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The new technological applications of nickel (Ni) raise concerns over its harmful effects on the environment and human health. Pomiferin isolated from Osage orange is evaluated in in vitro and in vivo laboratory bioassays. This study focused the effects of pomiferin on Ni-caused hepatic injury and its underlying mechanisms. With this aim, Sprague-Dawley rats received 10 mg/kg nickel chloride (NiCl 2 ) for 7 d by intraperitoneal injections. Pomiferin was given orally once a day at different doses (75, 150, and 300 mg/kg) for 20 d after exposure to NiCl 2 . Animals were anesthetized and livers were carefully collected to evaluate oxidative stress, inflammation, vascular injury, and hepatic function. Also, immunofluorescence analysis of apoptosis and DNA damage was performed on rat hepatic tissues. NiCl 2 increased MDA production while reducing SOD, CAT, and GPx activity. NiCl 2 induced the production of inflammatory cytokines and also platelet activation in hepatic tissue. Moreover, there were significant increases in AST, ALT, and LDH levels. NiCl 2 also caused significant pathological changes in hepatic. Additionally, it remarkably induced up-regulations of apoptotic marker and 8-OHdG expressions by immunofluorescence labeling in liver cells. Whereas, pomiferin significantly attenuated lipid peroxidation and increased antioxidant defense system in liver. Also, the use of pomiferin prevented deregulated inflammatory process by signaling pathways nuclear factor kappa B (NFκB)/COX-2/TNF-α/IL-1β/IL-6. In addition, pomiferin diminished histopathologic evidence of hepatic toxicity and significantly lower expressions of caspase 3 and 8-OHdG were observed in liver cells. Pomiferin seems to counteract the deleterious effects of NiCl 2 on hepatic tissue through different cellular and signaling mechanisms.

In this study, we aimed to identify the toxic effects of chlorpyrifos exposure on the tissues of common carp. For this purpose, we evaluated histopathological changes in the brain, gills, liver, kidney, testis, and ovaries after 21 days of chlorpyrifos exposure. Activation of 8-OHdG, cleaved caspase-3, and iNOS were assesed by immunofluorescence assay in chlorpyrifos-exposed brain and liver tissue. Additionally, we measured the expression levels of caspase-3, caspase-8, iNOS, MT1, CYP1A, and CYP3A genes in chlorpyrifos-exposed brain tissue, as well as the expression levels of FSH and LH genes in chlorpyrifos-exposed ovaries, using qRT-PCR. We observed severe histopathological lesions, including inflammation, degeneration, necrosis, and hemorrhage, in the evaluated tissues of common carp after both high and low levels of exposure to chlorpyrifos. We detected strong and diffuse signs of immunofluorescence reaction for 8-OHdG, iNOS, and cleaved caspase-3 in the chlorpyrifos-exposed brain and liver tissues. Furthermore, we found that chlorpyrifos exposure significantly upregulated the expressions of caspase-3, caspase-8, iNOS, and MT1, and also moderately upregulated CYP1A and CYP3A in the brain tissue of exposed carp. We also noted downregulation of FSH and LH gene expressions in chlorpyrifos-exposed ovary tissues. Based on our results, chlorpyrifos toxication caused crucial histopathological lesions in vital organs, induced oxidative stress, inflammation, and apoptosis in liver and brain tissues, and triggered reproductive sterility in common carp. Therefore, we can propose that chlorpyrifos toxication is highly dangerous to the health of common carp. Moreover, chlorpyrifos pollution in the water could threaten the common carp population. Use of chlorpyrifos should be restricted, and aquatic systems should be monitored for chlorpyrifos pollution., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

The liver is the primary site for fructose metabolism; therefore, the liver is susceptible to fructose related metabolic disturbances including metabolic insulin dysfunction, dyslipidemia and inflammation. We investigated whether astaxanthin (ASX) can modify hepatic nuclear factor-kappa B (NF-κB)/sirtuin-1 (SIRT-1) expression to alter oxidative stress caused by ingestion of excess fructose in rats. The animals were divided randomly into two x two factorially arranged groups: two regimens were given either water (W) or 30% fructose in drinking water (F). These two groups were divided further into two subgroups each: two treatments, either orally with 0.2 ml olive oil (OO) or 1 mg ASX/kg/day in 0.2 ml olive oil (ASX). Fructose administration increased serum glucose, triglycerides and very low density lipoproteins, and decreased serum concentration of high density lipoproteins; fructose did not alter serum total cholesterol. Excess fructose decreased hepatic superoxide dismutase (SOD) and increased hepatic NF-κB and MDA levels. ASX treatment increased hepatic SIRT-1 and decreased hepatic NF-κB and malondialdehyde (MDA) levels. ASX treatment decreased hepatic NF-κB and increased SOD levels, but did not alter MDA level in rats fed high fructose. ASX administration ameliorated oxidative stress caused by excess fructose by increasing hepatic NF-κB and SIRT-1 expression. [ABSTRACT FROM AUTHOR]

