The aminoglycoside Gentamicin is a commonly used antibiotic counteracting the Gram-ve microorganisms. Rats administered with Gentamicin showing a reduced testicular weight and inhibited spermatogenesis, as gentamicin generates ROS, decreasing the antioxidant reserve and accelerate mitochondrial dysfunction which then leads to apoptosis and testicular tissue destruction. This study was designed to investigate the protective effects of curcumin and/or quercetin on the gentamicin induced testicular damage or toxicity in sexually mature adult rats. Pre-treatment with curcumin and/or quercetin, markedly inhibited and ameliorated the reduction in sperm count, viability, motility and sperm production in gentamicin treated rats. Moreover, curcumin and/or quercetin, significantly reduce teratospermia including head or tail abnormalities that observed in the gentamicin treated rats. These abnormalities were effectively normalized by curcumin and/or quercetin pretreatment improving the testicular tissue via counteracting of ROS, improvement of spermatogenesis and ameliorate the sperms quality and quantity. In conclusion supplementation of curcumin and/or quercetin improving the sperm count and morphology via testicular cell repair, counteracting the undesirable effect of gentamicin.
Aflatoxin-contaminated food poses a serious risk to both human and animal health. Copper (1)-nicotinate (Cu +-nicotinate) complex potentiated the prophylactic effect against chronic aflatoxicosis in the experimental animals through the synthesis of less toxic metabolites M1 and Q1 which are easily excreted in urine. To investigate the action of the safety Cu +-nicotinate complex on gene expression of Cytochrome 450 (CYP450) system, the liver tissue samples of orally administered rats for 3 weeks with aflatoxin B1 (AFB1; 30 µg/kg body weight), with and without association of the copper complex (400 µg/kg body weight) were assayed for their gene expression of CYP450 families including 1A2, 3A2 and 2C11 as well as histopathological examination of the hepatic tissue samples was performed. The obtained data denoted that the Cu +-nicotinate complex significantly reduced gene expression of CYP2C11 and CYP3A2 that enhancing the most toxic epoxide metabolite. On the contrary, this complex enhanced the expression of CYP1A2 that synthesize the less toxic metabolite M1 and Q1. The histopathological examination mostly confirmed such observation as the signs of aflatoxicosis were absent in Cu +-nicotinate-treated group. Consequently, it could be predicted that the Cu +-nicotinate complex may be medically used as an inhibitory food additive agent against exposure of aflatoxicosis in the intact animals since the complex contains the copper and nicotinic acid, the two daily required biochemical elements for sustaining live in healthy conditions.
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