Recent advances in cadmium toxicity research suggest an association between cadmium and vascular diseases. However, the mechanisms of cadmium implications in vascular diseases are not yet explained. The objective of our present study is to explore the mechanism of cadmium induced endothelial dysfunction. Doses of 0, 1 and 5microM cadmium chloride were used to test the effects of cadmium on nitric oxide induced tube formation, cellular migration and subcellular actin polymerization in ECV-304 endothelial cells. An egg-yolk vascular bed model was used to study the effects of cadmium on angiogenesis. Results of the present study show that 5microM cadmium chloride effectively inhibited angiogenesis, cellular migration and tube formation. Phalloidin staining, which represents actin polymerization of endothelial cells, reveals that cadmium induces an altered F-actin pattern, which could be the prime cause for cadmium mediated inhibition of cellular migration and angiogenesis. Cadmium was also found to inhibit nitric oxide production in endothelial cells in a calcium free medium, which further hints that cadmium might impair endothelial functions by inhibiting endothelial nitric oxide synthase.
FFB prevents selenite-induced cataractogenesis in albino rat pups, possibly by maintaining antioxidant status and ionic balance through Ca(2+) ATPase pump, inhibition of lipid peroxidation, calpain activation, and protein insolubilization, which have been reported in this article for the first time.
FMO was effective in preventing cataractogenesis in selenite model by enhancing the activities of antioxidant enzyme, reducing the intensity of lipid peroxidation, and inhibiting free radical generation.
These results indicate that ECM influences activation, transdifferentiation and survival of HSCs, and suggest that apart from diffusible factors, the surrounding ECM also influences HSC behavior critical in both the progression of the fibrosis and the restitution of the liver during recovery after hepatic injury.
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