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Background: Mitochondria could be an important target for ultraviolet radiation (UVR)-induced skin damage. Therefore, protecting mitochondria using mitochondria-targeted antioxidants may protect skin from UV-induced photodamage., Methods: In the present study, UVR-induced skin damage model was developed by irradiating male Wistar rats with UVB at a dose of 120 mJ/cm 2 , twice a week for a period of 5 weeks. Mito-TEMPO was administered intraperitoneally (0.1 mg/kg b.w.) twice a week for 5 weeks. After 5 weeks of treatment period, animals were sacrificed and the dorsal skin tissues were collected. Physical examinations of the skin for analyzing wrinkle formation and epidermal thickening were carried out. Skin tissues were used for the evaluation of histopathological changes, mitochondrial dysfunction analysis, and mitochondrial membrane potential., Results: Physical and histological examination showed that mito-TEMPO protected from the damaging effect of UVB radiation. A significant increase in mitochondrial reactive oxygen species (mtROS) generation with a concomitant increase in mitochondrial lipid peroxidation (mtLPO) was observed in UV-irradiated groups. UV-induced generation of mtROS and mtLPO formation was effectively reduced by mito-TEMPO. Mito-TEMPO pre-treatment improved mitochondrial complex II activity, which was significantly reduced in the UV-irradiated group., Conclusion: The results suggested that mito-TEMPO effectively protected skin tissue against UV-induced oxidative stress and damage., (© 2024 The Author(s). Photodermatology, Photoimmunology & Photomedicine published by John Wiley & Sons Ltd.)

Background: Butin is a naturally occurring compound with a wide range of medicinal properties, including anti-inflammatory, anti-arthritic, and antioxidant properties. Particulate matter 2.5 (PM 2.5 ) and ultraviolet B (UVB) radiation contribute to skin cell damage via the induction of oxidative stress., Methods: This study sought to assess the protective effects of butin against damage triggered by PM 2.5 and UVB in human HaCaT keratinocytes. Assessments were performed to evaluate cell viability, apoptosis, and cellular component damage., Results: Butin exhibited its protective ability via the inhibition of PM 2.5 -induced reactive oxygen species generation, lipid peroxidation, DNA damage, protein carbonylation, and mitochondrial damage. Butin reduced the PM 2.5 -induced c-Fos and phospho-c-Jun protein levels as well as mitogen-activated protein kinase. Furthermore, butin mitigated PM 2.5 - and UVB-induced apoptosis., Conclusion: Butin had the potential as a pharmaceutical candidate for treating skin damage caused by PM 2.5 and UVB exposure., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Photobiomodulation (PBM) has emerged as a potentially effective therapeutic approach to modulate cellular functions. This study aimed to examine the impact of PBM on reactive oxygen species (ROS), lipid peroxidation, and glutathione-related antioxidant defense systems in rabbit eye tissues. A polychromatic light source with an intensity of 2.6 J/cm 2 /min was used for PBM treatment in New Zealand White rabbits for 12 min. The PBM group (n = 8) received treatments every 2 days for a total of 12 sessions, whereas the control group (n = 8) did not undergo any PBM light exposure during the same period. The application of PBM significantly elevated ROS-mediated glutathione levels, along with increased activities of glutathione peroxidase and reductase, particularly in corneal tissue (p ≤ 0.05). In conclusion, PBM treatment effectively enhances antioxidant defense mechanisms in the eye, particularly in corneal tissue, suggesting its potential as a therapeutic strategy for managing oxidative stress-related ocular conditions., (© 2024 The Author(s). Journal of Biophotonics published by Wiley‐VCH GmbH.)

Naturally Occurring Radioactive Materials (NORM) contribute to everyone's natural background radiation dose. The technologically advanced activities of the gas and oil sectors produce considerable amounts of radioactive materials as industrial by-products or waste products. The goal of the current study is to estimate the danger of long-term liability to Technologically Enhanced Naturally Occurring Radioactive Materials (TE-NORM) on blood indices, neurotransmitters, oxidative stress markers, and β-amyloid in the cerebral cortex of rats' brains. Twenty adult male albino rats were divided into two equal groups (n = 10): control and irradiated. Irradiated rats were exposed to a total dose of 0.016 Gy of TE-NORM as a whole-body chronic exposure over a period of two months. It should be ''The results showed no significant changes in RBC count, Hb concentration, hematocrit percentage (HCT%), and Mean Corpuscular Hemoglobin Concentration (MCHC). However, there was a significant increase in the Mean Corpuscular Volume of RBCs (MCV) and a significant decrease in cell distribution width (RDW%) compared to the control. Alteration in neurotransmitters is noticeable by a significant increase in glutamic acid and significant decreases in serotonin and dopamine. Increased lipid peroxidation, decreased glutathione content, superoxide dismutase, catalase, and glutathione peroxidase activities indicating oxidative stress were accompanied by increased β-amyloid in the cerebral cortex of rats' brains. The findings of the present study showed that chronic radiation liability has some harmful effects, that may predict the risks of future health problems in occupational radiation exposure in the oil industries. Therefore, the control of exposure and application of sample dosimetry is recommended for health and safety., Competing Interests: Declaration of competing interest We would like to declare that there is NO any conflict of interest for any person to submit or publish the manuscript entitled “Hematological and neurological impact studies on the exposure to naturally occurring radioactive materials” in the journal of Applied Radiation and Isotopes., (Copyright © 2024. Published by Elsevier Ltd.)

The aim of this study was to investigate whether simultaneous irradiation at 660 and 808 nm generates different patterns of oxidative/antioxidative activities compared to consecutive irradiation. Primary cultures of gingival keratinocytes and fibroblasts were exposed to a diose laser (660 ± 2 nm and 808 ± 2 nm, 100 mW, 0.09 cm 2 spot area) using double irradiation with the two wavelengths (consecutive or simultaneous) for 6, 10, and 20 s. The two irradiation regimens did not increase cell viability in any of the experimental conditions. Lipid peroxidation was increased after consecutive irradiation in epithelial cells, which was not detected after simultaneous irradiation. After 20s of the simultaneous mode, ROS levels increased, but antioxidative balance decreased. In the fibroblasts, the two double irradiations induced ROS reduction, increase in lipid peroxidation, and improvement of antioxidative balance, mainly after the 20 s irradiation time. In conclusion, simultaneous and consecutive irradiation induced distinct oxidative stress modulation in oral epithelial cells and fibroblasts. The imbalance in the oxidative system observed after longer exposures, allied with the absence of a significant increase in the viability of the two cell types, suggests a contraindication for longer simultaneous irradiation in clinical situations that demand cellular stimulation., (© 2023 The American Society for Photobiology.)

In this paper, we demonstrated the biological effects of acute low-dose neutrons on the whole body of rats and investigated the impact of that level of neutron dose to induce an in vivo radio-adaptive response. To understand the radio-adaptive response, the examined animals were exposed to acute neutron radiation doses of 5 and 10 mSv, followed by a 50 mSv challenge dose after 14 days. After irradiation, all groups receiving single and double doses were kept in cages for one day before sampling. The electron paramagnetic resonance (EPR) method was used to estimate the radiation-induced radicals in the blood, and some hematological parameters and lipid peroxidation (MDA) were determined. A comet assay was performed beside some of the antioxidant enzymes [catalase enzyme (CAT), superoxide dismutase (SOD), and glutathione (GSH)]. Seven groups of adult male rats were classified according to their dose of neutron exposure. Measurements of all studied markers are taken one week after harvesting, except for hematological markers, within 2 h. The results indicated lower production of antioxidant enzymes (CAT by 1.18-5.83%, SOD by 1.47-17.8%, and GSH by 11.3-82.1%). Additionally, there was an increase in red cell distribution width (RDW) (from 4.61 to 25.19%) and in comet assay parameters such as Tail Length, (from 6.16 to 10.81 µm), Tail Moment, (from 1.17 to 2.46 µm), and percentage of DNA in tail length (DNA%) (from 9.58 to 17.32%) in all groups exposed to acute doses of radiation ranging from 5 to 50 mSv, respectively. This emphasizes the ascending harmful effect with the increased acute thermal neutron doses. The values of the introduced factor of radio adaptive response for all markers under study reveal that the lower priming dose promotes a higher adaptation response and vice versa. Ultimately, the results indicate significant variations in DNA%, SOD enzyme levels, EPR intensity, total Hb concentration, and RDWs, suggesting their potential use as biomarkers for acute thermal neutron dosimetry. Further research is necessary to validate these measurements as biodosimetry for radiation exposure, including investigations involving the response impact of RAR with varied challenge doses and post-irradiation behavior., (© 2024. The Author(s).)

