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Aims: Oxidative stress and neuronal death are the primary reasons for the progression of amyloid-beta (Aβ) deposition and cognitive deficits in Alzheimer's disease (AD). Ecdysterone (ecdy), a common derivative of ecdysteroids, possesses free radical scavenging and cognitive-improving effects. High-intensity interval training (HIIT) can be a therapeutic strategy for improving cognitive decline and oxidative stress. The present study was aimed to evaluate the effect of HIIT exercise and ecdy consumption synergistically on the changes in learning and memory functions, activities of hippocampal antioxidant enzymes, and neuronal population after AD induced by Aβ in male rats., Materials and Methods: Following ten days of Aβ injection, HIIT exercise and ecdy treatment (10 mg/kg/day; P.O.) were initiated and continued for eight consecutive weeks in rats. At the end of the treatment period, the rat's learning and memory functions were assessed using Morris water maze and passive avoidance tests. The activity of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GRx), and changes in neuronal population were evaluated in rats' brains., Results: The results indicated that Aβ injection disrupted spatial/passive avoidance learning and memory in both tests, accompanied by a decrease in the SOD and CAT (as endogenous antioxidants) in rats' hippocampus. Additionally, Aβ injection resulted in neuronal loss in the cerebral cortex and hippocampus. Although the consumption of ecdy separately improved spatial/passive avoidance learning and memory impairments, recovered hippocampal activity of SOD, CAT, GRx, and prevented the hippocampal neuronal loss, its combination along with HIIT resulted in a more powerful and effective amelioration in all the above-mentioned Aβ-neuropathological changes., Conclusion: Our results confirm that a combination of HIIT and ecdy treatment could be a promising potential therapeutic option against AD-associated cognitive decline, owing to their free radical scavenging and neuroprotective properties., (Copyright © 2022. Published by Elsevier Inc.)

It has been shown that the development of coronavirus infection (COVID-19), especially in severe cases, is accompanied by hypoxia as a result of several pathological processes: alveolar blood supply disorders, hemolysis, COVID-associated coagulopathy. Under these conditions, the level of reactive oxygen species is increased and it is more likely that free-radical damage to biomolecules is caused by the process of free-radical fragmentation than oxidation. In contrast to the oxidation process, free-radical fragmentation reactions are more effectively inhibited by oxidizing agents than reducing agents. Therefore, the use of substances possessing both reducing and oxidizing properties, such as natural and synthetic quinones, bioflavonoids, curcuminoids, should reduce the probability of biomolecule destruction by oxidation as well as free-radical fragmentation processes.HighlightsCOVID-19 is accompanied by the iron release from the heme and «silent» hypoxiaROS initiate fragmentation reactions of biomolecules under conditions of hypoxiaBlocking of fragmentation process by oxidizers may lead to mitigation of COVID-19.

3-hydroxytyrosol (HT) is the main phenolic compound found in olive oil with known antioxidant, anti-inflammatory, and antimicrobial properties in several dermatological conditions, both when taken in the form of olive oil or pure in cosmeceutical formulations. To date, its direct effect on the wound healing process and the molecular mechanisms involved have not yet been elucidated. Thus, in the present study, we aimed to explore its effects in vitro in epidermal keratinocyte cultures focusing on the molecular mechanism implied. HT was able to induce keratinocyte proliferation in the low micromolar range, increasing the expression of cyclin dependent kinases fundamental for cell cycle progression such as CDK2 and CDK6. Furthermore, it increased cell migration through the activation of tissue remodeling factors such as matrix metalloproteinase-9 (MMP-9) protein. Then, we evaluated whether HT also showed antioxidant activity at this concentration range, protecting from H 2 O 2 -induced cytotoxicity. The HT prevented the activation of ATM serine/threonine kinase (ATM), Checkpoint kinase 1 (Chk1), Checkpoint kinase 2 (Chk2), and p53, reducing the number of apoptotic cells. Our study highlighted novel pharmacological properties of HT, providing the first evidence of its capability to induce keratinocyte migration and proliferation required for healing processes and re-epithelialization.

Electronic cigarettes (ECs) are categorized into generations which differ in terms of design, aerosol production, and customizability. Current and former smokers prefer third-generation devices that satisfy tobacco cravings more effectively than older generations. Recent studies indicate that EC aerosols from first- and second-generation devices contain reactive carbonyls and free radicals and can cause in vitro cytotoxicity. Third-generation ECs have not been adequately studied. Further, previous studies have focused on cells from the respiratory tract, whereas those of the oral cavity, which is exposed to high levels of EC aerosols, have been understudied. We quantified the production of reactive carbonyls and free radicals by a third-generation EC and investigated the induction of cytotoxicity and oxidative stress in normal and cancerous human oral cell lines using a panel of eight commercial EC liquids. We found that EC aerosols produced using a new atomizer contained formaldehyde, acetaldehyde, and acrolein, but did not contain detectable levels of free radicals. We found that EC aerosols generated from only one of the eight liquids tested using a new atomizer induced cytotoxicity against two human oral cells in vitro . Treatment of oral cells with the cytotoxic EC aerosol caused a concomitant increase in intracellular oxidative stress. As atomizer age increased with repeated use of the same atomizer, carbonyl production, radical emissions, and cytotoxicity increased. Overall, our results suggest that third-generation ECs may cause adverse effects in the oral cavity and normal EC use, which involves repeated use of the same atomizer to generate aerosol, may enhance the potential toxic effects of third-generation ECs.

Free radicals are generated in our body by several systems. A balance among free radicals and antioxidants is an important matter for appropriate physiological function. If free radicals become greater than the ability of the body to control them, a case known as oxidative stress appears, as a result of that, a number of human diseases spread in the body. Antioxidants can contribute to facingthis oxidative stress. The present review provides a brief overview of free radicals, oxidative stress, some natural antioxidants and the relationship between them., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

The objective of this study was to explore the effect of magnesium acetate (MA) addition on the endo-polyphenol yield by Phellinus baumii and establish a feasible additive strategy. The optimal three-point MA addition strategy (0.05 g/L concentration of MA added at 0 h and 6 h, 0.9 g/L concentration of MA added at 12 h) was employed to obtain maximum endo-polyphenol yield. The maximum endo-polyphenol production was reached at 1.22 g/L, which was 1.39-fold higher than that of the control. Additionally, the endo-polyphenol showed stronger antioxidant activity in vitro compared with the control, including DPPH· scavenging capacity (78.76%) and Trolox equivalent antioxidant capacity (TEAC) (32.28 μmol Trolox/g sample). HPLC analysis showed that the endo-polyphenol production of the crude ethanol extracts was significantly higher than that of the control. Hispidin was isolated and identified from the ethanol extract of the culture mycelia from Ph. baumii with the three-point MA addition strategy. Hispidin showed a strong ability to scavenge DPPH free radicals and TEAC, equivalent to positive (vitamin C) value of 89.41% and 75.98%, respectively. Furthermore, hispidin protected H2O2-induced PC12 cells injured by decreased oxidative stress level. These results indicated that the MA multi-stage addition strategy was dependable, and could be used to develop new natural antioxidants for foods or medicines.

