Abstract
Gentamycin is an aminoglycoside antibiotic commonly used against Gram-negative bacteria. This study was designed to investigate the testicular toxicity of gentamicin in adult rats. Gentamicin was given to rats at 0, 60, 80 or 100 mg/kg/day for 10 consecutive days. The absolute weight of testes reduced significantly in relation to the dose, while gentamicin at a dose of 60 mg/kg did not show any significant change in the relative testes weight. Sperm count and motility and daily sperm production decreased in a dose-related manner. Serum testosterone level was significantly decreased after gentamicin treatment in a dose-dependent manner. The activities of LDH-X was decreased while that of caspases-3 &-9 were significantly increased in a dose-related manner. H2O2 production and lipid peroxidation were significantly increased while the activities of SOD, CAT, GPX and GR, in addition to, the non-enzymatic GSH level were significantly decreased suggesting that gentamicin-induced oxidative stress. The biochemical findings were confirmed by histopathological examination of the testis. Atrophy, degeneration and loss of spermatogenesis were observed after gentamicin treatment. The findings of this study indicate that gentamicin induces oxidative stress associated with impairment of spermatogenesis, in addition to apoptosis. These data provide insight into the mode of action of gentamicin-induced impairment of spermatogenesis in the rat testis.
•Gentamicin inhibited spermatogenesis.•Gentamicin decreased testes weight, decreased sperm count, motility and daily sperm production.•It decreased serum testosterone, decreased testicular LDH-X activity and increased testicular caspase-3 & -9 activities.•It induced oxidative stress.•Genatmicin induced histopathological abnormalities.