Sperm Oxidative Damage Research Articles

Antioxidative potential of Quercetin against hydrogen peroxide induced oxidative stress in spermatozoa in vitro

This study was carried out to test the antioxidant effects of Quercetin on sperm parameters and antioxidant enzymes in male rats assessed in vitro after H(2) 0(2) -mediated sperm oxidative damage. Spermatozoa were incubated with Quercetin (10, 100 and 200 μm), H(2) O(2) alone (100 μm) and Quercetin (100, 200 μm) + H(2) O(2) (100 μm) repectively, for 3 h at 32 °C. After that, sperm parameters (motility, viability and abnormal morphology), malondialdehyde, superoxide dismutase, catalase and glutathione peroxidase levels were determined. We found that exposure to H(2) O(2) let to significant increase in lipid peroxidation (LP) and abnormal morphology associated with significant decrease in sperm motility, viability and antioxidant enzymes activities. When Quercetin was added in culture medium, it improved activities of antioxidant enzymes and protected spermatozoa against the deleterious effect of H(2) O(2) on sperm parameters and LP. This study demonstrated that supplementation with Quercetin could protect spermatozoa against H(2) O(2) -mediated sperm damage.

Protective effect of resveratrol on sperm oxidative damage caused by methyl-parathion exposure in mice

Protective effect of resveratrol on sperm oxidative damage caused by methyl-parathion exposure in mice

Male reproductive toxicity of trichloroethylene: sperm protein oxidation and decreased fertilizing ability.

The objective of the present study was to characterize and investigate potential mechanisms for the male reproductive toxicity of trichloroethylene (TCE). Male rats exposed to TCE in drinking water exhibited a dose-dependent decrease in the ability to fertilize oocytes from untreated females. This reduction in fertilizing ability occurred in the absence of treatment-related changes in combined testes/epididymides weight, sperm concentration, or sperm motility. In addition, flow cytometric analysis showed that there were no treatment-related differences in sperm mitochondrial membrane potential or acrosomal stability. TCE caused slight histological changes in efferent ductule epithelium, coinciding with the previously reported ductule localization of cytochrome P450 2E1. However, no alterations were noted in the testis or in any segment of the epididymis. Because there were no treatment-related changes to sperm indices and no clear pathological lesions to explain the reduced fertilization, the present study investigated TCE-mediated sperm oxidative damage. Oxidized proteins were detected by immunochemical techniques following the derivatization of sperm protein carbonyls with dinitrophenyl hydrazine. Immunochemical staining of whole, intact sperm showed the presence of halos of oxidized proteins around the head and midpiece of sperm from TCE-treated animals. The presence of oxidized sperm proteins was confirmed by Western blotting using in vitro-oxidized sperm as a positive control. Thiobarbituric acid reactive substances analyses showed a dose-dependent increase in the level of lipid peroxidation in sperm from treated animals, as well. Oxidative damage to sperm may explain the diminished fertilizing capacity of exposed animals and provide another mechanism by which TCE can adversely affect reproductive capabilities in the male.