The identification of conserved genes and pathways that regulate lifespan but also healthspan has resulted in an improved understanding of the link between nutrients, signal transduction proteins, and aging but has also provided evidence for the existence of multiple "longevity programs," which are selected based on the availability of nutrients. Periodic fasting and other dietary restrictions can promote entry into a long-lasting longevity program characterized by cellular protection and optimal function but can also activate regenerative processes that lead to rejuvenation, which are independent of the aging rate preceding the restricted period. Thus, a "juventology"-based strategy can complement the traditional gerontology approach by focusing not on aging but on the longevity program affecting the life history period in which mortality is very low and organisms remain youthful, healthy, and fully functional., (© 2018 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.)

Tucked inside our cells, we animals (and plants, and fungi) carry mitochondria, minuscule descendants of bacteria that invaded our common ancestor 2 billion years ago. This unplanned breakthrough endowed our ancestors with a convenient, portable source of energy, enabling them to progress towards more ambitious forms of life. Mitochondria still manufacture most of our energy; we have evolved to invest it to grow and produce offspring, and to last long enough to make it all happen. Yet because the continuous generation of energy is inevitably linked to that of toxic free radicals, mitochondria give us life and give us death. Stripping away clutter and minutiae, here we present a big-picture perspective of how mitochondria work, how they are passed on virtually only by mothers, and how they shape the lifestyles of species and individuals. We discuss why restricting food prolongs lifespan, why reproducing shortens it, and why moving about protects us from free radicals despite increasing their production. We show that our immune cells use special mitochondria to keep control over our gut microbes. And we lay out how the fabrication of energy and free radicals sets the internal clocks that command our everyday rhythms-waking, eating, sleeping. Mitochondria run the show.

The loss of pancreatic β-cells plays a central role in the pathogenesis of both type 1 and type 2 diabetes, and many studies have been focused on ways to improve glucose homeostasis by preserving, expanding and improving the function of β-cell. Elevated levels of free fatty acids such as palmitate might contribute to the loss of β-cells. A marine squid, Loliolus beka has long been used as a food in Korea, China, Japan and Europe due to its tender meat and high taurine content. Here, we investigated the protective effects of a hot water extract of Loliolus beka meat (LBM) against palmitate toxicity in Ins-1 cells, a rat β-cell line. Treatment with LBM extract protected against palmitate-induced cytotoxicity and scavenged overproduction of nitric oxide, alkyl, and hydroxyl radicals. In addition, LBM extract protected against palmitate-induced DNA damage and β-cell dysfunction. These findings suggest that LBM protects pancreatic β-cells from palmitate-induced damage. LBM could be a potential therapeutic functional food for diabetes.

During the perinatal period, free radicals (FRs) are involved in several physiological roles such as the cellular responses to noxia, the defense against infectious agents, the regulation of cellular signaling function, and the induction of a mitogenic response. However, the overproduction of FRs and the insufficiency of an antioxidant mechanism result in oxidative stress (OS) which represents a deleterious process and an important mediator of damage to the placenta and the developing fetus. After birth, OS can be magnified by other predisposing conditions such as hypoxia, hyperoxia, ischemia, hypoxia ischemia-reperfusion, inflammation, and high levels of nonprotein-bound iron. Newborns are particularly susceptible to OS and oxidative damage due to the increased generation of FRs and the lack of adequate antioxidant protection. This impairment of the oxidative balance has been thought to be the common factor of the so-called "free radical related diseases of prematurity," including retinopathy of prematurity, bronchopulmonary dysplasia, intraventricular hemorrhage, periventricular leukomalacia, necrotizing enterocolitis, kidney damage, and oxidative hemolysis. In this review, we provide an update focused on the factors influencing these diseases refining the knowledge about the role of OS in their pathogenesis and the current evidences of such relationship. Mechanisms governing FR formation and subsequent OS may represent targets for counteracting tissue damage.

Oxidative stress plays an important role in the pathogenesis of various chronic liver diseases (CLD) and increasing evidence have confirmed the contributory role of oxidative stress in the pathogenesis of drugs and chemical-induced CLD. Chronic liver injury is manifested as necrosis, cholestasis, fibrosis, and cirrhosis. Chronic administration of anti-tubercular, anti-retroviral, immunosuppressive drugs is reported to induce free radical generation during their biotransformation in the liver. Further, these reactive intermediates are said to induce profibrogenic cytokines, several inflammatory markers, collagen synthesis during the progression of hepatic fibrosis. Oxidative stress and free radicals are reported to induce activation and proliferation of hepatic stellate cells in the injured liver leading to the progression of CLD. Hence, to counteract or to scavenge these reactive intermediates, several plant-derived antioxidant principles have been effectively employed against oxidative stress and came out with promising results in human and experimental models of CLD. This review summarizes the relationships between oxidative stress and different liver pathogenesis induced by drugs and xenobiotics, focusing upon different chronic liver injury induced by alcohol, antitubercular drugs and hyperactivity of antiretroviral drugs in HIV patients, viral hepatitis infection induced oxidative stress., (Copyright © 2018 Pan-Arab Association of Gastroenterology. Published by Elsevier B.V. All rights reserved.)

This study compared the radioprotective effects of high-molecular-weight poly-gamma-glutamate (γ-PGA, average molecular mass 3,000 kDa) and a reduced form of glutathione (GSH, a known radioprotector) on calf thymus DNA damage. The radiation-induced DNA damage was measured on the basis of the decreased fluorescence intensity after binding the DNA with ethidium bromide. All the experiments used ⁶⁰Co gamma radiation at 1,252 Gy, representing 50% DNA damage. When increasing the concentration of γ-PGA from 0.33 to 1.65 μM, the DNA protection from radiation-induced damage also increased, with a maximum of 87% protection. Meanwhile, the maximal DNA protection when increasing the concentration of GSH was only 70%. Therefore, γ-PGA exhibited significant radioprotective effects against gamma irradiation.

Purpose of Review: Low-dose oxygen (LDO) supplementation is used by millions of COPD patients worldwide. The therapeutic benefits of LDO supplementation are well known. There are also several concerns regarding the potential for cellular harm from LDO in COPD patients. This review summarizes the current arguments and evidence pertaining to this important topic., Recent Findings: LDO therapy has been used in COPD patients for more than 50 years. Over the years, data from randomized controlled trials has confirmed that LDO provides survival benefit in COPD patients with severe hypoxemia. Recent data, however, show that LDO does not provide any morality benefit for patients with a less severe degree of hypoxemia. There are several theoretical concerns regarding use of LDO in COPD patients, including radiation-like cellular risks because of oxygen toxicity. However, none of these have been validated in human clinical trials and remain somewhat peripheral to the clinician deciding whether or not to initiate LDO in a hypoxemic COPD patient., Summary: There is high-quality evidence that LDO is both well tolerated and highly efficacious for patients with COPD. There are several theoretical concerns regarding damage from oxygen free radicals from LDO in COPD patients. However, none of these have been validated or confirmed in human clinical trial data. Thus, the benefits of LDO clearly outweigh the risks from any theoretical concerns about oxygen toxicity.

