Transplacental exposure to vinclozolin induces epididymal and testicular toxicity in adult male rats

Abstract

Vinclozolin (3-(3-5-dichlorophenyl)-5-methyl-oxazolidine-2,4-dione) is extensively used in the viticulture, agriculture and commercial horticulture to control several fungal pathogens and has been shown to induce reproductive abnormalities in male rats, causing reduced fertility. The mechanism of action of vinclozolin on male reproductive system is not clear. In the present study we investigated whether prenatal administration of vinclozolin induces oxidative stress in the testes and changes in sperm quality and quantity in epididymis in adult male rats. Pregnant rats were injected with 1, 5 and 10 mg vinclozolin/Kg body weight on 1st, 7th and 14th day of pregnancy and allowed to deliver. Male pups were maintained up to postnatal day 100 and used for assessing testicular and epididymal toxicity. Embryonic exposure to vinclozolin significantly decreased in the sperm density, number of motile sperm, viable sperm and HOS tail coiled sperm in adult rats. Significant increase in the levels of lipid peroxidation with a significant reduction in the activity levels of superoxide dismutase and catalase in testis was observed in rats exposed to vinclozolin during embryonic development. It can be concluded that prenatal exposure to vinclozolin induced oxidative stress in testis of adult rats thereby decreases the sperm quantity and deteriorates sperm quality.