Gamma-irradiation-induced testicular oxidative stress and apoptosis: Mitigation byl-carnitine

The current study evaluated the potential ameliorative and protective impacts ofl-carnitine (L-CAR) against gamma-irradiation (RAD)-induced oxidative stress and apoptosis in mice testes. Male Swiss mice were allocated into four groups (n = 7). Group 1 served as a control that received saline intraperitoneally (IP). Group 2 received L-CAR (10 mg/kg bw/day; IP in saline) for 17 days. Group 3 received saline for 17 days and on day 7 exposed to RAD at a dose of 0.1 Gy per day for consecutive 10 days. Group 4 (L-CAR + RAD), received L-CAR same as in group 2 and on day 7 exposed to RAD for consecutive 10 days. Testicular antioxidants (malondialdehyde,MDA; gamma-glutamyl-cysteine synthetase,gGCS; and catalase) were altered by gamma-irradiation. Preadministration of L-CAR protected gamma-irradiated mice from altered changes induced by gamma-irradiation. gamma-Irradiation affected the mRNA expression of pro-apoptotic, apoptotic, and anti-apoptotic genes (c-jun, c-fos, Bcl-xl, caspase-3, andBAX). All altered genes were ameliorated by priorl-carnitine administration to gamma-irradiated mice. Testicular cells showed deformities and edema with congestion in seminiferous tubules and strong immunoreactivity forcaspase-9and a decrease in immunoreactivity of Bcl-2 in histological and immunohistochemical examination. Prior administration of L-CAR to gamma-irradiated mice protected this group from reported changes incaspase-9andBcl-2immunostaining. In conclusion, the current study provides evidence for the protective and ameliorative impacts of L-CAR against gamma-irradiation-induced testicular oxidative stress and apoptosis at biochemical, molecular, and cellular levels.