Relatively high doses of psychostimulants induce neurotoxicity on the dopaminergic system and self-injurious behavior (SIB) in rodents. However the underlying neuronal mechanisms of SIB remains unclear. Dopamine receptor antagonists, N-methyl-D-aspartic acid (NMDA) receptor antagonists, Nitric Oxide Synthase (NOS) inhibitors and free radical scavengers significantly attenuate methamphetamine-induced SIB. These findings indicate that activation of dopamine as well as NMDA receptors followed by radical formation and oxidative stress, especially when mediated by NOS activation, is associated with methamphetamine-induced SIB. On the other hand, an increase in the incidence of polydrug abuse is a major problem worldwide. Coadministered methamphetamine and morphine induced lethality in more than 80% in mice, accompanied by an increase in the number of poly (ADP-ribose) polymerase (PARP)-immunoreactive cells in the heart, kidney and liver. The lethal effect and the increase in the incidence of rupture or PARP-immunoreactive cells induced by the coadministration of methamphetamine and morphine were significantly attenuated by pretreatment with a phospholipase A2 inhibitor or a radical scavenger, or by cooling of body from 30 to 90 min after drug administration. These results suggest that free radicals play an important role in the increased lethality induced by the coadministration of methamphetamine and morphine. Therefore, free radical scavengers and cooling are beneficial for preventing death that is induced by the coadministration of methamphetamine and morphine. These findings may help us better understand for masochistic behavior, which is a clinical phenomenon on SIB, as well as polydrug-abuse-induced acute toxicity.

Frequent air travelers and airplane pilots may develop various types of illnesses. The environmental risk factors associated with air travel syndromes (ATS) or air travel-related adverse health outcomes raised concerns and need to be assessed in the context of risk management and public health. Accordingly, the aim of the present review was to determine ATS, risk factors, and mechanisms underlying ATS using scientific data and information obtained from Medline, Toxline, and regulatory agencies. Additional information was also extracted from websites of organizations, such as the International Air Transport Association (IATA), International Association for Medical Assistance to Travelers (IAMAT), and International Civil Aviation Organization (ICAO). Air travelers are known to be exposed to environmental risk factors, including circadian rhythm disruption, poor cabin air quality, mental stress, high altitude conditions, hormonal dysregulation, physical inactivity, fatigue, biological infections, and alcoholic beverage consumption. Consequences of ATS attributed to air travel include sleep disturbances (e.g., insomnia), mental/physical stress, gastrointestinal disorders, respiratory diseases, circulatory-related dysfunction, such as cardiac arrest and thrombosis and, at worst, mechanical and terrorism-related airplane crashes. Thus safety measures in the cabin before or after takeoff are undertaken to prevent illnesses or accidents related to flight. In addition, airport quarantine systems are strongly recommended to prepare for any ultimate adverse circumstances. Routine monitoring of environmental risk factors also needs to be considered. Frequently, the mechanisms underlying these adverse manifestations involve free radical generation. Therefore, antioxidant supplementation may help to reduce or prevent adverse outcomes by mitigating health risk factors associated with free radical generation.

Background: Exposure to elevated levels of particulate matter (PM) is associated with increased risk of morbidity and mortality due to respiratory tract viral infections in infants. Recent identification of environmentally persistent free radicals (EPFRs) in the PM from a variety of combustion sources suggests its role in the enhancement of disease severity of lower respiratory tract infections (LRTI). Our previous studies demonstrated that acute exposure to EPFRs induces pulmonary immunosuppression allowing for enhanced influenza disease severity. Here, we determine the mechanism of EPFR-induced immunosuppression and its impact on the immune response towards influenza infection., Methods: Neonatal mice (3 days old) were acutely exposed to DCB (combustion derived PM with chemisorbed EPFR) for seven consecutive days. Four days post-exposure (dpe), mice were infected with influenza virus. Pulmonary T cell phenotypes including regulatory T cells (Tregs) were analyzed by flow cytometry. The role of IL10 in EPFR-induced exacerbation of influenza disease severity was determined by administering recombinant IL10 (rIL10) to wild type mice or by using IL10 deficient (IL10 -/- ) neonatal mice. Mice were assessed for morbidity by measuring percent weight change and pulmonary viral load., Results: Neonatal mice exposed to EPFRs had a significant increase in pulmonary Tregs and the immunosuppressive cytokine IL10 following influenza infection, which coincided with decreased protective T cell responses to influenza infection at 6 dpi. Depletion of Tregs in EPFR-exposed neonatal mice resulted in increased protective, adaptive T cell responses, whereas adoptive transfer of Tregs from EPFR-exposed neonates to air-exposed neonatal mice suppressed adaptive T cell responses towards influenza infection. Further, treatment with rIL10 could recapitulate EPFR-induced exacerbation of morbidity and pulmonary viral load compared to air exposed and influenza infected mice, whereas, EPFR-exposed IL10 -/- neonates exhibited significant reductions in morbidity, pulmonary viral load and adaptive T cell responses following influenza infection., Conclusions: Neonatal exposure to EPFRs induced Tregs and IL10 resulting in suppressed adaptive T cell responses and enhanced influenza disease severity in neonatal mice. Depletion of Tregs increased adaptive T cell responses and deficiency of IL10 reduced morbidity and conferred enhanced protection against influenza virus.

Through natural selection, living organisms have evolved well-adapted survival strategies over time. The shallow salt waters of Moorea lagoon are the site of accumulation of microbial mats called "Kopara," in the native Polynesian language. This unique ecosystem is rich in film-forming exopolysaccharides (EPSs) secreted by microorganisms within the biofilm, as a mean to protect themselves from environmental stress (strong ultraviolet [UV], pH, salinity … ). Using blue biotechnology, a manufacturing process was developed to obtain an EPS with skin benefits. The active ingredient (EPS-229) protects against urban pollution, including free radicals, heavy metals, hydrocarbons, and PM 2.5 (particulate matter with a size lower than 2.5 μm)., Methods: The anti-lipid peroxidation action of EPS-229 was studied in an in vitro UVB-irradiated keratinocyte culture model, using lipophilic fluorescent probe. The chelating properties of EPS-229 were evaluated in tubo in the presence of cadmium and lead. The protective effect of EPS-229 on pollution-exposed skin explants was investigated through quantification of released malondialdehyde (MDA) and histological observation of skin morphology using optical microscopy. Clinical evaluation of the protective and cleansing efficacy of a water solution containing EPS-229 (0.02% and 0.01% w/v, respectively) was performed, against placebo, on a panel of 18 volunteers. For these studies, the forearms of volunteers were treated with EPS-229 before (anti-adhesion affect) or after (cleansing effect) application of PM 2.5 (iron particles of 1 μm). The presence of skin-adherent particles was observed and quantified by image analysis, using specific digital masks., Results: In vitro , EPS-229 significantly protected keratinocyte cell membranes from lipid peroxidation. A decrease of 28% was achieved when a concentration of 0.001% w/v EPS-229 was applied to the cell culture. In tubo , EPS-229 also presented strong chelating properties. Maximal adsorption was estimated at 154 mg/g (1.37 mmol/g) of EPS-299 for cadmium and at 250 mg/g (1.21 mmol/g) of EPS-229 for lead. In the skin explant model of pollution exposure, EPS-229 (0.03% w/v) reduced MDA production by 44%, preserved cell integrity, improved dermal-epidermal cohesion, and normalized the collagen network. In vivo , treatment of skin with EPS-229 before exposure to PM 2.5 created a protective film limiting particle adhesion. When used in a cleansing solution after exposure to PM 2.5 , EPS-229 formed a mesh that entrapped particles and removed them from the skin surface., Conclusion: Inspired by the French Polynesia Kopara unique ecosystem, a bioactive exopolysaccharide (EPS-229) has been developed that offers protection from environmental aggression. As a biomimetic shield at the surface of the skin, EPS-229 provides an immediate multiprotective action that efficiently fights the harmful effects of urban pollution and smog.

