The protective effects of melatonin, vitamin E, and selenium alone or in combination were tested against cadmium-induced oxidative damage in rat testes. A total of 60 male rats were equally divided into five study groups, one of which acted as control receiving subcutaneous injections of physiological saline. The remaining four groups were treated with subcutaneous injections of cadmium chloride at a dose of 1 mg/kg weight. The first study group received no treatment. The second group was treated with a combination of 60 mg/kg vitamin E and 1 mg/kg sodium selenite. Group 3 was treated with 10 mg/kg melatonin, and the fourth group received a combination of vitamin E, sodium selenite, and melatonin at the doses mentioned above. After 1 month, the animals were killed, and the testes were excised for histological inspection and determination of tissue malondialdehyde and the activity of superoxide dismutase. The animals receiving no treatment showed significantly higher malondialdehyde levels and reduced activity of the enzyme (p < 0.05). Treatment with antioxidants resulted in a significant reduction in malondialdehyde when compared to the nontreated animals (p < 0.05) and an increase in the superoxide dismutase activity that was almost the same as the controls. The combination of melatonin, vitamin E, and selenium appears to have the more profound effect against cadmium-induced testicular injury.
Opiate abuse has been a matter of serious concern in male adolescents. This study investigates the effects of chronic morphine administration on serum luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone levels, testicular histology, and body and testes weight in developing male rats. Animals were subcutaneously injected with morphine (5 mg/kg) or saline (1 mL/kg) twice daily for 30 days. Body weight determinations and injections were carried out under light ether anesthesia. At the end of the experiments, the rats were decapitated and blood samples were collected. Serum levels of LH and FSH were measured. Chronic morphine administration significantly decreased decreased serum testosterone (p < .02) and LH (p < .01) levels, but not FSH release compared to controls. Morphine exposure reduced body weight (p < .01), but had no significant effect on the testicular weight. When the testicular tissue was histologically examined, structural features of the seminiferous tubules and Leydig cells were similar in both saline and morphine-treated animals. The results suggest that opiates affect testosterone release through the hypothalamo-hypophyseal-gonadal axis rather than by a local testicular mechanism. Chronic morphine exposure during sexual maturation may have long-term endocrine disturbances in male rats.
The present study was performed to determine the protective effects of melatonin alone and vitamin E with selenium combination against cadmium-induced oxidative damage in rat liver. A total of 60 male rats were equally divided into five groups, one of which acted as control receiving subcutaneous injections of physiological saline. The remaining four groups were treated with subcutaneous injections of cadmium chloride at a dose of 1 mg/kg weight. The first study group received no treatment. The second group was treated with a combination of 60 mg/kg vitamin E and 1 mg/kg sodium selenite. Group 3 was treated with 10 mg/kg melatonin, and the four group received a combination of vitamin E, sodium selenite, and melatonin at the doses mentioned above. After 1 month, the animals were killed, and liver and kidneys were excised for histopathological inspection and determination of tissue malondialdehyde and the activity of superoxide dismutase. The animals receiving no treatment showed significantly higher malondialdehyde levels and reduced activity of superoxide dismutase (p < 0.05). Treatment with antioxidants resulted in a significant reduction in malondialdehyde when compared to nontreated animals (p < 0.05) and increase in the enzyme activity that was almost the same as the controls. The pathological findings were also in parallel with the results of the biochemical analysis. In conclusion, all the agents tested had protective effects against cadmium-induced oxidative damage.
The toxic effects of lead(II) have been studied in Escherichia coli cells. Using microcalorimetric analysis, it was shown that E. coli growth was inhibited in the presence of Pb2+ resulting from damage to the cell membrane and that Pb2+ takes part in the metabolism of cells. Treatment with lysozyme confirms damage to the cell's outer membrane. Similarities between the ionic radii and charge/radius ratio cause Pb(II) to replace Ca(II) at the binding sites of lipopolysacharides, leading to rupture of protecting areas on the cell's surface. Consequently, the protection and functionality of outer membrane is lost, thus becoming the basis for the biological effect of Pb2+ on E. coli.
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