Background: Exposure to environmental stressors like particulate matter (PM) and ultraviolet radiation (UV) induces cutaneous oxidative stress and inflammation and leads to skin barrier dysfunction and premature aging. Metals like iron or copper are abundant in PM and are known to contribute to reactive oxygen species (ROS) production., Aims: Although it has been suggested that topical antioxidants may be able to help in preventing and/or reducing outdoor skin damage, limited clinical evidence under real-life exposure conditions have been reported. The aim of the present study was to evaluate the ability of a topical serum containing 15% ascorbic acid, 0.5% ferulic acid, and 1% tocopherol (CF Mix) to prevent oxinflammatory skin damage and premature aging induced by PM + UV in a human clinical trial., Methods: A 4-day single-blinded, clinical study was conducted on the back of 15 females (18-40 years old). During the 4 consecutive days, the back test zones were treated daily with or without the CF Mix, followed by with/without 2 h of PM and 5 min of UV daily exposure., Results: Application of the CF Mix prevented PM + UV-induced skin barrier perturbation (Involucrin and Loricrin), lipid peroxidation (4HNE), inflammatory markers (COX2, NLRP1, and AhR), and MMP9 activation. In addition, CF Mix was able to prevent Type I Collagen loss., Conclusion: This is the first human study confirming multipollutant cutaneous damage and suggesting the utility of a daily antioxidant topical application to prevent pollution induced skin damage., (© 2024 The Authors. Journal of Cosmetic Dermatology published by Wiley Periodicals LLC.)

This study summarizes the response of cyanobacterium Spirulina subsalsa HKAR-19 under simulated light conditions of photosynthetically active radiation (PAR), PAR+UV-A (PA), and PAR+UV-A+UV-B (PAB). Exposure to UV radiation caused a significant (P < 0.05) decrease in chlorophyll a, phycocyanin, and total protein. In contrast, total carotene content increased significantly (P < 0.05) under PA and PAB with increasing irradiation time. The photosynthetic efficiency of photosystem II also decreased significantly in PA and PAB radiation. We have also recorded a decrease in the fluorescence emission intensity of phycocyanin under PA and PAB exposure. The phycocyanin fluorescence shifted towards shorter wavelengths (blue-shift) after 72 h of PA and PAB exposure. Intracellular reactive oxygen species (ROS) levels increased significantly in PA and PAB. Fluorescence microscopic images showed an increase in green fluorescence, indicating ROS generation in UV radiation. We have also quantified ROS generation using green and red fluorescence ratio represented as G/R ratio. A 2-6-fold increase in antioxidative enzymes activity was observed to overcome the damaging effects caused by UV stress as compared to untreated control cultures. The lipid peroxidation was assessed in terms of malondialdehyde content which increases significantly (P < 0.05) as the duration of exposure increases. These results suggest that a combined effect of PAR, UV-A, and UV-B was more deleterious than an individual one., (© 2023. Institute of Microbiology, Academy of Sciences of the Czech Republic, v.v.i.)

Purpose: The products of lipid peroxidation have been implicated in human diseases and aging. This prompted us to investigate the response to conventional (CONV) versus FLASH irradiation of oxylipins, a family of bioactive lipid metabolites derived from omega-3 or omega-6 polyunsaturated fatty acids through oxygen-dependent non-enzymatic as well as dioxygenase-mediated free radical reactions., Methods and Materials: Ultrahigh performance liquid chromatography coupled to tandem mass spectrometry was used to quantify the expression of 37 oxylipins derived from eicosatetraenoic, eicosapentaenoic and docosahexaenoic acid in mouse lung and in normal or cancer cells exposed to either radiation modality under precise monitoring of the temperature and oxygenation. Among the 37 isomers assayed, 14-16 were present in high enough amount to enable quantitative analysis. The endpoints were the expression of oxylipins as a function of the dose of radiation, normoxia versus hypoxia, temperature and post-irradiation time., Results: In normal, normoxic cells at 37°C radiation elicited destruction and neosynthesis of oxylipins acting antagonistically on a background subject to rapid remodeling by oxygenases. Neosynthesis was observed in the CONV mode only, in such a way that the level of oxylipins at 5 minutes after FLASH irradiation was 20-50% lower than in non-irradiated and CONV-irradiated cells. Hypoxia mitigated the differential CONV versus FLASH response in some oxylipins. These patterns were not reproduced in tumor cells. Depression of specific oxylipins following FLASH irradiation was observed in mouse lung at 5 min following irradiation, with near complete recovery in 24 hours and further remodeling at one week and two months post-irradiation., Conclusions: Down-regulation of oxylipins was a hallmark of FLASH irradiation specific of normal cells. Temperature effects suggest that this process occurs via diffusion-controlled, bimolecular recombination of a primary radical species upstream from peroxyl radical formation and evoke a major role of the membrane composition and fluidity in response to the FLASH modality., (Copyright © 2024 Elsevier Inc. All rights reserved.)

UVA exposure disturbs the metabolism of skin cells, often inducing oxidative stress and inflammation. Therefore, there is a need for bioactive compounds that limit such consequences without causing undesirable side effects. The aim of this study was to analyse in vitro the effects of the phytocannabinoids cannabigerol (CBG) and cannabidiol (CBD), which differ in terms of biological effects. Furthermore, the combined use of both compounds (CBG+CBD) has been analysed in order to increase their effectiveness in human skin fibroblasts and keratinocytes protection against UVA-induced alternation. The results obtained indicate that the effects of CBG and CBD on the redox balance might indeed be enhanced when both phytocannabinoids are applied concurrently. Those effects include a reduction in NOX activity, ROS levels, and a modification of thioredoxin-dependent antioxidant systems. The reduction in the UVA-induced lipid peroxidation and protein modification has been confirmed through lower levels of 4-HNE-protein adducts and protein carbonyl groups as well as through the recovery of collagen expression. Modification of antioxidant signalling (Nrf2/HO-1) through the administration of CBG+CBD has been proven to be associated with reduced proinflammatory signalling (NFκB/TNFα). Differential metabolic responses of keratinocytes and fibroblasts to the effects of the UVA and phytocannabinoids have indicated possible beneficial protective and regenerative effects of the phytocannabinoids, suggesting their possible application for the purpose of limiting the harmful impact of the UVA on skin cells.

UV irradiation significantly alters nanoplastics (NPs) physicochemical properties, thus affecting their biological toxicity. This study is the first to assess the influence of virgin and UV-aged polystyrene NPs (v-PS NPs, a-PS NPs) on the intestinal barrier of ICR mice. We found that a-PS NPs can cause more severe intestinal barrier damage compared with v-PS NPs. The reason may be attributed to that a-PS NPs produced more ROS in intestinal tissue. Moreover, the strong oxidizing property of hydroxyl radicals (·OH) generated from the a-PS NPs can damage cell membranes through lipid peroxidation, thereby leading to a low clearance rate of ·OH due to the impaired intestinal tissue function, in turn, causing more ROS to accumulate and inducing severe oxidative damage. This research underscores the crucial role of ·OH in mediating oxidative damage from UV-aged nanoparticles, emphasizing the need to consider environmental factors in assessing NPs toxicity., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

The prevalence of Light-emitting diodes (LEDs) has exposed us to an excessive amount of blue light (BL) which causes various ophthalmic diseases. Previous studies have shown that conjunctiva is vulnerable to BL. In this study, we aimed to investigate the underlying mechanism of BL-induced injury in conjunctiva. We placed C57BL/6 mice and human conjunctival epithelial cell lines (HCECs) under BL (440 nm ± 15 nm, 0.2 mW/cm 2 ) to establish a BL injury model in vivo and in vitro. Immunohistochemistry and MDA assay were used to identify lipid peroxidation (LPO) in vivo. HE staining was applied to detect morphological damage of conjunctival epithelium. DCFH-DA, C11-BODIPY 581/591, Calcein-AM, and FeRhoNox™-1 probes were performed to identify ferroptosis levels in vitro. Real-time qPCR and Western blotting techniques were employed to uncover signaling pathways of blue light-induced ferroptosis. Our findings demonstrated that BL affected tear film instability and induced conjunctival epithelium injury in vivo. Ferrostatin-1 significantly alleviated blue light-induced ferroptosis in vivo and in vitro. BL downregulates the levels of solute carrier family 7 member 11 (SLC7A11), Ferritin heavy chain (FTH1), and glutathione peroxidase (GPX4) by inhibiting the activation and translocation of the Signal transducer and activator of transcription 3 (STAT3) from inducing Fe 2+ burst, ROS and LPO accumulation, ultimately resulting in ferroptosis. This study will offer new insight into BL-induced conjunctival injury and LED-induced dry eye., Competing Interests: Declaration of competing interest There are no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier B.V.)