The literature on the anti-neoplastic effects of Pt drugs provides substantial evidence that free radical may be involved in the formation of Pt-DNA adducts and other cytotoxic effects. The conditions specific to cancerous tumours are more conducive to free radical mechanisms than the commonly accepted hydrolysis nucleophilic-electrophilic mechanism of Pt-DNA adduct formation. Molecular orbital studies of the adiabatic attachment of hydrated electrons to Pt drugs reveal that there is a significant lengthening of the Pt-X bond (where X is Cl, O in cisplatin, carboplatin and some pyrophosphate-Pt drugs but not oxaliplatin) in the anion radical species. This observation is consistent with a dissociative electron transfer (DET) mechanism for the formation of Pt-DNA adducts. A DET reaction mechanism is proposed for the reaction of Pt drugs with guanine which involves a quasi-inner sphere 2 electron transfer process involving a transient intermediate 5 co-ordinated activated anion radical species {R2Pt---Cl(G)(Cl)•}*(-) (where R is an ammine group, and G is guanine) and the complex has an elongated Pt---Cl (or Pt---O) bond. A DET mechanism is also proposed when Pt drugs are activated by reaction with free radicals such as HO•, CO3•(-), O2•(-) but do not react with DNA bases to form adducts, but form Pt-protein adducts with proteins such ezrin, FAS, DR5, TNFR1 etc. The DET mechanism may not occur with oxaliplatin., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Many polyphenols that contain more than two phenolic hydroxyl groups are natural antioxidants and can provide health benefits to humans. These polyphenols include, for example, oleuropein, hydroxytyrosol, catechin, chlorogenic acids, hesperidin, nobiletin, and isoflavones. These have been studied widely because of their strong radical-scavenging and antioxidative effects. These effects may contribute to the prevention of diseases, such as diabetes. Insulin secretion, insulin resistance, and homeostasis are important factors in the onset of diabetes, a disease that is associated with dysfunction of pancreatic β-cells. Oxidative stress is thought to contribute to this dysfunction and the effects of antioxidants on the pathogenesis of diabetes have, therefore, been investigated. Here, we summarize the antioxidative effects of polyphenols from the perspective of their radical-scavenging activities as well as their effects on signal transduction pathways. We also describe the preventative effects of polyphenols on diabetes by referring to recent studies including those reported by us. Appropriate analytical approaches for evaluating antioxidants in studies on the prevention of diabetes are comprehensively reviewed.

The requirements on sunscreens have essentially changed, since some years ago it was demonstrated that approximately 50% of free radicals, that are formed in the skin by solar radiation, originate from the visible and infrared regions of the solar spectrum. In addition, a critical radical concentration threshold could be found. If this concentration, the free radical threshold value (FRTV), is exceeded, sunburn, immunosuppression and skin cancer may develop. Application of sunscreens and lotions protects against sunburn in the UV region of the solar spectrum and therefore is frequently used to extend people's stay in the sun. However, this behaviour can enhance the concentration of free radicals formed in the visible and infrared regions of the solar spectrum, so that the critical radical threshold is exceeded and the skin may be damaged., (Copyright© 2016 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.)

Stress is known to precipitate neuropsychiatric diseases, and depending upon its nature and intensity it can also influence the functioning of the immune system. Melatonin (N-acetyl-5-methoxy tryptamine) a pineal gland hormone and potent antioxidant is known to protect against many diseases. Effect of melatonin in stress-induced neuro-immunomodulation is not well elucidated. Therefore in the present study, the protective effects of melatonin were evaluated in restraint stress (RS)-induced behavioral and immunological changes in rats. RS for 1 h significantly reduces (i) percentage of open-arm entries and (ii) percentage of time spent on open-arm in elevated plus maze (EPM) test parameters (p < 0.01) and significant increase in MDA levels in brain homogenate when compared to non-RS control groups (p < 0.05). In immunological studies, both humoral and cell-mediated immune responses to antigen were significantly suppressed by RS for 1 h for 5 consecutive days, as evidenced by significant reduction in (i) anti-SRBC antibody titre, (ii) PFC counts, (iii) percentage change in paw volume, and (iv) Th1 (IFN-γ) and Th2 (IL-4) cytokine levels (p < 0.001 in all parameters). These RS-induced immunological changes were associated with significantly increased lipid peroxidation (MDA) levels in serum and significantly decreased activity of (i) SOD, (ii) CAT, and (iii) GSH levels in RS (X5)-exposed group (p < 0.02). Pretreatment with melatonin (10, 50, and 100 mg/kg) significantly reversed these RS-induced changes in EPM test parameters and humoral and cell-mediated immunological parameters, as well as oxidative stress markers in a dose-dependent manner by differential degrees (p < 0.001). Results are strongly suggestive of the involvement of free radicals during stress-induced neurobehavioral and immunological changes. These changes were significantly restored by melatonin pretreatment. We can conclude that melatonin may have a protective role during such stress-induced neuro-immunomodulation.

