Reproductive Hormones and Sperm Parameter Alteration in Chromium (III) Nitrate and Lead Acetate-Treated Male Wistar Rats: Possible Role of PI3K/Akt Pathway

Abstract

The effects of heavy metals such as lead have been well-reported to interfere with testicular steroidogenesis and spermatogenesis, but conflicting reports exist regarding the reproductive effects of trivalent chromium. This study investigated the hormonal, sperm quality, and quantity changes in chromium (III) nitrate and lead acetate-treated male Wistar rats. Twenty male Wistar rats were divided into four groups (n=5): control, 300µg/kg chromium (III) nitrate (Cr(NO3)3), 15 mg/kg lead acetate (Pb), and Pb combined with Cr(NO3)3. Oral exposures to Pb and Cr(NO3)3 were for 42 days. The ELISA method was used for the evaluation of serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone levels, testicular 17β-hydroxysteroid dehydrogenase (17β-HSD), phosphoinositide-3-kinase (PI3K) and protein kinase B (Akt). Epididymal sperms were assessed microscopically. Lead acetate negatively affects serum levels of FSH, LH, testosterone, 17β-HSD, sperm motility, immotile sperm, PI3K/Akt activities, sperm viability, and sperm abnormalities. Also, Cr(NO3)3 caused a reduction in LH and testosterone levels. The combined exposure of Pb and Cr(NO3)3 group showed significant hormonal, 17β-HSD, and Akt suppression. The combined treatment improved sperm motility, viability, and PI3K, while sperm immotility and abnormal sperm morphology were reduced. The negative impacts of the lead acetate and chromium (III) nitrate on testicular steroidogenesis partially impair spermatogenesis. Hence, the findings of this study emphasize the need to discourage the use of chromium (III) nitrate as an antioxidant supplement due to the possibility that its prolonged use can lead to male infertility through impairment of steroidogenesis and spermatogenesis.