Background: This work was carried out to compare the modifying roles of ascorbic and metformin during Ehrlich (ESC) tumor-bearing mice irradiation., Methods: Fifty Swiss albino male mice were segmented into seven groups, including one control group and six Ehrlich induced tumors treated with ascorbic, ascorbic plus radiation, metformin, metformin plus radiation, and radiation only. Many tests, including behavioral, biochemical, immunohistochemistry, gene expression, DNA fragmentation, oxidative stress markers, and EPR, were performed to interrogate the modifying effects on tumor and liver tissues., Results: Remarkable apoptosis was found in metformin irradiated animals compared to irradiated ascorbic counterparts. The irradiated metformin mice showed the greatest reduction in PCNA. There was a significant reduction of DNA fragmentation in the liver tissues of the irradiated metformin group. Irradiated metformin and irradiated ascorbic acid animals showed a reduced signal of ERK as well as c-Fos genes. There was a tendency of metformin and metformin irradiated animals to reduce MDA levels in liver tissues. ESC-bearing mice treated with ascorbic or metformin showed an improvement in the spontaneous alternation percentage (SAP%) and improved short-term memory. There was also an improvement in long memory tests., Conclusions: The study added more preclinical evidence on the utility of metformin in cancer treatment during radiotherapy. Metformin was shown to reduce lipid peroxidation in irradiated healthy tissues, increase tumor cytotoxicity, downregulate critical pathways involved in tumor progression and proliferation, and enhance tumor apoptosis. Controlled clinical trials using metformin are highly warranted., (Copyright © 2022. Published by Elsevier Ltd.)

Oxidative stress and lipid peroxidation are major causes of skin injury induced by ultraviolet (UV) irradiation. Ferroptosis is a form of regulated necrosis driven by iron-dependent peroxidation of phospholipids and contributes to kinds of tissue injuries. However, it remains unclear whether the accumulation of lipid peroxides in UV irradiation-induced skin injury could lead to ferroptosis. We generated UV irradiation-induced skin injury mice model to examine the accumulation of the lipid peroxides and iron. Lipid peroxides 4-HNE, the oxidative enzyme COX2, the oxidative DNA damage biomarker 8-OHdG, and the iron level were increased in UV irradiation-induced skin. The accumulation of iron and lipid peroxidation was also observed in UVB-irradiated epidermal keratinocytes without actual ongoing ferroptotic cell death. Ferroptosis was triggered in UV-irradiated keratinocytes stimulated with ferric ammonium citrate (FAC) to mimic the iron overload. Although GPX4 protected UVB-injured keratinocytes against ferroptotic cell death resulted from dysregulation of iron metabolism and the subsequent increase of lipid ROS, keratinocytes enduring constant UVB treatment were markedly sensitized to ferroptosis. Nicotinamide mononucleotide (NMN) which is a direct and potent NAD + precursor supplement, rescued the imbalanced NAD + /NADH ratio, recruited the production of GSH and promoted resistance to lipid peroxidation in a GPX4-dependent manner. Taken together, our data suggest that NMN recruits GSH to enhance GPX4-mediated ferroptosis defense in UV irradiation-induced skin injury and inhibits oxidative skin damage. NMN or ferroptosis inhibitor might become promising therapeutic approaches for treating oxidative stress-induced skin diseases or disorders., (Copyright © 2021 The Authors. Published by Elsevier B.V. All rights reserved.)

Radiotherapy promotes tumor cell death and senescence through the induction of oxidative damage. Recent work has highlighted the importance of lipid peroxidation for radiotherapy efficacy. Excessive lipid peroxidation can promote ferroptosis, a regulated form of cell death. In this review, we address the evidence supporting a role of ferroptosis in response to radiotherapy and discuss the molecular regulators that underlie this interaction. Finally, we postulate on the clinical implications for the intersection of ferroptosis and radiotherapy.

UV radiation is known to induce a multiple changes in the metabolism of skin-building cells, what can affect the functioning not only neighboring cells, but also, following signal transduction releasing into the blood vessels, the entire body. Therefore, the aim of this study was to analyze the proteomic disturbances occurred in plasma of chronically UVA/UVB irradiated rats and define the effect on these changes of skin topically applied cannabidiol (CBD). Obtained results showed significant changes in the expression of numerous anti-inflammatory and signaling proteins including: NFκB inhibitor, 14-3-3 protein, protein kinase C, keratin, and protein S100 after UV irradiation and CBD treatment. Moreover, the effects of UVA and UVB were manifested by increased level of lipid peroxidation products-protein adducts formation. CBD partially prevented all of these changes, but in a various degree depending on the UV radiation type. Moreover, topical treatment with CBD resulted in the penetration of CBD into the blood and, as a consequence, in direct modifications to the plasma protein structure by creating CBD adducts with molecules, such as proline-rich protein 30, transcription factor 19, or N-acetylglucosamine-6-sulfatase, what significantly changed the activity of these proteins. In conclusion, it may be suggested that CBD applied topically may be an effective compound against systemic UV-induced oxidative stress, but its effectiveness requires careful analysis of CBD's effects on other tissues of the living organism., (© 2021. The Author(s).)

In recent decades, atmospheric pollution led to a progressive reduction of the ozone layer with a consequent increase in UV-B radiation. Despite the high adaptation of olive trees to the Mediterranean environment, the progressive increase of UV-B radiation is a risk factor for olive tree cultivation. It is therefore necessary to understand how high levels of UV-B radiation affect olive plants and to identify olive varieties which are better adapted. In this study we analyzed two Italian olive varieties subjected to chronic UV-B stress. We focused on the effects of UV-B radiation on RubisCO, in terms of quantity, enzymatic activity and isoform composition. In addition, we also analyzed changes in the activity of antioxidant enzymes (SOD, CAT, GPox) to get a comprehensive picture of the antioxidant system. We also evaluated the effects of UV-B on the enzyme sucrose synthase. The overall damage at biochemical level was also assessed by analyzing changes in Hsp70, a protein triggered under stress conditions. The results of this work indicate that the varieties (Giarraffa and Olivastra Seggianese) differ significantly in the use of specific antioxidant defense systems, as well as in the activity and isoform composition of RubisCO. Combined with a different use of sucrose synthase, the overall picture shows that Giarraffa optimized the use of GPox and opted for a targeted choice of RubisCO isoforms, in addition to managing the content of sucrose synthase, thereby saving energy during critical stress points.

Lipid oxidation is ubiquitous in cell life under oxygen and essential for photodynamic therapy (PDT) of carcinomas. However, the mechanisms underlying lipid oxidation in rather complex systems such as plasma membranes remain elusive. Herein, Langmuir monolayers were assembled with the lipid extract of glandular breast cancer (MCF7) cells and used to probe the molecular interactions allowing adsorption of the photosensitizer (PS) erythrosine B and subsequent photooxidation outcomes. Surface pressure (π) versus area (cm 2 /mL) isotherms of MCF7 lipid extract shifted to larger areas upon erythrosine incorporation, driven by secondary interactions that affected the orientation of the carbonyl groups and lipid chain organization. Light-irradiation increased the surface area of the MCF7 lipid extract monolayer containing erythrosine owing to the lipid hydroperoxidation, which may further undergo decomposition, resulting in the chain cleavage of phospholipids and membrane permeabilization. Incorporation of erythrosine by MCF7 cells induced slight toxic effects on in vitro assays, differently of the severe phototoxicity caused by light-irradiation, which significantly decreased cell viability by more than 75% at 2.5 × 10 -6 mol/L of erythrosine incubated for 3 and 24 h, reaching nearly 90% at 48 h of incubation. The origin of the phototoxic effects is in the rupture of the plasma membrane shown by the frontal (FSC) and side (SSC) light scattering of flow cytometry. Consistent with hydroperoxide decomposition, membrane permeabilization was also confirmed by cleaved lipids detected in mass spectrometry and subsidizes the necrotic pathway of cell death., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Radon inhalation decreases the level of lipid peroxide (LPO); this is attributed to the activation of antioxidative functions. This activation contributes to the beneficial effects of radon therapy, but there are no studies on the risks of radon therapy, such as DNA damage. We evaluated the effect of radon inhalation on DNA damage caused by oxidative stress and explored the underlying mechanisms. Mice were exposed to radon inhalation at concentrations of 2 or 20 kBq/m3 (for one, three, or 10 days). The 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels decreased in the brains of mice that inhaled 20 kBq/m3 radon for three days and in the kidneys of mice that inhaled 2 or 20 kBq/m3 radon for one, three or 10 days. The 8-OHdG levels in the small intestine decreased by approximately 20-40% (2 kBq/m3 for three days or 20 kBq/m3 for one, three or 10 days), but there were no significant differences in the 8-OHdG levels between mice that inhaled a sham treatment and those that inhaled radon. There was no significant change in the levels of 8-oxoguanine DNA glycosylase, which plays an important role in DNA repair. However, the level of Mn-superoxide dismutase (SOD) increased by 15-60% and 15-45% in the small intestine and kidney, respectively, following radon inhalation. These results suggest that Mn-SOD probably plays an important role in the inhibition of oxidative DNA damage., (© The Author(s) 2021. Published by Oxford University Press on behalf of The Japanese Radiation Research Society and Japanese Society for Radiation Oncology.)

