musicHydrogen sulfide prevents tissue damage in sodium selenite-induced liver injury in mice. Sodium selenite (Na2SeO3) is a powerful oxidant that

Tanjavur Urumi Melam Pushpavanam Kuppusamy Songgolkes

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tanjavur urumi melam pushpavanam kuppusamy songgolkes Category:Indian musical groups Category:Folk music groups Category:Performers of Hindu musicHydrogen sulfide prevents tissue damage in sodium selenite-induced liver injury in mice. Sodium selenite (Na2SeO3) is a powerful oxidant that could induce acute liver failure. However, whether hydrogen sulfide (H2S) has the protective effect on selenite-induced liver damage remains unclear. In this study, we explored the effects of H2S on Na2SeO3-induced liver injury in mice and the mechanism underlying this protection. Our data showed that Na2SeO3 induced acute liver injury, as evidenced by elevated serum enzyme activities and histological changes of the liver, with a marked elevation of oxidative stress. Na2SeO3 induced the generation of H2S in vivo. Pretreatment with H2S donor GYY4137 (500 µg/kg, ip) 1 h before Na2SeO3 (3.5 mg/kg, ip) significantly attenuated liver damage by inhibiting oxidative stress. Furthermore, GYY4137 significantly decreased the levels of serum enzyme activities and oxidative stress markers. Interestingly, GYY4137 also reversed the reduction in the activity of hepatic antioxidative enzymes. These findings indicate that H2S protects against selenite-induced liver injury and oxidative stress by inhibiting oxidative stress in mice.Cancer patients do not always respond well to radiation therapy. For example, they can develop severe and untreatable radiation induced side effects. Our laboratory has been investigating the role of the nitric oxide (NO) system in radiation induced fibrosis of the intestines. NO is a free radical that is generated by radiation therapy and generated by stromal cells during the normal response to injury in the intestine. One of the consequences of NO is increased smooth muscle tone which is associated with an increased sensitivity to norepinephrine. NO is also capable of altering the proliferation and apoptosis of stromal cells. In normal intestine, NO has been shown to stimulate apoptosis and inhibit proliferation of intestinal smooth muscle cells (SMC). However, these same mechanisms may be involved in radiation induced fibrosis. Our research has shown that the NO system is important in the pathogenesis of radiation induced fibrosis in the intestine. Experiments with endothelial cell (EC) specific NO synthase (N

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