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

The current study evaluated the potential ameliorative and protective impacts of l-carnitine (L-CAR) against γ-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; γ-glutamyl-cysteine synthetase, gGCS; and catalase) were altered by γ-irradiation. Preadministration of L-CAR protected γ-irradiated mice from altered changes induced by γ-irradiation. γ-Irradiation affected the mRNA expression of pro-apoptotic, apoptotic, and anti-apoptotic genes (c-jun, c-fos, Bcl-xl, caspase-3, and BAX). All altered genes were ameliorated by prior l-carnitine administration to γ-irradiated mice. Testicular cells showed deformities and edema with congestion in seminiferous tubules and strong immunoreactivity for caspase-9 and a decrease in immunoreactivity of Bcl-2 in histological and immunohistochemical examination. Prior administration of L-CAR to γ-irradiated mice protected this group from reported changes in caspase-9 and Bcl-2 immunostaining. In conclusion, the current study provides evidence for the protective and ameliorative impacts of L-CAR against γ-irradiation-induced testicular oxidative stress and apoptosis at biochemical, molecular, and cellular levels.

Keywords: antioxidants; apoptosis-associated genes; gene regulation; l-carnitine; reactive oxygen species; γ-irradiation.