The mammalian target of rapamycin (mTOR) is a sensor of nutrient status and plays an important role in cell growth and metabolism. Although inhibition of mTOR signaling promotes tumor cell death and several mTOR inhibitors have been used clinically, recent reports have shown that co-treatment with MHY1485, an mTOR activator, enhances the anti-cancer effects of anti-PD-1 antibody and 5-fluorouracil. However, it remains unclear whether MHY1485 treatment alters the effects of radiation on tumor cells. In this study, the radiosensitizing effects of MHY1485 were investigated using murine CT26 and LLC cell lines. We examined mTOR signaling, tumor cell growth, colony formation, apoptosis, senescence, oxidative stress, p21 accumulation and endoplasmic reticulum (ER) stress levels in cells treated with MHY1485 and radiation, either alone or together. We found that MHY1485 treatment inhibited growth and colony formation in both cell lines under irradiation and no-irradiation conditions, results that were not fully consistent with MHY1485's known role in activating mTOR signaling. Furthermore, we found that combined treatment with MHY1485 and radiation significantly increased apoptosis and senescence in tumor cells in association with oxidative stress, ER stress and p21 stabilization, compared to radiation treatment alone. Our results suggested that MHY1485 enhances the radiosensitivity of tumor cells by a mechanism that may differ from MHY1485's role in mTOR activation., (© The Author(s) 2021. Published by Oxford University Press on behalf of The Japanese Radiation Research Society and Japanese Society for Radiation Oncology.)

Graves' disease (GD), the most common cause of hyperthyroidism, is an autoimmune disease directly caused by circulating autoantibodies that bind and activate the TSH receptor, inducing metabolic activation of the thyroid gland; this may be associated with important cardiac (atrial fibrillation) and ocular (ophthalmopathy) complications. Treating GD with real curative intent implies the full elimination of the functioning thyroid parenchyma using surgery or radioactive iodine therapy (RAI). RAI has been used in humans with hyperthyroidism since 1941, thanks to the pioneering work of a physician (Dr. Saul Hertz) and a physicist (Dr. Arthur Roberts). The rationale of RAI is based on the effect of radiation of 131 I on target cells leading to DNA damage, both directly, through breakage of molecular bonds, and indirectly through the formation of free radicals. In particular, irradiation causes a broad spectrum of cellular damage due to the production of reactive oxygen species and lipid peroxidation of the plasma membrane. Thus, RAI-related cellular death takes place through both apoptosis and necrosis. The aim of this review was to summarize indications, efficacy, safety profile, and dosimetric aspects of RAI treatment in patients affected by GD.

Ultraviolet (UV) irradiation is an important risk factor in cataractogenesis. Lens epithelial cells (LECs), which are a highly metabolically active part of the lens, play an important role in UV-induced cataractogenesis. The purpose of this study was to characterize cell compounds such as nucleic acids, proteins, and lipids in human UV C-irradiated anterior lens capsules (LCs) with LECs, as well as to compare them with the control, non-irradiated LCs of patients without cataract, by using synchrotron radiation-based Fourier transform infrared (SR-FTIR) micro-spectroscopy. In order to understand the effect of the UV C on the LC bio-macromolecules in a context of cataractogenesis, we used the SR-FTIR micro-spectroscopy setup installed on the beamline MIRAS at the Spanish synchrotron light source ALBA, where measurements were set to achieve a single-cell resolution with high spectral stability and high photon flux. UV C irradiation of LCs resulted in a significant effect on protein conformation with protein formation of intramolecular parallel β-sheet structure, lower phosphate and carboxyl bands in fatty acids and amino acids, and oxidative stress markers with significant increase of lipid peroxidation and diminishment of the asymmetric CH 3 band.

The discovery of regulated cell death processes has enabled advances in cancer treatment. In the past decade, ferroptosis, an iron-dependent form of regulated cell death driven by excessive lipid peroxidation, has been implicated in the development and therapeutic responses of various types of tumours. Experimental reagents (such as erastin and RSL3), approved drugs (for example, sorafenib, sulfasalazine, statins and artemisinin), ionizing radiation and cytokines (such as IFNγ and TGFβ1) can induce ferroptosis and suppress tumour growth. However, ferroptotic damage can trigger inflammation-associated immunosuppression in the tumour microenvironment, thus favouring tumour growth. The extent to which ferroptosis affects tumour biology is unclear, although several studies have found important correlations between mutations in cancer-relevant genes (for example, RAS and TP53), in genes encoding proteins involved in stress response pathways (such as NFE2L2 signalling, autophagy and hypoxia) and the epithelial-to-mesenchymal transition, and responses to treatments that activate ferroptosis. Herein, we present the key molecular mechanisms of ferroptosis, describe the crosstalk between ferroptosis and tumour-associated signalling pathways, and discuss the potential applications of ferroptosis in the context of systemic therapy, radiotherapy and immunotherapy.

d-Galactosamine (d-GalN) is a well-known toxin that causes many metabolic and morphological abnormalities resulting in advanced renal failure and liver damage. Occupational exposure to low-level ionizing radiation (<1 Gy) was shown to enhance cell protection via attenuating an established inflammatory process. The present study was therefore aimed to investigate the protective impact of Amphora coffaeiformis extract and low dose gamma radiation against d-GalN induced renal damage in rats. Forty-eight adult male Swiss albino rats were distributed equally into eight groups. The measurements included antioxidants activities (superoxide dismutase, catalase and glutathione peroxidase) as well as lipid peroxidation level in kidney tissue. Also, kidney function tests and inflammatory markers (tumor necrosis factor alpha and nuclear factor kappa-light-chain-enhancer of activated B cells) were measured. Additionally, relative quantification of kidney nuclear factor erythroid 2-related factor 2 (Nrf-2) gene was estimated. Histopathological examination was also performed in kidney tissue. The results revealed decreases in antioxidant activities and downregulation of Nrf-2 expression accompanied by increases in lipid peroxidation level, kidney function tests and inflammatory markers in d-GaIN group. The treatment with Amphora algal extract and low dose gamma radiation ameliorated the previous measurements which were harmony with histopathological findings. In conclusion, A coffaeiformis extract and low dose gamma radiation provided marked functional and histological effects in the treating acute renal damage induced by d-GalN in rats., (© 2020 Wiley Periodicals LLC.)

Photobiomodulation with 808 nm laser light electively stimulates Complexes III and IV of the mitochondrial respiratory chain, while Complexes I and II are not affected. At the wavelength of 1064 nm, Complexes I, III, and IV are excited, while Complex II and some mitochondrial matrix enzymes seem to be not receptive to photons at that wavelength. Complex IV was also activated by 633 nm. The mechanism of action of wavelengths in the range 900-1000 nm on mitochondria is less understood or not described. Oxidative stress from reactive oxygen species (ROS) generated by mitochondrial activity is an inescapable consequence of aerobic metabolism. The antioxidant enzyme system for ROS scavenging can keep them under control. However, alterations in mitochondrial activity can cause an increment of ROS production. ROS and ATP can play a role in cell death, cell proliferation, and cell cycle arrest. In our work, bovine liver isolated mitochondria were irradiated for 60 sec, in continuous wave mode with 980 nm and powers from 0.1 to 1.4 W (0.1 W increment at every step) to generate energies from 6 to 84 J, fluences from 7.7 to 107.7 J/cm 2 , power densities from 0.13 to 1.79 W/cm 2 , and spot size 0.78 cm 2 . The control was equal to 0 W. The activity of the mitochondria's complexes, Krebs cycle enzymes, ATP production, oxygen consumption, generation of ROS, and oxidative stress were detected. Lower powers (0.1-0.2 W) showed an inhibitory effect; those that were intermediate (0.3-0.7 W) did not display an effect, and the higher powers (0.8-1.1 W) induced an increment of ATP synthesis. Increasing the power (1.2-1.4 W) recovered the ATP production to the control level. The interaction occurred on Complexes III and IV, as well as ATP production and oxygen consumption. Results showed that 0.1 W uncoupled the respiratory chain and induced higher oxidative stress and drastic inhibition of ATP production. Conversely, 0.8 W kept mitochondria coupled and induced an increase of ATP production by increments of Complex III and IV activities. An augmentation of oxidative stress was also observed, probably as a consequence of the increased oxygen consumption and mitochondrial isolation experimental conditions. No effect was observed using 0.5 W, and no effect was observed on the enzymes of the Krebs cycle., Competing Interests: The authors declare no conflicts of interest., (Copyright © 2021 Andrea Amaroli et al.)

