Propargylglycine aggravates liver damage in LPS-treated rats: Possible relation of nitrosative stress with the inhibition of H2S formation

Background: Hydrogen sulfide (H2S) is a naturally occurring gaseous transmitter, which may play important roles in normal physiology and disease. Here, we investigated the effect of endogenously formed H2S in the endotoxemic organ injury

The protective effect of resveratrol against cyclosporine A-induced oxidative stress and hepatotoxicity

The immunosuppressive agent cyclosporine A (CsA) has hepatotoxic potential. Increased reactive oxygen species (ROS) formation is among the causes leading to hepatotoxicity. This study aimed to investigate the effect of resveratrol (RES) on CsA-induced oxidative stress and hepatotoxicity in rats. Rats were treated with RES (10 mg/kg/day; i.p.) for 14 days. CsA (25 mg/kg/day; s.c.) was given during the last seven days together with RES. Serum alanine aminotransferase and aspartate aminotransferase activities together with hepatic histopathological examinations were performed. ROS, thiobarbituric acid reactive substances (TBARS), advanced oxidation protein products (AOPPs), ferric reducing antioxidant power, and glutathione levels as well as superoxide dismutase, and glutathione peroxidase activities were measured in the liver tissue. RES ameliorated histopathological changes and decreased hepatic ROS, TBARS, and AOPP levels significantly. However, antioxidant parameters did not change in CsA-treated rats. Our results indicate that RES treatment may be effective in decreasing CsA-induced oxidative stress and hepatotoxicity

Changes in Prooxidant-Antioxidant Balance in Tissues of Rats Following Long-term Hyperglycemic Status

Introduction. Reactive oxygen species play an important role in the pathogenesis of organ damage in diabetes mellitus. Streptozotosin (STZ) is a commonly employed compound to produce diabetes mellitus and these animals exhibit most of diabetic complications. Methods. In our study, diabetes was induced by a single intraperitoneal injection of STZ at a dose of 50 mg/kg in rats and they were killed 12 weeks after STZ. Endogenous lipid peroxide levels, enzymatic and non-enzymatic antioxidants were measured in liver, heart, kidney, brain, and testis tissues to investigate the effect of long-term hyperglycemic state. The susceptibility of diabetic tissues to oxidative stress was also examined in in vitro oxidizing system containing ascorbic acid and iron. Results. We found that prooxidant and antioxidant balance has changed in favor of prooxidation in the tissues of diabetic rats. The susceptibility of liver to oxidative stress increased; however, this susceptibility did not change in heart, kidney, brain, and testis of diabetic rats. Conclusion. Our results indicate that long-term hyperglycemic state disturbs hepatic prooxidant-antioxidant balance at an earlier period and more pronouncedly than other tissues

Response of liver to lipopolysaccharide treatment in male and female rats

Gender is considered to be an important factor in endotoxin-induced tissue damage. Our aim was to examine the role of sex on the prooxidant-antioxidant status, necrotic and apoptotic events in the liver of lipopolysaccharide (LPS)-treated rats. We determined levels of lipid peroxides, non-enzymatic and enzymatic antioxidants, and expressions of apoptosis-related proteins, antiapoptotic B cell lymphoma-2 (Bcl-2) and proapoptotic Bax, caspase-3 activity and apoptotic cell numbers in the liver. Hepatic histopathology and serum alanine transaminase (ALT) and aspartate transaminase (AST) activities were also investigated. Male and female Wistar rats (180-200g) were injected with LPS (10 mg/kg, i.p.) and examinations were performed 6 h after the injection. Significant increases in hepatic thiobarbituric acid reactive substances and diene conjugate levels were observed in male and female rats following LPS treatment. However, there were no changes in hepatic glutathione, vitamin E and vitamin C levels together with superoxide dismutase, glutathione peroxidase and glutathione transferase activities. LPS treatment caused significant increases in serum ALT and AST activities and lymphocyte infiltration and necrotic changes in the livers. Bcl-2 and Bax expressions, caspase-3 activity and apoptotic cell numbers were also found to be increased in both groups. In conclusion, no sex-dependent difference was observed in the changed hepatic prooxidant-antioxidant status of rats following LPS treatment. Besides, the process leading to apoptosis and necrosis in the liver showed a similar pattern in both gender of rats. (C) 2012 Elsevier GmbH. All rights reserved

Effect of carnosine treatment on oxidative stress in serum, apoB-containing lipoproteins fraction and erythrocytes of aged rats

One of the mechanisms underlying the aging process is proposed to be oxidative damage by free radicals. Carnosine (beta-alanyl-L-histidine) is a dipeptide with antioxidant properties. In this study, we investigated the effect of carnosine supplementation on oxidative stress in serum, apoB-containing lipoproteins (LDL + VLDL) and erythrocytes of young and aged rats. At the initiation of the study, young and aged rats were 5 and 22 months old, respectively. Carnosine (250 mg/kg, daily, ip) was administered for 1 month to young and aged rats. We found that serum malondialdehyde (MDA) and diene conjugate (DC) levels and endogenous DC and copper-induced MDA levels in the LDL + VLDL fraction increased in aged rats, but there was no change in plasma antioxidant activity. Endogenous DC and H(2)O(2)-induced MDA. levels were also higher, but glutathione (GSH) levels were lower in erythrocytes of aged rats. Administration of carnosine for 1 month to aged rats resulted in decreased levels of MDA and DC in serum, the LDL + VLDL fraction and erythrocytes and increased levels of GSH in erythrocytes. Our findings indicate that in vivo carnosine treatment may be useful for the decrease in aged-induced oxidative stress in serum, the LDL + VLDL fraction and erythrocytes

Vascular endothelial growth factor G+405C polymorphism may contribute to the risk of developing papillary thyroid carcinoma

BackgroundPapillary thyroid carcinoma (PTC) is the most common endocrine malignancy. Vascular endothelial growth factor (VEGF) is a mediator implicated with cell proliferation, differentiation and migration, and monocyte/macrophage chemotaxis. In present study, we aimed to investigate the relationship between VEGF gene polymorphisms (G+405C, T-460C, and A-2578C) and PTC susceptibility