Ethnopharmacological Relevance: Cataract is the clouding or opacity that develops in the eye's lens and is considered to be an unavoidable consequence of aging due to irreversible lens damage. Free radicals and oxidant species are reported to be the major factor responsible for the onset and pathology of cataract. No pharmacological measures are formulated to treat cataract blindness and surgical removal of the opaque lens is the only remedy till date. Boosting of antioxidant potential of the lens is proved to prevent cataract and many indigenous plants have been screened for anticataractogenic potential in the last decades. The objective of the present study was to determine whether Cassia tora leaves; the plant employed in traditional medicine for eye rejuvenation and ailments, can prevent cataract in neonatal rats., Materials and Methods: Cataract was induced by a single subcutaneous injection of sodium selenite at a dose of 4 μg/g body weight on the 10th day and Cassia tora leaves was administered orally from 8th day upto 12th day at a concentration of 5 μg/g body weight. After 30 days; lens morphology, oxidant-antioxidant equilibrium, glutathione metabolism, cytoskeletal protein/gene expressions were monitored., Results: Lens morphology, biochemical analysis and expression studies supported the anticataractogenic effect of Cassia tora leaves., Conclusion: In summary, it can be suggested that the consumption of these leaves afford protection to the lens with its antioxidant action and seems to be a new therapeutic approach against cataract by preventive protection., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Human organisms have many defence mechanisms able to neutralise the harmful effects of the reactive species of oxygen. Antioxidants play an important role in reducing the oxidative damage to the human organism. Carotenoids are among the strongest antioxidants. They have 11 coupled double bonds, so they can be classified as polyisoprenoids, show low polarity and can occur in acyclic, monocyclic or bicyclic forms. The carotenoids of the strongest antioxidant properties are lycopene, lutein, astaxanthin and β-carotene. Carotenoids with strong antioxidant properties have found wide application in medical, pharmaceutical and cosmetic industries. These compounds are highly active against both reactive oxygen species and free radicals. Comparing β-carotene, astaxanthin and lycopene with other antioxidants (e.g. vitamin C and E), it can be concluded that these compounds have higher antioxidant activity, e.g. against singlet oxygen. Astaxanthin is a stronger antioxidant compared to β-carotene, vitamin E and vitamin C, respectively 54, 14 and 65 times. Carotenoids have a salutary effect on our body, making it more resistant and strong to fight chronic diseases. The purpose of this article is to review the literature concerning free radicals and their adverse effects on the human body and carotenoids, as strong, natural antioxidants.

Importance: The Healthy Brain Initiative 2013-2018 seeks to optimize brain health as we age. Free radical injury is an important effector of molecular and cellular stress in the aging brain that derives from multiple sources., Objective: To identify potentially modifiable risk factors associated with increased markers of brain oxidative stress., Design, Setting, and Participants: This cross-sectional, academic multicenter study consisted of 320 research volunteers (172 women) aged 21 to 100 years who were medically healthy and cognitively normal., Main Outcomes and Measures: Free radical injury to the brain was assessed using cerebrospinal fluid (CSF) F2-isoprostane (F2-IsoP) concentrations correlated with age, sex, race, cigarette smoking, body mass index, inheritance of the ε4 allele of the apolipoprotein E gene (APOE), and CSF biomarkers of Alzheimer disease., Results: The concentration of CSF F2-IsoP increased with age by approximately 3 pg/mL (approximately 10%) from age 45 to 71 years in medically healthy, cognitively normal adults (P < .001). The CSF F2-IsoP concentration increased by approximately more than 10% for every 5-U increase in body mass index (P < .001). Current smoking had an approximately 3-fold greater effect on CSF F2-IsoPs compared with age (P < .001). Women had greater mean CSF F2-IsoP concentrations than men at all ages after adjusting for other factors (P = .02). Neither the concentration of CSF Alzheimer disease biomarkers nor inheritance of the APOE ε4 allele was associated with the CSF F2-IsoP concentration in this group of medically healthy, cognitively normal adults (P > .05). The association between CSF F2-IsoP concentrations and race was not significant after controlling for the effect of current smoking status (P = .45)., Conclusions and Relevance: Our results are consistent with an age-related increase in free radical injury in the human brain and uniquely suggest that this form of injury may be greater in women than in men. Our results also highlighted 2 lifestyle modifications (ie, body mass index and smoking) that would have an even greater effect on suppressing free radical injury to the brain than would suppressing the processes of aging. These results inform efforts to achieve success in the Healthy Brain Initiative 2013-2018.

One of the less well-documented, potentially modifiable stroke risk factor is the obstructive sleep apnea. Obstructive sleep apnea increases cardiovascular morbidity and mortality, including stroke risk. The article summarizes the pathophysiological factors in sleep apnea syndrome which can increase stroke risk.

Objective: Perinatal hypoxia-induced free radical formation is an important cause of hypoxic-ischaemic encephalopathy and subsequent neurodevelopmental disabilities. Allopurinol reduces the formation of free radicals, which potentially limits hypoxia-induced brain damage. We investigated placental transfer and safety of allopurinol after maternal allopurinol treatment during labour to evaluate its potential role as a neuroprotective agent in suspected fetal hypoxia., Design: We used data from a randomised, double-blind multicentre trial comparing maternal allopurinol versus placebo in case of imminent fetal hypoxia (NCT00189007)., Patients: We studied 58 women in labour at term, with suspected fetal hypoxia prompting immediate delivery, in the intervention arm of the study., Setting: Delivery rooms of 11 Dutch hospitals., Intervention: 500 mg allopurinol, intravenously to the mother, immediately prior to delivery., Main Outcome Measures: Drug disposition (maternal plasma concentrations, cord blood concentrations) and drug safety (maternal and fetal adverse events)., Results: Within 5 min after the end of maternal allopurinol infusion, target plasma concentrations of allopurinol of ≥2 mg/L were present in cord blood. Of all analysed cord blood samples, 95% (52/55) had a target allopurinol plasma concentration at the moment of delivery. No adverse events were observed in the neonates. Two mothers had a red and/or painful arm during infusion., Conclusions: A dose of 500 mg intravenous allopurinol rapidly crosses the placenta and provides target concentrations in 95% of the fetuses at the moment of delivery, which makes it potentially useful as a neuroprotective agent in perinatology with very little side effects., Trial Registration: The study is registered in the Dutch Trial Register (NTR1383) and the Clinical Trials protocol registration system (NCT00189007).

Introduction: Previous studies have demonstrated that oxidative stress by mediating the excessive production of reactive oxygen species is involved in tissue damage and organ failure during and after surgery. The impact of the preoperative immunonutrition including antioxidants on the postoperative course of patients undergoing hepatic surgery was investigated in this pilot study., Patients and Methods: Twenty-three living donor liver transplantation (LDLT) donors were randomly assigned to either an experimental (AO) group, received a commercial supplement enriched with antioxidant nutrients for each of the 5 days immediately prior to surgery while maintaining normal food intake, or a control (CT) group, administered no supplement. Antioxidative capacity was measured by spectrophotometry of patient serum using a free-radical analytical system., Results: The antioxidative capacity of 90.9% patients in the AO group increased after immunonutrition. Compared to the CT group, the AO group was found to have higher antioxidant capacity and transferrin levels; lower WBC, lymphocyte, and neutrophil counts; and briefer duration of postoperative fever during the postsurgical period. No significant differences were found between the 2 groups regarding the nutritional parameters; liver functioning parameters; immunological parameters; intraoperative factors; postoperative outcomes., Conclusion: Preoperative immunonutrition including antioxidants might play a beneficial role in improving postsurgical immunological response but the modest biological advantage was not associated with any significant clinical outcome.