Ultraviolet B (UVB) light corresponds to 5% of ultraviolet radiation. It is more genotoxic and mutagenic than UVA and causes direct and indirect cellular damage through the generation of reactive oxygen species (ROS). Even after radiation, ROS generation may continue through activation of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) enzyme. Long-term exposure can progress to premature skin aging and photocarcinogenesis. To prevent damage that is caused by UVB radiation, several studies have focused on the topical administration of compounds that have antioxidant properties. 2-Acetylphenothiazine (ML171) is a potent and selective inhibitor of NOX1. The present study investigated the antioxidant potential and photoprotective ability of ML171 in UVB-irradiated L929 fibroblasts. ML171 had considerable antioxidant activity in both the DPPH • and xanthine/luminol/xanthine oxidase assays. ML171 did not induce cytotoxicity in L929 fibroblasts and increased the viability of UVB-irradiated cells. ML171 also inhibited ROS production, the enzymatic activity of NOX, depolarization of the mitochondrial membrane, and DNA damage. Additionally, ML171 protected cell membrane integrity and induced fibroblast migration. These results suggest that the incorporation of ML171 in topical administration systems may be a promising strategy to mitigate UVB-induced oxidative damage in L929 fibroblasts., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Exposure to reactive oxygen species can easily result in serious diseases, such as hyperproliferative skin disorders or skin cancer. Herbal extracts are widely used as antioxidant sources in different compositions. The importance of antioxidant therapy in inflammatory conditions has increased. Innovative formulations can be used to improve the effects of these phytopharmacons. The bioactive compounds of Plantago lanceolata (PL) possess different effects, such as anti-inflammatory, antioxidant, and bactericidal pharmacological effects. The objective of this study was to formulate novel liquid crystal (LC) compositions to protect Plantago lanceolata extract from hydrolysis and to improve its effect. Since safety is an important aspect of pharmaceutical formulations, the biological properties of applied excipients and blends were evaluated using assorted in vitro methods on HaCaT cells. According to the antecedent toxicity screening evaluation, three surfactants were selected (Gelucire 44/14, Labrasol, and Lauroglycol 90) for the formulation. The dissolution rate of PL from the PL-LC systems was evaluated using a Franz diffusion chamber apparatus. The antioxidant properties of the PL-LC systems were evaluated with 2,2-diphenyl-1-picrylhydrazyl (DPPH) and malondialdehyde (MDA) assessments. Our results suggest that these compositions use a nontraditional, rapid-permeation pathway for the delivery of drugs, as the applied penetration enhancers reversibly alter the barrier properties of the outer stratum corneum. These excipients can be safe and highly tolerable thus, they could improve the patient's experience and promote adherence.

Ultra-violet (UV) radiation (UVR) causes significant oxidative injury to retinal pigment epithelium (RPE) cells. Obacunone is a highly oxygenated triterpenoid limonoid compound with various pharmacological properties. Its potential effect in RPE cells has not been studied thus far. Here in ARPE-19 cells and primary murine RPE cells, obacunone potently inhibited UVR-induced reactive oxygen species accumulation, mitochondrial depolarization, lipid peroxidation and single strand DNA accumulation. UVR-induced RPE cell death and apoptosis were largely alleviated by obacunone. Obacunone activated Nrf2 signaling cascade in RPE cells, causing Keap1-Nrf2 disassociation, Nrf2 protein stabilization and nuclear translocation. It promoted transcription and expression of antioxidant responsive element-dependent genes. Nrf2 silencing or CRISPR/Cas9-induced Nrf2 knockout almost reversed obacunone-induced RPE cytoprotection against UVR. Forced activation of Nrf2 cascade, by Keap1 knockout, similarly protected RPE cells from UVR. Importantly, obacunone failed to offer further RPE cytoprotection against UVR in Keap1-knockout cells. In vivo , intravitreal injection of obacunone largely inhibited light-induced retinal damage. Collectively, obacunone protects RPE cells from UVR-induced oxidative injury through activation of Nrf2 signaling cascade.

Not much information is available to substantiate the possible role of γ -aminobutyric acid (GABA) signaling in mitigating water-deficit stress in snap bean ( Phaseolus vulgaris L.) plants under semiarid conditions. Present work aims to investigate the role of exogenous GABA (foliar application; 0.5, 1 and 2 mM) in amelioration of drought stress and improvement of field performance on snap bean plants raised under two drip irrigation regimes (100% and 70% of water requirements). Water stress led to significant reduction in plant growth, leaf relative water content (RWC), cell membrane stability index (CMSI), nutrient uptake (N, P, K, Ca, Fe and Zn), pod yield and its content from protein and total soluble solids (TSS). Meanwhile, lipid peroxidation (malondialdehyde content- MDA), osmolyte content (free amino acids- FAA, proline, soluble sugars) antioxidative defense (activity of superoxide dismutase- SOD, catalase- CAT, peroxidase- POX and ascorbate peroxidase- APX) and the pod fiber content exhibited significantly increase due to water stress. Exogenous GABA application (especially at 2 mM) revealed partial normalization of the effects of drought stress in snap bean plants. GABA-induced mitigation of drought stress was manifested by improvement in growth, water status, membrane integrity, osmotic adjustment, antioxidant defense and nutrient acquisition. Furthermore, GABA application during water stress in snap bean plants resulted in improvement of field performance being manifested by increased pod yield and its quality attributes. To sum up, exogenous GABA appears to function as an effective priming molecule to alleviate drought stress in snap bean plants under semiarid conditions.

Purpose: Baicalein (an anti-ferroptosis drug) was recently reported to synergistically improve the survival rate of mice following a high dose of total body irradiation with anti-apoptosis and anti-necroptosis drugs. At the same time, our group has demonstrated that ferrostatin-1, a ferroptosis inhibitor, improves the survival rate of a mouse model of hematopoietic acute radiation syndrome to 60% for 150 days ( p  < .001). These phenomena suggest that ferroptosis inhibition can mitigate radiation damage. In this study, we continued to study the mechanisms by which ferrostatin-1 alleviated radiation-induced ferroptosis and subsequent hematopoietic acute radiation syndrome., Materials and Methods: Male ICR mice (8-10 weeks old) were exposed to doses of 0, 8, or 10 Gy irradiated from a 137 Cs source. Ferrostatin-1 was intraperitoneally injected into mice 72 h post-irradiation. Bone marrow mononuclear cells (BMMCs) and peripheral blood cells were counted. The changes in iron-related parameters, lipid metabolic enzymes, lipid peroxidation repair molecules (glutathione peroxidase 4, glutathione, and coenzyme Q10), and inflammatory factors (TNF-α, IL-6, and IL-1β) were evaluated using biochemical or antibody techniques., Results: Ferrostatin-1 increased the number of red and white blood cells, lymphocytes, and monocytes in the peripheral blood after total body irradiation in mice by mitigating the ferroptosis of BMMCs. Total body irradiation induced ferroptosis in BMMCs by increasing the iron and lipid peroxidation levels and depleting the acyl-CoA synthetase long-chain family member 4 (ASCL4), lipoxygenase 15, glutathione peroxidase 4, and glutathione levels. Ferroptotic BMMCs did not release TNF-α, IL-6, or IL-1β at the early stage of radiation exposure. Ferrostatin-1 mitigated the lipid peroxidation of radiation-induced ferroptosis by attenuating increases in levels of hemosiderin and liable iron pool and decreases in levels of ASCL4 and glutathione peroxidase 4., Conclusions: The onset of total body irradiation-induced ferroptosis in BMMCs involved changes in iron, lipid metabolic enzymes, and anti-lipid peroxidation molecules. Ferrostatin-1 could be a potential radiation mitigation agent by acting on these targets.

