Chakraborti T, Ghosh S K, Michael J R, Batabyal S K, Chakraborti S
Department of Biochemistry and Biophysics, University of Kalyani, West Bengal, India.
Mol Cell Biochem. 1998 Oct;187(1-2):1-10. doi: 10.1023/a:1006802903504.
Although oxidants such as superoxide (O2.) and hydrogen peroxide (H2O2) play a role in host-mediated destruction of foreign pathogens yet excessive generation of oxidants may lead to a variety of pathological complications in the cardiovascular system. An important mechanism by which oxidants cause dysfunction of the cardiovascular system appears to be due to the increase in intracellular free Ca2+ concentration. Oxidants cause cellular Ca2+ mobilization by modulating activities of a variety of regulators such as Na+/H+ and Na+/Ca2+ exchangers, Na+/K+ ATPase and Ca2+ ATPase and Ca2+ channels that are associated with Ca2+ transport in the plasma membrane and the sarco(endo)plasmic reticular membrane of myocardial cells. Recent research have suggested that the increase in Ca2+ level by oxidants plays a pivotal role in inducing several protein kinases such as protein kinase C, tyrosine kinase and mitogen activated protein kinases. Oxidant-mediated alteration of different signal transduction systems and their interations eventually regulate a variety of pathological conditions such as atherosclerosis, apoptosis and necrosis in the myocardium.
尽管超氧阴离子（O2.）和过氧化氢（H2O2）等氧化剂在宿主介导的对外来病原体的破坏中发挥作用，但氧化剂的过度产生可能导致心血管系统出现多种病理并发症。氧化剂导致心血管系统功能障碍的一个重要机制似乎是细胞内游离Ca2+浓度的增加。氧化剂通过调节多种调节剂的活性来引起细胞Ca2+动员，这些调节剂如Na+/H+和Na+/Ca2+交换体、Na+/K+ ATP酶、Ca2+ ATP酶以及与心肌细胞质膜和肌浆（内质）网中Ca2+转运相关的Ca2+通道。最近的研究表明，氧化剂引起的Ca2+水平升高在诱导几种蛋白激酶如蛋白激酶C、酪氨酸激酶和丝裂原活化蛋白激酶中起关键作用。氧化剂介导的不同信号转导系统的改变及其相互作用最终调节多种病理状态，如动脉粥样硬化、心肌细胞凋亡和坏死。
