Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2008) 16 P262

ECE2008 Poster Presentations Endocrine disruptors (9 abstracts)

Lipid peroxidation, antioxidant enzymes activities in testis and spermatotoxicity of rats during short-term exposure to atrazine

Sunny O Abarikwu 3 , Adebukola C Adesiyan 1 , Titilola O Oyejola 1 , Mathew O Oyeyemi 2 & Olatunde O Farombi 1


1Drug Toxicology Research Laboratories, Faculty of Basic Medical Sciences, University of Ibadan, Ibadan, Nigeria; 2Department of Veterinary Surgery and Reproduction,Faculty of Verterinary Medicine, University of Ibadan, Ibadan, Nigeria; 3Division of Biochemistry, College of Natural Sciences, Redeemer’s University, Redemption City, Nigeria.


Atrazine is a chloro-s-triazine herbicide that has been in used worldwide for over 4 decades now. Its endocrine disrupting effects have been shown in mammals but the specific mechanism or mechanisms of action remain unknown. The aim of this study was to evaluate the acute effects of atrazine on testicular antioxidant systems and on some spermatological parameters in rats.

Atrazine was administered to wistar rats at a dose equivalent to 120 mg/kg or 200 mg/kg b. wt daily for seven days. The results indicate a decrease in the terminal body weight and food consumption in both treated groups. Testicular and epididymal sperm number, spermatozoa viability and motility in atrazine treated animals decreased significantly. Therefore atrazine treatment provoked a significant decrease in daily spermatozoal production. The induction of abnormal sperms was increased by atrazine. These effects were seen in a dose dependent manner. While there were no significant effects on lipid peroxidation, superoxide dismutase (SOD) and catalase (CAT) activities and H2O2-generation in the atrazine groups, glutathione (GSH) and glutathione-S-transferase (GST) activities in the testis after the last day of treatment showed a significant increase vs control. The epithelium of the seminiferous tubules showed normal histology.

Possibly the dose and duration of exposure was inadequate to induce tissue pathology or that atrazine have a direct effect on spermatozoa. Our study has added the information that oral atrazine exposure attributes to alterations in spermatological parameters without significant effects on the parameters of testicular oxidative stress. This appears not to be mediated by the seminiferous tubules epithelium and may be secondarily related to the restricted food intake and growth rate. Furthermore, our data implicates the GSH/GST status as sensitive markers for atrazine testicular toxicity during short-term exposure.

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