Plants often encounter light intensities exceeding the capacity of photosynthesis (excessive light) mainly due to biotic and abiotic factors, which lower CO 2 fixation and reduce light energy sinks. Under excessive light, the photosynthetic electron transport chain generates damaging molecules, hence leading to photooxidative stress and eventually to cell death. In this review, we summarize the mechanisms linking the excessive absorption of light energy in chloroplasts to programmed cell death in plant leaves. We highlight the importance of reactive carbonyl species generated by lipid photooxidation, their detoxification, and the integrating role of the endoplasmic reticulum in the adoption of phototolerance or cell-death pathways. Finally, we invite the scientific community to standardize the conditions of excessive light treatments., (Copyright © 2020 The Author. Published by Elsevier Inc. All rights reserved.)

To understand how olives reconfigure their metabolism to face stress shock episodes, plants from the economically relevant olive ( Olea europaea cv. Cobrançosa) were exposed to high UV-B radiation (UV-B, 12 kJ m -2 d -1 ) or heat shock (HS, 40 °C) for two consecutive days. The physiological responses and some important lipophilic compounds were evaluated immediately (day 0) and 30 days after UV-B or HS episodes. Both treatments induced a reduction of the olive physiological performance, particularly increasing cell membrane damages and proline pool and at the same time reducing chlorophyll levels, the quantum yield of photosystem II (Φ PSII ), and the efficiency of excitation energy capture by open photosystem II (PSII) reaction centers ( F' v / F' m ). Nevertheless, the HS episode caused more adverse effects, additionally reducing the pool of protective pigments (carotenoids) and the maximum efficiency of PSII (with F 0 increase). In the UV-B treatment, despite the higher lipid peroxidation, the activation of some stress protective mechanisms ( e . g ., increase of NPQ and carotenoids and remobilization of some metabolites, such as phytol and proline) might have contributed to avoiding photoinhibition. Thirty days after stress relief, the performance of olives from both treatments recovered similarly, in part due to the metabolites' adjustments that contributed to strengthened stress protection (an increase of long-chain alkanes) and provided energy (through the use of soluble sugars, mannitol, and myo-inositol) for re-establishment. Other metabolites, like anthocyanins and squalene, also have an important role in responding specifically to HS or UV-B recovery for helping in the oxidative damage control. These data contribute to understanding how young olive plants may deal with climatic episodes when being transferred from nurseries to field orchards, under the actual context of climate change.

Background: UV radiation and its impact on living organisms became an essential concern over the past three decades and will be essential in the years to come. So, the present investigation was devoted to examining the impact of artificial UV-B radiation on the accumulation of amino acids and MDA contents as well as some antioxidant enzymes activities in three freshwater cyanobacterial species; Planktothrix cryptovaginata, Nostoc carneum and Microcystis aeruginosa , one freshwater green alga; Scenedesmus acutus and one marine cyanobacterium; Microcystis ., Methods: The algal cultures were exposed directly to artificial UV-B radiation for 1, 3, 5, and 7 hours and amino acids, MDA contents, and the antioxidant enzyme activities; CAT, POD, APX, and SOD were analyzed., Results: The data obtained indicated that alteration in MDA and antioxidant enzymes by UV stress depends on the algal species and the exposure time. The treatment of the investigated algae with different periods of UV-B exposure stimulated the biosynthesis of some individual amino acids and inhibited the accumulation of some others. In some cases, exposure to UV-B was accompanied by the disappearance of some amino acids. In addition, UV-B exposure for 3 hours stimulated the accumulation of total amino acids in M. aeruginosa and S. acutus , while 7 hours of UV-B enhanced the biosynthesis of total amino acids in M. aeruginosa only from the investigated algae., Conclusion: Exposure of some cyanobacteria and green algae to UV-B radiation stimulated the biosynthesis of some individual amino acids and inhibited the accumulation or accompanied by the disappearance of some others. However, the alteration in MDA and antioxidant enzymes by UV stress depends on the algal species and the exposure time.

We assessed the radioprotective and mitigative actions of sodium diclofenac, a non-steroidal anti-inflammatory drug using cultured human peripheral blood as a model. Both pre- and post-irradiation treatments with the drug reduced gamma radiation-induced formation of dicentric chromosome, cytochalasin-blocked micronuclei and γ-H2AX foci in human peripheral blood lymphocytes. This work supports the concept that sodium diclofenac may be a useful radiation countermeasure agent., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Increasing studies demonstrated that photobiomodulation (PBM) influenced specific biological effects in cells, tissues and organs, and these effects rely on the production of light irradiation. In this study, we aimed to precisely manipulate the spatial arrangement of adhesion cells in a traditional culture condition with 450 nm low intensity laser. Through 450 nm laser PBM, the adhesion of the cultured cells was significantly improved and resisted the digestion of 0.1% trypsin. Combined with a computer aided design system (CAD) and computer numerical control (CNC) system, the designed laser irradiation pattern induced the specific cell micropattern in the culture dish. RNA sequencing and biochemical experiments confirmed that the 450 nm laser prompted low-density lipoprotein (LDL) bonding to the cell surface and induced lipid peroxidation, which crosslinked and modified the protein molecules on the irradiated cell surface. In this way, the peroxidation product-modified proteins resisted trypsin proteolysis, ultimately leading to a differential detachment between the irradiated and non-irradiated cells under trypsin treatment. This convenient method did not require special biomaterial processing, has no impact on cell viability and functions, and required no changes to the conventional cell culture conditions. The photo-induced cell capturing is a great complement to existing tools by providing spatial resolution., (Copyright © 2020 Elsevier B.V. All rights reserved.)

A fucose-rich fucoidan was purified from brown seaweed Saccharina japonica , of which the UVB protective effect was investigated in vitro in keratinocytes of HaCaT cells and in vivo in zebrafish. The intracellular reactive oxygen species levels and the viability of UVB-irradiated HaCaT cells were determined. The results indicate that the purified fucoidan significantly reduced the intracellular reactive oxygen species levels and improved the viability of UVB-irradiated HaCaT cells. Furthermore, the purified fucoidan remarkably decreased the apoptosis by regulating the expressions of Bax/Bcl-xL and cleaved caspase-3 in UVB-irradiated HaCaT cells in a dose-dependent manner. In addition, the in vivo UV protective effect of the purified fucoidan was investigated using a zebrafish model. It significantly reduced the intracellular reactive oxygen species level, the cell death, the NO production, and the lipid peroxidation in UVB-irradiated zebrafish in a dose-dependent manner. These results suggest that purified fucoidan has a great potential to be developed as a natural anti-UVB agent applied in the cosmetic industry.

Fucoidan, a sulphated polysaccharide, plays a vital role in reducing cellular oxidative damage by exerting potential antioxidant activity. However, because of the negative surface charges of oligofucoidan, it shows poor oral intestinal absorption. To overcome this drawback, the oligofucoidan polysaccharides self-assembled with opposite charge based polysaccharides (chitosan) to form the chitosan-fucoidan polysaccharides (C 1 -F 3 P) nanoparticles (NPs) of 190-230 nm in size. The oligofucoidan and C 1 -F 3 P NPs were studied for their radioprotective property using mice exposed to 5 Gy radiation. The C 1 -F 3 P NPs prevents radiation induced lipid peroxidation and restores intestinal enzymatic and non-enzymatic antioxidants (p < 0.05) status. In addition, hematoxylin-eosin staining revealed the radioprotective effect of oligofucoidan and C 1 -F 3 P NPs by mitigating the loss of crypt and villi in the small intestine. Thus, the present study demonstrated that C 1 -F 3 P NPs can be considered as a radioprotective agent that can be used for the prevention and treatment of Gy-radiation-induced intestine injury., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020. Published by Elsevier B.V.)

