N-acetyl cysteine attenuates diazinon exposure-induced oxidative stress in rat testis.
Summary of "N-acetyl cysteine attenuates diazinon exposure-induced oxidative stress in rat testis."
The aim of this study was to investigate the gonadotoxic effects of diazinon and its mechanism of action with special reference to its possible reactive oxygen species generating potential in rat testis and the protective effect of N-Acetyl Cysteine (NAC) on the exposure of diazinon. The vehicle was given orally to the control group and NAC, diazinon, combination of NAC and diazinon were given to three treatment groups for 4 weeks. Testis lipid peroxidation levels were higher in diazinon group than in control although lipid peroxidation levels were lower in diazinon + NAC group than in diazinon group. The reduced glutathione (GSH) levels were lower in diazinon group than in control and NAC group although its levels were higher in diazinon + NAC group than in diazinon group. Vitamin C, Vitamin E and β-carotene concentrations were also lower in diazinon group than in control and NAC groups. Vitamin E and β-carotene concentrations were higher in diazinon + NAC group than diazinon group. Glutathione peroxidase activity and vitamin A concentrations in the testis did not show any difference between the four groups. In conclusion, we observed that NAC treatment modulated diazinon-induced oxidative injury in the rat testis. These findings suggest that NAC supplementation can be useful in testis oxidative injury caused by the organophosphate insecticides.
Department of Urology, Faculty of Medicine, Suleyman Demirel University, Isparta, Turkey.
This article was published in the following journal.
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/22742659
- DOI: http://dx.doi.org/10.1111/j.1439-0272.2012.01329.x
Medical and Biotech [MESH] Definitions
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
An enzyme that catalyzes the biosynthesis of cysteine in microorganisms and plants from O-acetyl-L-serine and hydrogen sulfide. This enzyme was formerly listed as EC 18.104.22.168.
A naturally occurring phenolic acid which is a carcinogenic inhibitor. It has also been shown to prevent paraquat-induced oxidative stress in rats. (From J Chromatogr A 1996;741(2):223-31; Biosci Biotechnol Biochem 1996;60(5):765-68).
The appearance of carbonyl groups (such as aldehyde or ketone groups) in PROTEINS as the result of several oxidative modification reactions. It is a standard marker for OXIDATIVE STRESS. Carbonylated proteins tend to be more hydrophobic and resistant to proteolysis.
A direct-acting oxidative stress-inducing agent used to examine the effects of oxidant stress on Ca(2+)-dependent signal transduction in vascular endothelial cells. It is also used as a catalyst in polymerization reactions and to introduce peroxy groups into organic molecules.
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