Aim: Long-term exposure of humans to low intensity radiofrequency electromagnetic radiation (RF-EMR) leads to a statistically significant increase in tumor incidence. Mechanisms of such the effects are unclear, but features of oxidative stress in living cells under RF-EMR exposure were previously reported. Our study aims to assess a production of initial free radical species, which lead to oxidative stress in the cell., Materials and Methods: Embryos of Japanese quails were exposed in ovo to extremely low intensity RF-EMR of GSM 900 MHz (0.25 µW/cm2) during 158-360 h discontinuously (48 c - ON, 12 c - OFF) before and in the initial stages of development. The levels of superoxide (O2·-), nitrogen oxide (NO·), thiobarbituric acid reactive substances (TBARS), 8-oxo-2'-deoxyguanosine (8-oxo-dG) and antioxidant enzymes' activities were assessed in cells/tissues of 38-h, 5- and 10-day RF-EMR exposed and unexposed embryos., Results: The exposure resulted in a significant persistent overproduction of superoxide and nitrogen oxide in embryo cells during all period of analyses. As a result, significantly increased levels of TBARS and 8-oxo-dG followed by significantly decreased levels of superoxide dismutase and catalase activities were developed in the exposed embryo cells., Conclusion: Exposure of developing quail embryos to extremely low intensity RF-EMR of GSM 900 MHz during at least one hundred and fifty-eight hours leads to a significant overproduction of free radicals/reactive oxygen species and oxidative damage of DNA in embryo cells. These oxidative changes may lead to pathologies up to oncogenic transformation of cells.

Introduction: The gastrointestinal tract is frequently exposed to noxious stimuli that may cause oxidative stress, inflammation and injury. Intraluminal pro-oxidants from ingested nutrients especially iron salts and ascorbic acid frequently consumed together, can lead to catalytic formation of oxygen-derived free radicals that ultimately overwhelm the cellular antioxidant defense and lead to cell damage., Hypothesis: Since the mechanisms remain sketchy, efforts have been exerted to evaluate the role of epigenetics in modulating components of endogenous enzymatic antioxidants in the intestine. To this end, Caco-2/15 cells were exposed to the iron-ascorbate oxygen radical-generating system., Results: Fe/Asc induced a significant increase in lipid peroxidation as reflected by the elevated formation of malondialdehyde along with the alteration of antioxidant defense as evidenced by raised superoxide dismutase 2 (SOD2) and diminished glutathione peroxidase (GPx) activities and genes. Consequently, there was an up-regulation of inflammatory processes illustrated by the activation of NF-κB transcription factor, the higher production of interleukin-6 and cycloxygenase-2 as well as the decrease of IκB. Assessment of promoter's methylation revealed decreased levels for SOD2 and increased degree for GPx2. On the other hand, pre-incubation of Caco-2/15 cells with 5-Aza-2'-deoxycytidine, a demethylating agent, or Trolox antioxidant normalized the activities of SOD2 and GPx, reduced lipid peroxidation and prevented inflammation., Conclusion: Redox and inflammatory modifications in response to Fe/Asc -mediated lipid peroxidation may implicate epigenetic methylation.

This article reviews current knowledge in khat (cathinone) research and its health impacts and toxicity in the cardiac system of khat chewers based on current evidence. The authors describe the process by which khat is postulated to induce multiple cardiac abnormalities by illustrating multiple case reports as described from around the world. The role of free radicals in inducing cardiac disease is also discussed. Future research areas are proposed to enhance our understanding of the mode of action of this toxicological drug., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Studies have found that natural antioxidants, which are free-radical scavengers, can reduce the risk of diseases caused by free radicals. This work investigated the antioxidant properties of duck proteins hydrolysates. The free-radical scavenging function of CP-1 (M(r) > 10 kDa), CP-2 (5 kDa < M(r) < 10 kDa) and CP-3 (M(r) < 5 kDa), obtained through ultrafiltration and gel filtration were evaluated. The results showed that the lower molecular weight fraction exhibited a stronger free-radical scavenging ability. The highest free-radical scavenging activity was detected in the fraction of p4 purified from CP-3 using Sephadex G-15 column chromatography. The 50% inhibitory value (IC(50)) of p4 for scavenging radicals of superoxide, hydroxyl and 1,1-diphenyl-2-pycrylhydrazyl (DPPH) were, respectively, 0.97 mg mL(-1), 0.84 mg mL(-1) and 1.84 mg mL(-1). Furthermore, the p4 fraction at a concentration of 10 μg mL(-1) increased cell viability from 84.8% to 94% under antioxidative stress in neuroblastoma SK-N-SH cells.

Free radicals play a key role in the development of several pathological conditions. Therefore, several methods have been developed to measure oxidative stress from bodily fluids including blood, urine and, more recently, saliva. Free radical and antioxidant defences within the oral cavity may play a key role in odontostomatological pathologies. This review provides an update of the literature concerning the association of oxidative stress with pathological conditions associated with the oral cavity. It focuses on the diagnostic and therapeutic importance of the tests based on saliva specimens in a preventive perspective., (© 2012 John Wiley & Sons A/S.)

Introduction: Preservatives in ophthalmic preparations are known to cause ocular surface damage. Excipients can also contribute to oxidative stress in the compromised ocular surface. We evaluated commonly used topical glaucoma medications to ascertain pH levels and the intrinsic presence of free radicals., Methods: Samples of 27 topical glaucoma preparations were analysed for total free radical presence using a Randox Kit for total antioxidant status. Analytical grade indicator paper was used to ascertain pH levels., Results: Free radical concentrations for these 27 glaucoma preparations ranged from 0 to 4.54 mmol/l, with a median value of 0.66 mmol/l (mean value of 0.662 mmol/l, SD 0.839). Levels of pH ranged from 4.0 to 7.4, with a median value of 6.5 (mean 6.252, SD 0.826). There was no evidence of a direct correlation between these two variables (r=0.232, P=0.275)., Conclusion: This study is the first to document the range of pH and concentrations of free radicals intrinsically present in commonly used glaucoma medications. Long-term exposure to preservatives, free radicals, and pH levels could all contribute to ocular surface damage. The effect of excipients could be responsible for patient intolerance when changing products in the compromised ocular surface.