The Chlorella vulgaris has been generally recognized as a promising microalgal model to study stress-related responses due to its ability to withstand against ionizing and non-ionizing radiation. The objective of the present study was to investigate the effect of CaCl 2 pre-treatment at different concentrations on the responses of microalga C. vulgaris under gamma radiation toxicity. Changes in growth, physiological parameters and biochemical compositions of the algae pretreated with 0.17 (normal), 5, and 10 mM CaCl 2 were analyzed under 300 Gy gamma irradiation and compared to those of gamma-free control. The results showed that parameters including specific growth rate, cell size, chlorophyll and protein contents, ascorbate peroxidase (APX), and superoxide dismutase (SOD) activity, Ferric Reducing Antioxidant Power (FRAP), and the ratios of nucleic acid to protein negatively affected by gamma irradiation. All these parameters, except for the ratios of nucleic acid to protein significantly increased in the algae when pretreated with a CaCl 2 content higher than normal concentration. The analysis also showed that parameters including catalase activity, proline, and carotenoid content, the level of lipid peroxidation, and electrolyte leakage (EL) significantly increased under gamma irradiation but not affected significantly under different CaCl 2 pre-treatments. Additionally, specific growth rate, chlorophyll a and protein content, APX and SOD activity, FRAP, lipid peroxidation, electrolyte leakage, and the ratios of nucleic acid to protein were the only parameters that significantly affected by the interaction of gamma toxicity and CaCl 2 pretreatment. Overall, the results suggested that regardless of the CaCl 2 effect, the algal cells responded to gamma radiation more efficiently by increasing proline, carotenoids content, and CAT activity. More important, it was concluded that calcium had an essential role in modifying the detrimental effect of gamma toxicity on the algae mainly by increasing the activity of ascorbate peroxidase and superoxide dismutase and maintaining the reducing antioxidant power (FRAP) of the cells at a high level., Competing Interests: Declaration of competing interest The authors declare no competing financial interests., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Purpose: Light intensity is one of the important environmental factors that have strong influence on larviculture. Culture of fish at high intensity of light generates harmful radicals in the body that can compromise their health and production. The present study aims to evaluate the effect of various light intensities on the physiology of rohu Labeo rohita fry. Materials and Methods: Rohu fry (13.56 ± 0.4 mg) were exposed at five different light intensities: 0.17 ± 0.005 (Lc, control), 1.45 ± 0.23 (L1), 2.69 ± 0.47 (L2), 3.93 ± 0.72 (L3) and 5.06 ± 0.95 Wm -2 (L4). After 90 days of culture, rohu were harvested. Results and Conclusions: A 2-5% mortality of rohu was recorded in L3 and L4 treatments. The average weight and specific growth rate were significantly ( p  < .05) higher in Lc treatment compared to others. The light intensity and swimming activity of rohu showed direct relationship, whereas, light intensity showed inverse relation with nitric oxide synthase and reduced glutathione levels. Significantly ( p  < .05) higher glutathione S-transferase and glutathione peroxidase activies were found in rohu exposed at L4 treatment. Higher light intensities resulted in oxidative stress in the muscles of rohu. Thiobarbituric acid reactive substances, carbonyl protein and heat shock protein 70 were significantly ( p  < .05) higher in rohu exposed at L4 compared to other treatments. Exposure of rohu fry to intense light resulted into physiological stress and immunosupression.

The physiological stress modeled by circulatory hypoxia activates LPO processes in various tissues. In posthypoxic period, the infrared low-intensity laser irradiation significantly decreased the chemiluminescence parameters in blood plasma, normalized the retinal levels of diene and triene conjugates, and decreased MDA in the rat brain attesting to the correcting effect of this irradiation during various types of physiological stresses.

Although radiation is widely used to treat cancers, resistance mechanisms often develop and involve activation of DNA repair and inhibition of apoptosis. Therefore, compounds that sensitize cancer cells to radiation via alternative cell death pathways are valuable. We report here that ferroptosis, a form of nonapoptotic cell death driven by lipid peroxidation, is partly responsible for radiation-induced cancer cell death. Moreover, we found that small molecules activating ferroptosis through system x c - inhibition or GPX4 inhibition synergize with radiation to induce ferroptosis in several cancer types by enhancing cytoplasmic lipid peroxidation but not increasing DNA damage or caspase activation. Ferroptosis inducers synergized with cytoplasmic irradiation, but not nuclear irradiation. Finally, administration of ferroptosis inducers enhanced the antitumor effect of radiation in a murine xenograft model and in human patient-derived models of lung adenocarcinoma and glioma. These results suggest that ferroptosis inducers may be effective radiosensitizers that can expand the efficacy and range of indications for radiation therapy.

Ultraviolet B (UVB) radiation triggers the activation of many reactive oxygen species (ROS)-sensitive signaling pathways, resulting in the induction of skin damage that can progress to premature skin aging with long-term exposure. Even after the cessation of UVB radiation, the activated photosensitizers can still cause cellular injury. Thus, the use of photoprotectors that inhibit or prevent intracellular ROS production during or after UV exposure is one alternative to counteract UV-induced oxidative damage. The present study investigated the photoprotective activity of protocatechuic acid (P0) and its alkyl esters ethyl protocatechuate (P2) and heptyl protocatechuate (P7) against UVB-induced damage in L929 fibroblasts by evaluating biomarkers of oxidative stress and photoaging. P0, P2 and P7 markedly increased cell viability after UVB exposure. This protective effect was related to the ability of these compounds to absorb UVB and restore cellular redox balance even 24 h after UVB exposure. P0, P2 and P7 also decreased oxidative damage to membrane lipids, mitochondrial membrane potential, and DNA. They also inhibited the nuclear translocation of NF-κB p65 and downregulated the expression of the photoaging-related proteins matrix metalloproteinases-1 and -9 and cyclooxygenase-2. As the lipophilicity of the P0 derivatives increased, their antioxidant potency increased, but more pronounced cytotoxic effects were also detected. In summary, P0 and P2 may be promising candidates for the prevention and treatment of UVB-induced skin photodamage and photoaging., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Chitosan, being one of the most promising biological macromolecules, has an immense scope in agriculture to boost crop growth and defense responses. In this study, chitosan was exposed to gamma rays in order to obtain a low molecular weight derivative. Viscometric characterization showed a sharp decrease in molecular weight and FTIR based analysis confirmed retention of structural integrity of the polymer upon gamma irradiation. Assessments of various physiological and biochemical attributes were carried out on sugarcane plantlets that were subjected to progressive water deficit stress. The irradiated chitosan was found to differentially ameliorate water deficit stress tolerance against that of normal chitosan through positive modulation of various gas exchange parameters alongside significant improvement in relative tissue water content, SOD activity, soluble sugars and adenine energetics. Furthermore, application of irradiated chitosan significantly reduced cell membrane damage, lipid peroxidation, H 2 O 2 and free-proline accumulations. This is the first report on the use of gamma irradiated chitosan to alleviate water deficit stress tolerance in sugarcane. Overall comparative assessments showed that differential plant responses were triggered upon foliar application of normal and gamma irradiated chitosan in sugarcane plants grown under water deficit stress conditions., (Copyright © 2019 Elsevier B.V. All rights reserved.)

The present study was premeditated to examine the radioprotective effects of aqueous Aloe vera gel extract against whole-body X-ray irradiation-induced hematological alterations and splenic tissue injury in mice. Healthy male balb/c mice were divided into four groups: group 1, control; group 2, A. vera (50 mg/kg body weight) administered per oral on alternate days for 30 days (15 times); group 3, X-ray exposure of 2 Gy (0.25 Gy twice a day for four consecutive days in the last week of the experimental protocol); and group 4, A. vera + X-ray. X-ray exposure caused alterations in histoarchitecture of spleen along with enhanced clastogenic damage as assessed by micronucleus formation and apoptotic index. Irradiation caused an elevation in proinflammatory cytokines like tumor necrosis factor and interleukin-6, total leucocyte counts, neutrophil counts and decreased platelet counts along with unaltered red blood cell counts and hemoglobin. Irradiation also caused an elevation in reactive oxygen species (ROS), lipid peroxidation (LPO) levels, lactate dehydrogenase activity and alterations in enzymatic and nonenzymatic antioxidant defense mechanism in plasma and spleen. However, administration of A. vera gel extract ameliorated X-ray irradiation-induced elevation in ROS/LPO levels, histopathological and clastogenic damage. It also modulated biochemical indices, inflammatory markers, and hematological parameters. These results collectively indicated that the A. vera gel extract offers protection against whole-body X-ray exposure by virtue of its antioxidant, anti-inflammatory and anti-apoptotic potential.

