ABSTRACT
Humans and animals are most sensitive to toxicant exposure during development. Dioxin, as an endocrine disruptor, is known to impair testicular functions and fertility. The present study was carried out to investigate the effects of quercetin on TCDD-induced toxicity in the testicular tissue of rats. Forty male albino rats were randomly divided into four groups (n = 10/group). Group I represent the control group; Group II administrated TCDD (27.5 μg/kg) via gavage for four week; Group III received quercetin (20 mg/kg bw.) Via gavage before TCDD administration; Group IV received quercetin alone (20 mg/kg bw). Biochemical markers included levels of testicular malondialdehyde formation and reduced glutathione as well as monitoring the activities of testicular superoxide dismutase, catalase, glutathione peroxidase, glutathione S-transferase were studied. Also, serum hormonal profiles of luteinizing hormone and testosterone were reported. Our results show that administration of TCDD induces testicular damage concerning oxidative stress parameters, serum hormone level and sperm parameters. In addition, the microscopic structures of the testis, including histological and immunohistochemical studies were evaluated. Exposure to TCDD induces histopathological changes in rats testis including degeneration of seminiferous tubules, tubular necrosis, intratubular vacuolization, widened lumen and deshaped germ cells. Marked increase of apoptotic activity was observed. Also, our results clearly demonstrate the ameliorative potential of quercetin in dioxin induced testicular damage.
ABSTRACT
The present study was conducted to evaluate the possible protective effect of selenium in reversing methyl parathion -induced testicular damage in male rats, using light and electron microscopy with reference to plasma testosterone (T) and lutenizing hormone (LH) levels. The animals were randomly divided into four groups, Group 1: control animals. Group 2: animals were treated with sodium selenite in a dose (10μg/kg b.w). Group 3: rats were given methyl parathion in a dose (0.28 mg/kg b.w). Group 4: rats were received sodium selenite prior to treatment with methyl parathion. Results showed that animals exposed to methyl parathion displayed a reduction in body and testicular weight and a reduction in seminiferous tubules diameter. At the end of the treatments plasma testosterone and LH concentrations were reduced significantly in methyl parathion-treated rats. Light and electron microscopy of testes from treated animals with methyl parathion showed disorganization of tubular elements with increased intercellular space. Also, revealed necrosis and cellular damage. In addition, a significant increase in sperm DNA fragmentation was detected. Selenium supplementation to rats given methyl parathion improved the testicular damage. In conclusion, Selenium may be useful for the prevention and treatment of methyl parathion -induced testicular damage.