Accumulation of molecular damage and increased molecular heterogeneity are hallmarks of photoaged skin and pathogenesis of human cutaneous disease. Growing evidence demonstrates the ability of molecular chaperone proteins and of pharmacologic chaperones to decrease the environmental stress and ameliorate the oxidation stress-related and glycation disease phenotypes, suggesting that the field of chaperone therapy might hold novel treatments for skin diseases and aging. In this review, we examine the evidence suggesting a role for molecular chaperone proteins in the skin and their inducer and protecting agents: pharmacologic chaperone imidazole dipeptide-based agents (carcinine and related compounds) in cosmetics and dermatology. Furthermore, we discuss the use of chaperone therapy for the treatment of skin photoaging diseases and other skin pathologies that have a component of increased glycation and/or free radical-induced oxidation in their genesis. We examine biologic activities of molecular and pharmacologic chaperones, including strategies for identifying potential chaperone compounds and for experimentally demonstrating chaperone activity in in vitro and in vivo models of human skin disease. This allows the protein to function and traffic to the appropriate location in the skin, thereby increasing protein activity and cellular function and reducing stress on skin cells. The benefits of imidazole dipeptide antioxidants with transglycating activity (such as carcinine) in skin care are that they help protect and repair cell membrane damage and help retain youthful, younger-looking skin. All skin types will benefit from daily, topical application of pharmacologic chaperone antioxidants, anti-irritants, in combination with water-binding protein agents that work to mimic the structure and function of healthy skin. General strategies are presented addressing ground techniques to improve absorption of usually active chaperone proteins and dipeptide compounds, include encapsulation into hydrophobic carriers, a combination with penetration enhancers, active electrical transport, or chemical modification to increase hydrophobicity.

Basic research, exploring the hypothesis that γ-hydroxyalkenal phospholipids are generated in vivo through oxidative cleavage of polyunsaturated phospholipids, is delivering a bonanza of molecular mechanistic insights into cardiovascular disease. Rather than targeting a specific pathology, these studies were predicated on the presumption that a fundamental understanding of lipid oxidation is likely to provide critical insights into disease processes. This investigational approach, from the chemistry of biomolecules to disease phenotype, that complements the more common opposite paradigm, is proving remarkably productive.

We identified a previously unrecognized component of airborne particulate matter (PM) formed in combustion and thermal processes, namely, environmentally persistent free radicals (EPFRs). The pulmonary health effects of EPFRs are currently unknown. In the present study, we used a model EPFR-containing pollutant-particle system referred to as MCP230. We evaluated the effects of MCP230 on the phenotype and function of bone marrow-derived dendritic cells (BMDCs) in vitro and lung dendritic cells (DCs) in vivo, and the subsequent T-cell response. We also investigated the adjuvant role of MCP230 on airway inflammation in a mouse model of asthma. MCP230 decreased intracellular reduced glutathione (GSH) and the GSH/oxidized glutathione ratio in BMDCs, and up-regulated the expression of costimulatory molecules CD80 and CD86 on DCs. The maturation of DCs was blocked by inhibiting oxidative stress or the uptake of MCP230. BMDCs exposed to MCP230 increased their antigen-specific T-cell proliferation in vitro. In a model of asthma, exposure to MCP230 exacerbated pulmonary inflammation, which was attributed to the increase of neutrophils and macrophages but not eosinophils. This result correlated with an increase in Th17 cells and cytokines, compared with non-MCP230-treated but ovalbumin (OVA)-challenged mice. The percentage of Th2 cells was comparable between OVA and OVA + MCP230 mice. Our data demonstrate that combustion-generated, EPFR-containing PM directly induced the maturation of DCs in an uptake-dependent and oxidative stress-dependent manner. Furthermore, EPFR-containing PM induced a Th17-biased phenotype in lung, accompanied by significant pulmonary neutrophilia. Exposure to EPFR-containing PM may constitute an important and unrecognized risk factor in the exacerbation and development of a severe asthma phenotype in humans.

Globally, tobacco use is associated with 5 million deaths per annum and is regarded as one of the leading causes of premature death. Major chronic disorders associated with smoking include cardiovascular diseases, several types of cancer, and chronic obstructive pulmonary disease (lung problems). Cigarette smoking (CS) generates a cumulative oxidative stress, which may contribute to the pathogenesis of chronic diseases. Mainstream and side stream gas-phase smoke each have about the same concentration of reactive free radical species, about 1 × 10(16) radicals per cigarette (or 5 × 10(14) per puff). This effect is critical in understanding the biologic effects of smoke. Several lines of evidence suggest that cigarette smoke constituents can directly activate vascular reactive oxygen species production. In this work we present multiple evidence that CS provide the important risk factors in many age-related diseases, and is associated with increased cumulative and systemic oxidative stress and inflammation. The cited processes are marked by increased white blood cell (leucocytes, WBCs) turnover. The data suggest an alteration of the circulating WBCs by CS, resulting in increased adherence to endothelial cells. Telomeres are complex DNA-protein structures located at the end of eukaryotic chromosomes. Telomere length shortens with biologic age in all replicating somatic cells. It has been shown that tobacco smoking enhances telomere shortening in circulating human WBCs. Telomere attrition (expressed in WBCs) can serve as a biomarker of the cumulative oxidative stress and inflammation induced by smoking and, consequently, show the pace of biologic aging. We originally propose that patented specific oral formulations of nonhydrolized carnosine and carcinine provide a powerful tool for targeted therapeutic inhibition of cumulative oxidative stress and inflammation and protection of telomere attrition associated with smoking. The longitudinal studies of the clinical population groups described in this study including elderly support the hypothesis that telomere length is a predictor of survival and therapeutic treatment requirement associated with smoking behavior.

Proline is an amino acid with an essential role for primary metabolism and physiologic functions. Hyperprolinemia results from the deficiency of specific enzymes for proline catabolism, leading to tissue accumulation of this amino acid. Hyperprolinemic patients can present neurological symptoms and brain abnormalities, whose aetiopathogenesis is poorly understood. This review addresses some of the findings obtained, mainly from animal studies, indicating that high proline levels may be associated to neuropathophysiology of some disorders. In this context, it has been suggested that energy metabolism deficit, Na(+),K(+)-ATPase, kinase creatine, oxidative stress, excitotoxicity, lipid content, as well as purinergic and cholinergic systems are involved in the effect of proline on brain damage and spatial memory deficit. The discussion focuses on the relatively low antioxidant defenses of the brain and the vulnerability of neural tissue to reactive species. This offers new perspectives for potential therapeutic strategies for this condition, which may include the early use of appropriate antioxidants as a novel adjuvant therapy, besides the usual treatment based on special diets poor in proline.

The possibility of using modified peroxyredoxins as powerful antioxidant agents has been considered. Peroxyredoxins immobilized on perfluorocarbon emulsions and PTD-modified peroxyredoxins have been studied. It has been shown that peroxyredoxins efficiently bind to particles of perfluorocarbon emulsions, while maintaining their antioxidant properties. A panel of PTD-modified peroxyredoxins has been created and peroxyredoxins most effective both in antioxidant properties and the ability to penetrate cells have been selected. The modified peroxyredoxins obtained may serve as the basis for the design of drug with powerful antioxidant action.

