thromboxane-b2 and nickel-chloride

This study was undertaken to examine the effects of nickel (Ni) on human platelet function. In a (concentration-dependent manner, Ni significantly inhibited the function of platelet aggregation induced by collagen. The phenomenon of lipid peroxidation was involved as Ni significantly increased malondialdehyde (MDA) levels with reduction in platelet reduced glutathione (GSH) and alpha-tocopherol content. Further, platelet thromboxane B2, formation was markedly inhibited and the levels of cyclic AMP were significantly elevated by Ni. Treatment with ascorbic acid (Vit C) significantly lowered the levels of MDA and increased the content of alpha-tocopherol and reduced GSH. Vit C also significantly increased platelet aggregation and thromboxane B2 when coincubated with Ni. Data show that Ni is toxic as evidenced by lipid peroxidative damage and inhibition of human platelet aggregation, but that ascorbic acid provides protection, at least partially, against this metal.

Topics: Ascorbic Acid; Blood Platelets; Cyclic AMP; Glutathione; Humans; In Vitro Techniques; Lipid Peroxidation; Nickel; Oxidative Stress; Platelet Aggregation; Thromboxane B2; Vitamin E