PURPOSE:To determine the antioxidant and anti-inflammatory effects of alfa lipoic acid (ALA) on the liver injury induced by methotrexate (MTX) in rats. METHODS:Thirty two rats were randomly assigned into four equal groups; control, ALA, MTX and MTX with ALA groups. Liver injury was performed with a single dose of MTX (20 mg/kg) to groups 3 and 4. The ALA was administered intraperitonealy for five days in groups 2 and 4. The other rats received saline injection. At the sixth day the rats decapitated, blood and liver tissue samples were removed for TNF-α, IL-1β, malondialdehyde, glutathione, myeloperoxidase and sodium potassium-adenosine triphosphatase levels measurement and histological examination. RESULTS:MTX administration caused a significant decrease in tissue GSH, and tissue Na + , K + ATPase activity and which was accompanied with significant increases in tissue MDA and MPO activity. Moreover the pro-inflammatory cytokines (TNF-α, IL-β)were significantly increased in the MTX group. On the other hand, ALA treatment reversed all these biochemical indices as well as histopathological alterations induced by MTX. CONCLUSION:Alfa lipoic acid ameliorates methotrexate induced oxidative damage of liver in rats with its anti-inflammatory and antioxidant effects.

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OBJECTIVE: We aimed to determine the possible protective effects of melatonin and agomelatine on an animal model of adriamycin nephrotoxicity by 99m Tc DMSA renal scintigraphy and biochemical methods. METHODS: Ten weeks old 49 male Wistar rats were randomly separated into seven groups; namely control (CON), adriamycin (ADR), melatonin (MEL), agomelatine (AGO), melatonin + adriamycin (MEL+ADR), agomelatine + adriamycin (AGO+ADR) and melatonin + agomelatine + adriamycin (MEL+AGO+ADR) groups. Nephrotoxicity was induced by a three-dose of 18 mg/kg adriamycin, i.p. at a 24 h interval on the 5th, 6th and 7th days. A dose of melatonin and agomelatine (40 mg/kg/i.p, the same doses) were injected for 7 days before and after the injected of ADR (18 mg/kg, i.p.), respectively. On the 8th day of the experiment, all animals were evaluated and scintigraphic and biochemical parameters were assessed, respectively. RESULTS: ADR signifi cantly increased blood urea nitrogen (1040 %) and plasma creatinine (1020 %), and decreased 99m Tc DMSA uptake levels (59 %) compared to the control (p < 0.001). Pretreatment with MEL, AGO, MEL+AGO mitigated these abnormalities produced by ADR in the kidney (p < 0.001). CONCLUSION: 99m Tc DMSA for the early determination of ADR-induced nephrotoxicity had an important role. Also, a signifi cant correlation was found between biochemical and scintigraphy parameters. Adriamycin caused signifi cant damages to kidneys that were reduced with MEL and AGO (Tab. 2, Fig. 3, Ref. 39).

We investigated changes in rat liver tissues following administration of thymoquinone (TQ) against 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced hepatotoxicity. Fifty rats were assigned randomly to five groups of 10 as follows: control, corn oil, TCDD, TQ and TCDD + TQ. Biochemical and histopathological analyses were conducted on liver tissue. We found that 30 day TCDD administration caused histopathological changes in liver including thickening of Glisson's capsule, intracytoplasmic vacuolization in hepatocytes, sinusoidal dilation, vascular and sinusoidal congestion and inflammatory cell infiltration. TCDD administration increased malondialdehyde (MDA), total oxidant status (TOS), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) levels in rat liver tissue and reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and total antioxidant status (TAS) levels compared to all other groups. In the TQ treated group, GSH, SOD, CAT and TAS levels increased compared to all other groups. MDA, TOS, ALT, AST, ALP levels decreased compared to all other groups. Our histological findings were consistent with the biochemical findings. The oxidative and histologic effects of TCDD were eliminated by TQ treatment. TCDD administration caused oxidative stress in rat liver and TQ administered with TCDD prevented TCDD induced hepatotoxicity. TQ could be considered an alternative anti-TCDD toxicity agent.

Exposure to acrylamide (Ac) through food is almost inevitable and this kind of toxicity may cause lifelong harm. In present study, we researched effects of Crocin (Cr) on testis histopathology in Ac‐induced testis of rats. Adult male rats were grouped as: group 1, 1 ml saline only; group 2, 50 mg/kg Cr only; group 3, 25 mg/kg Ac only and group 4, 25 mg/kg Ac + 50 mg/kg Cr. All administrations were given as 1 ml/day by gavage for 21 days. It was found that Ac adversely influenced the levels of FSH, testosterone and LH in the blood serum; malondialdehyde (MDA), total antioxidant status (TOS), oxidative stress index (OSI)/ glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), total antioxidant status (TAS) oxidant/antioxidant parameters in testis tissue (p < .01) and the histopathological parameters like Johnson's score, seminiferous tubule diameter, seminiferous epithelial height and H‐score for caspase‐3 immunoreactivity. In contrary, Cr treatment resulted in increase in testosterone, follicle stimulating hormone (FSH), luteinizan hormone (LH) levels and SOD, CAT, GSH, TAS levels (p < .01) and improved all the histopathological changes. In conclusion, Cr has a promising protective potential against Ac‐caused toxic damages in testicular tissue.

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