The purpose of this study was to examine whether the administration of nickel (Ni) was associated with cell apoptosis and also to evaluate whether post acute oral exposure to hyperoside would cause histopathologic alterations in rats. Four groups of male Sprague- Dawley rats (n = 7) used in this study were as follows: a control group and groups treated with Ni (as NiCI2, 13 mg/kg), hyperoside (Hyp) (50 mg/kg), and Ni + Hyp. Routine histopathological examination methods such as hematoxylin and eosin (H&E), periodic acid-Schiff (PAS), and Congo red staining for amyloid deposits were applied at the end of the experiment. In addition, biochemical analyses of the rats' brain tissues were carried out. Immunofluorescence (IF) labeling for active caspase 3 was used in the brain sections taken from the Ni-administrated rats to demonstrate the effect of Hyp on the active caspase 3 expression. The rats treated with Ni (13 mg/kg body weight) showed a significant reduction in antioxidant enzyme activities such as superoxide dismutase, catalase, and glutathione peroxidase. Furthermore, a significant increase was observed in the levels of thiobarbituric acid reagents. Our data suggested that Ni exposure may contribute to brain damage pathogenesis by mediating neuronal death and increasing the oxidative stress in the rat brain. All these alterations were ameliorated by Hyp administration. [ABSTRACT FROM AUTHOR]

Deltamethrin is a widely used synthetic pyrethroid pesticide that protects agricultural yields, including crops, fruits, and vegetables from insect-pests. It is known that deltamethrin toxication leads to metabolic disorders and has detrimental effects on the brain and liver in different organisms. However, the harmful effects of deltamethrin toxication on aquatic animals remain unclear. In the present study, we aimed to evaluate the adverse effects of deltamethrin toxication by performing a histopathological examination, an immunofluorescence assay, and a qRT-PCR on common carp. We observed that a low-dose (0.04 μM) and a high-dose (0.08 μM) of deltamethrin exposure caused lamellar cells hyperplasia and inflammatory cells infiltration in the gills, hyperemia, diffuse hydropic degenerations and focal necrosis in the hepatocytes, necrotic changes in the neurons, and also induced activation of inducible Nitric Oxide Synthase (iNOS) and 8-hydroxy-2-deoxyguanosine (8-OHdG) in the gills, liver, and brain depending on the exposure time (24 h, 48 h, 72 h and 96 h). In addition, deltamethrin toxication caused the up-regulation of caspase-3 and the inducible Nitric Oxide Synthase (iNOS) of the gene expression depending on the dose (0.04 μM and 0.08 μM) and the exposure time in the brain ( p < 0.05, p < 0.01, p < 0.001 ). Our results indicated that long-term deltamethrin exposure could lead to inflammation, oxidative stress, DNA damage, and apoptosis on the different organs in common carp. Thus, deltamethrin toxication is dangerous for common carp populations, and the usage of deltamethrin should be controlled and restricted in agricultural areas. [ABSTRACT FROM AUTHOR]

ABSTRACT Cisplatin (CP) treatment causes the damage in male reproductive system. Carvacrol (CARV) is an antioxidant that is naturally found in some plants. We aimed to investigate the effect of CARV on CP-induced reproductive toxicity in male rats. Eighteen adult male Sprague-Dawley rats were used. The control group ( n = 6) was treated orally with physiological saline (PS) daily for 14 days and a single intraperitoneal (IP) PS injection on day 10. The CP group ( n = 6) was administered with daily oral PS for 14 days and a single IP injection of 10 mg/kg CP on day 10. The CARV + CP group ( n = 6) was treated with daily 75 mg/kg oral CARV for 14 days and a single IP injection of 10 mg/kg CP on day 10. CP treatment caused the damage on some spermatological parameters (motility, live sperm rate, and abnormal sperm rate), increased the oxidative stress, and induced testicular degeneration and apoptosis. However, CARV treatment mitigates CP-induced reproductive toxicity. [ABSTRACT FROM AUTHOR]

Linuron is a widely used herbicide to control grasses and annual broad leaf weeds. It is known that linuron has toxic effects on different organisms. However, the toxic effects of linuron on aquatic organisms, especially fish, is completely unknown. Thus, we aimed to investigate changes in 8-hydroxy-2-deoxyguanosine (8-OHdG) and nuclear factor kappa B (NFkB) activity, histopathological changes, antioxidant responses and acetylcholinesterase (AChE) activity in rainbow trout brain after exposure to linuron. Fish were exposed to 30 μg/L, 120 μg/L and 240 μg/L concentrations of linuron for twenty-one days. Brain tissues were taken from fish for 8-OHdG and NFkB activity, histopathological examination and determination of superoxide dismutase (SOD), catalase (CAT) enzyme activity, lipid peroxidation (LPO), and reduced glutathione (GSH) levels. Our data indicated that high linuron concentrations caused a decrease in GSH levels, SOD and CAT activities in brain tissues ( p < 0.05). LPO levels were significantly increased by 240 μg/L linuron. All concentrations caused a significant inhibition in brain AChE enzyme activity ( p < 0.05). Immunopositivity was detected for 8-OHdG and NFkB, and linuron exposure caused histopathological damage to the brain tissues. The results of this study can provide useful information for understanding of linuron-induced toxicity. [ABSTRACT FROM AUTHOR]