Microcystis blooms and their associated microcystins pose a significant health risk to humans. Microcystis normally occurs as colonies in eutrophic water bodies, and its physiological tolerance to algaecides is dissimilar to that of unicellular forms. However, the differences of physiological response to algaecides between unicellular and colonial Microcystis have been poorly explored. The current study investigated the effects of hexane extract of Acorus calamus rhizome (HEACR) on the physiological and photosynthetic mechanisms of unicellular and colonial M. aeruginosa in the laboratory. We analyzed the cell density, reactive oxygen species (ROS) level, malonaldehyde (MDA) content, photosynthetic pigments, capsular polysaccharide (CPS), and photosystem (PS II) parameters of the two morphological forms of Microcystis. Our results show that HEACR suppresses the growth of both unicellular and colonial M. aeruginosa, increases the intracellular ROS level and cause lipid peroxidation, as well as exerting a detrimental effect on chlorophyll a (chl a) content and photosynthetic efficiency. Almost 100% inhibition was observed for unicellular and colonial M. aeruginosa after 3 d exposure to 50 and 100 mg L -1 HEACR, respectively. The ROS level increase, MDA accumulation, the chl a decrease and carotenoid increase in unicellular M. aeruginosa were all more obvious than that in colonial cells. The fall in photosynthetic efficiency of unicellular M. aeruginosa were also more significant than that of colonial cells. After 3d exposure, the maximum quantum yield of PS II photochemistry (Fv/Fm), effective quantum yield of PS II photochemistry (Fv'/Fm') and effective quantum yield of photochemical energy conversion in PS II (YII) of unicellular M. aeruginosa was almost totally inhibited by 20 mg L -1 HEACR, while the F v /F m , F v '/F m ' and YII of colonial M. aeruginosa decreased by 43%, 26% and 66% for 100 mg L -1 of HEACR, respectively. Comparing the two morphological forms of Microcystis, colonies show a greater increase in CPS level to more effectively resist the stress of HEACR and to mitigate ROS generation thereby better defending against oxidative damage. Furthermore, colonial M. aeruginosa shows better photoprotection ability than the unicellular form when exposed to HEACR. The colonies also sustain their maximum electron transport rate, increase their tolerance to strong light, and maintain a higher ability to disperse excess energy. These results demonstrated that HEACR can significantly interfere with the growth and physiological processes of both unicellular and colonial M. aeruginosa, but that colonial M. aeruginosa has a greater ability to adjust physiological tolerance to resist the stresses of HEACR., (Copyright © 2019. Published by Elsevier B.V.)

High dose rates of ionizing radiation have been reported to cause adverse effects such as reduction in reproduction and growth, and damage to protein and lipids in primary producers. However, the relevant effects of ionizing radiation are still poorly understood in aquatic plants. This study was intended to characterize the biological effects and modes of action (MoAs) of ionizing radiation using gamma radiation as the prototypical stressor and duckweed Lemna minor as a model organism. Lemna minor was exposed to 1, 14, 24, 46, 70 mGy/h gamma radiation dose rates from a cobalt-60 source for 7 days following the testing principles of the OECD test guideline 221. A suite of bioassays was applied to assess the biological effects of gamma radiation at multiple levels of biological organization, including detection of reactive oxygen species (ROS), oxidative stress responses (total glutathione, tGSH; lipid peroxidation, LPO), DNA damage, mitochondrial dysfunctions (mitochondrial membrane potential, MMP), photosynthetic parameters (chlorophyll a, chl a; chlorophyll b, chl b; carotenoids; Photosystem II (PSII) performance; CO 2 uptake), intercellular signaling (Ca 2+ release) and growth. Gamma radiation increased DNA damage, tGSH level and Ca 2+ content together with reduction in chlorophyll content, maximal PSII efficiency and CO 2 uptake at dose rates between 1 and 14 mGy/h, whereas increases in cellular ROS and LPO, inhibition of MMP and growth were observed at higher dose rates (≥24 mGy/h). A network of toxicity pathways was proposed to portray the causal relationships between gamma radiation-induced physiological responses and adverse outcomes to support the development of Adverse Outcome Pathways (AOPs) for ionizing radiation-mediated effects in primary producers., (Copyright © 2019 Elsevier B.V. All rights reserved.)

A comparative study of melanin and ommochrome-containing samples, isolated from the black soldier fly (BSF) by enzymatic hydrolysis, alkaline and acid alcohol extraction or by acid hydrolysis, was carried out. Melanin was isolated both as a melanin-chitin complex and as a water-soluble melanin. Acid hydrolysis followed by delipidization yielded a more concentrated melanin sample, the electron spin resonance (ESR) signal of which was 2.6 × 10 18 spin/g. The ommochromes were extracted from the BSF eyes with acid methanol. The antiradical activity of BSF melanins and ommochromes was determined by the method of quenching of luminol chemiluminescence. It has been shown that delipidization of water-soluble melanin increases its antioxidant properties. A comparison of the antioxidant activity of BSF melanins and ommochromes in relation to photoinduced lipid peroxidation was carried out. The ESR characteristics of native and oxidized melanins and ommochromes were studied. It is assumed that H. illucens adult flies can be a useful source of natural pigments with antioxidant properties.

Radiation is known to be associated with pathology of various human diseases. This study has focused on the effect of radiation on glucose homeostasis with regard to metabolic function of liver and pancreas and the effect of polysaccharide from the fruiting bodies of Auricularia auricular (SNAAP) on glucose metabolism. The 60 Co-γ-radiated mice displayed destroyed redox equilibrium, accompanied by increased blood glucose accumulation, decreased insulin and hepatic glycogen contents, impaired blood glucose tolerance ability, abnormal changes in activities of glucose metabolism-related enzymes and damaged hepatic and pancreatic function, while SNAAP can restore the disordered glucose metabolism to some extent. Increased phosphorylation of JNK and FoxO1, reduced phosphorylation of Akt and GSK-3β and increased expression of PEPCK, G6Pase and GYS2 in the liver as well as the decreased expression of PDX1, GLUT2 and IRS1 in the pancreas of radiated mice were recovered after treated with SNAAP, leading to an improved gluconeogenesis and glycogen synthesis. These findings clearly indicate that SNAAP has significant potency in radiation-induced glucose metabolism disorder through modulating the JNK pathway in the liver as well as the PDX1/GLUT2 in the pancreas., (Copyright © 2019. Published by Elsevier B.V.)

Purpose: The present study focused on the role of primary metabolites, antioxidant activities in black gram ( Vigna mungo L. Hepper) variety Vamban-4 under the impact of gamma irradiation. Materials and methods: The black gram seeds were irradiated at a different dose of gamma rays viz., 200, 400, 600, 800, 1000 and 1200 Gray (Gy), and analyzed the changes of biochemical and antioxidant contents. Results: Biochemical contents increased with increasing doses up to 800 Gy and reduced at higher dose viz.,1000 and 1200 Gy of gamma-ray treatment, while malondialdehyde content increased at higher dose 1200 Gy compared to control, this indicates that the formation of more lipid peroxidation at higher radiation level. Gamma irradiation enhanced the activity of antioxidant enzymes such as catalase, peroxidase and superoxide dismutase with increasing doses rather than control plants. These studies depict that the effect of gamma irradiation on seeds increased the free radicals compared to control, which emphasize by the Electron spin resonance spectroscopy (ESR). Gamma irradiated seed samples contain more fractions of protein, lipids, amino acid and polysaccharides compared to control plants observed from the Fourier infrared transform spectroscopy (FTIR). Conclusion: The present result concludes that cellular metabolites and the antioxidant enzymes increased and these alterations of metabolism due to the effect of gamma rays which induced free radical production in seeds and plants grown under irradiation stress. These results confirm that the exposure of gamma irradiation produced free radicals as well as counteract by antioxidant enzymes and in addition to that accumulation and alteration of primary metabolites.

The present work was conducted to study how restoration of perturbed oxidant and antioxidant homeostasis is achieved in the UV-C radiation exposed cells of cyanobacterium Nostoc muscorum Meg1. Exposure to varying doses of UV-C radiation (6, 12, 18 and 24 mJ/cm 2 ) showed damage to ultrastructures especially cytoplasmic membrane, cell wall and organisation of thylakoid membranes of the cyanobacterium under transmission electron microscope (TEM). All doses of UV-C exposure significantly induced most of the enzymatic antioxidant {catalase, superoxide dismutase (SOD) and glutathione reductase (GR)} activities, their protein levels (western blot analysis) and mRNA levels (real time PCR analysis) within the first hour of post UV-C radiation incubation period. In the same way, contents of many non-enzymatic antioxidants such as ascorbic acid, reduced glutathione, proline, phenol and flavonoids were also augmented in response to such UV-C radiation exposure. Although notable increase in ROS level was only seen in cultures treated with 24 mJ/cm 2 UV-C exposure which also registered increase in protein oxidation (22%) and lipid peroxidation (20%), this boost in both enzymatic and non-enzymatic antioxidants was significant in all radiation exposed cells indicating cell's preparation to combat rise in oxidants. Further, albeit all antioxidants increased considerably, their levels were restored back to control values by day seventh re-establishing physiological redox state for normal metabolic function. The combined efficiency of the enzymatic and non-enzymatic antioxidants were so effective that they were able to bring down the increase levels of ROS, lipid peroxidation and protein oxidation to the physiological levels within 1 h of radiation exposure signifying their importance in the defensive roles in protecting the organism from oxidative toxicity induced by UV-C radiation exposure., (Copyright © 2019 Elsevier B.V. All rights reserved.)