Aim: To investigate the therapeutic effects of antioxidants on the clinical and biochemical outcome of patients with nasal polyposis., Methods: Thirty-four patients with nasal polyposis were divided into two groups receiving either intranasal steroid or intranasal steroid plus per-oral vitamins A, C and E and selenium. Paranasal sinus computed tomography, endoscopy, and polyp tissue and serum sampling were conducted pre- and post-therapy. Serum levels of malondialdehyde, superoxide dismutase, nitrite and myeloperoxidase and tissue levels of malondialdehyde and superoxide dismutase were measured. Group results were compared using the Mann-Whitney U test and Wilcoxon signed-rank test., Results: Both groups had significantly lower tissue parameters, computed tomography scores and serum malondialdehyde levels, comparing pre- versus post-treatment results. Post-treatment, the steroid plus antioxidant group had significantly lower tissue malondialdehyde levels and a greater fall in tissue and serum malondialdehyde, compared with the steroid group., Conclusion: Serum and tissue levels of malondialdehyde (an oxidative marker) were significantly decreased by adding antioxidants to standard therapy. This is the first report of the positive effects of adding antioxidants to steroid therapy for nasal polyposis.

Reserpine-induced orofacial dyskinesia in rats is an animal model of tardive dyskinesia that has been linked with free radical generation and oxidative stress. In the present study, reserpine (1 mg kg(-1), s.c.) was given to rats on days 1, 3 and 5 to induce orofacial dyskinesia, which is characterised by increased vacuous chewing and tongue protrusion. Sub-chronic treatment with Korean ginseng extract from day 1 to day 21 along with reserpine on days 1, 3 and 5 significantly and dose-dependently (100 and 200 mg kg(-1)) reduced reserpine-induced vacuous chewing movements and tongue protrusions. Reserpine-treated animals also showed poor retention of memory in the elevated plus maze paradigm. The sub-chronic Korean ginseng extract administration significantly reversed reserpine-induced retention deficits. Biochemical analysis revealed that repeated reserpine treatment significantly induced lipid peroxidation and decreased glutathione (GSH) levels in the brains of rats. Reserpine-treated rats also showed decreased levels of antioxidant defence enzymes, superoxide dismutase (SOD), and catalase. Sub-chronic administration of Korean ginseng extract dose-dependently and significantly reduced lipid peroxidation and restored decreased GSH levels by repeated reserpine treatment. It also significantly reversed the reserpine-induced decrease in brain SOD and catalase levels in rats. The present study concludes that oxidative stress might play an important role in reserpine-induced abnormal oral movements, and Korean ginseng extract could be useful in the treatment of drug-induced dyskinesia and amnesia.

Single strand breaks are induced in DNA plasmids, pBR322 and pUC19, in aqueous media exposed to strong fields generated using ultrashort laser pulses (820 nm wavelength, 45 fs pulse duration, 1 kHz repetition rate) at intensities of 1-12  TW cm(-2). The strong fields generate, in situ, electrons and radicals that induce transformation of supercoiled DNA into relaxed DNA, the extent of which is quantified. Introduction of electron and radical scavengers inhibits DNA damage; results indicate that OH radicals are the primary (but not sole) cause of DNA damage.

Multivitamin/multimineral complexes are the most common dietary supplements. Unlike minerals in foods that are incorporated in bioorganic structures, minerals in dietary supplements are typically in an inorganic form. These minerals can catalyze the generation of free radicals, thereby oxidizing antioxidants during digestion. Here we examine the ability of a matrix consisting of an amino acid and non-digestible oligosaccharide (AAOS) to blunt metal-catalyzed oxidations. Monitoring of ascorbate radical generated by copper shows that ascorbate is oxidized more slowly with the AAOS matrix than with copper sulfate. Measurement of the rate of oxidation of ascorbic acid and Trolox® by catalytic metals confirmed the ability of AAOS to slow these oxidations. Similar results were observed with iron-catalyzed formation of hydroxyl radicals. When compared to traditional forms of minerals used in supplements, we conclude that the oxidative loss of antioxidants in solution at physiological pH is much slower when AAOS is present.

Oxidative stress (OS) is defined as an unbalance between prooxidant and antioxidant factors that can lead to cellular and tissue damage.The newborn, especially if preterm, is highly prone to OS and to the toxic effect of free radicals (FR). At birth, the newborn is exposed to a relatively hyperoxic environment caused by an increased oxygen bioavailability with greatly enhanced generation of FR. Additional sources (inflammation, hypoxia, ischemia, glutamate, and free iron release) occur magnifying OS. In the preterm baby, the perinatal transition is accompanied by the immaturity of the antioxidant systems and the reduced ability to induce efficient homeostatic mechanisms designed to control overproduction of cell-damaging FR. Improved understanding of the pathophysiological mechanism involved in perinatal brain lesions helps to identify potential targets for neuroprotective interventions, and the knowledge of these mechanisms has enabled scientists to develop new therapeutic strategies that have confirmed their neuroprotective effects in animal studies. Considering the growing role of OS in preterm newborn morbidity in respect to the higher risk of FR damage in these babies, a strict control of oxygen administration, lutein, melatonin, and hypothermia show great promise as potential neuroprotectants. This review provides an overview of the pathogenesis of free radical-mediated diseases of the newborn and the antioxidant strategies for now tested to reduce the OS and its damaging effects.

Cells ability to evade cell death and to proliferate post geno-/cell-toxic stresses, likely leads to formation of cancer. Activation of p38MAPK and p53 following these stresses help protect cells against cancer development by initiating apoptosis. The duration of p38MAPK and p53 activation is regulated by the WIP1 phosphatase. BRCA1-IRIS triggers WIP1 expression in p53-dependent and -independent manner. BRCA1-IRIS triggers the expression and cytoplasmic localization of the mRNA stabilization and translation inducer, HuR that binds p53 and PPM1D mRNA. Hence, BRCA1-IRIS overexpression inactivates p38MAPK and/or p53 by upregulating WIP1 expression. BRCA1-IRIS abrogation of the homeostatic balance maintained by p38MAPK-p53-WIP1 pathway suppressed cell death induced by a lethal dose of UVC, high dosages of etoposide or H2O2, and allowed cells to survive and proliferate post geno-/cell-toxic stresses. This mechanism represents a new link between geno-/cell-toxic stress and aggressive breast cancer formation in p53 wild-type cells., (Hawaii Medical Journal Copyright 2010.)

It was studied that type 2 diabetes mellitus is connected with increased plasma lipid peroxidation (lipid peroxidation expressed as malondialdehyde). This review aimed to evaluate the state of lipid peroxidation among type 2 diabetic subjects. Present finding showed that lipid peroxidation increased in type 2 diabetes mellitus. Increased lipid peroxidation maybe is associated with some diseases such as cancer, cardiovascular diseases and diabetes mellitus. Lipid peroxidation has an important role in the pathogenesis and the complications of diabetes. Antioxidants have been found to prevent the progression and occurrence of diabetes. There are several mechanisms that may cause lipid peroxidation affront in diabetic subjects, although, their precise contributions are not completely clear. We proposed that production of free radicals can be reduced by preventing high blood glucose levels and by the control of instabilities in blood glucose levels. A contributor to these instabilities in blood glucose is glycaemic control by using of fast blood sugar test. Furthermore, the earlier assessment of the advancement of diabetes that firmly control of blood glucose can be obtained; the greater will be the decrease in diabetic complications. Patients with type 2 diabetes may have very high physiological antioxidants requirements.