Arvelo Francisco
Laboratorio de Cultivo de Tejidos y Biología de Tumores, Instituto de Biología Experimental, Facultad de Ciencias, Universidad Central de Venezuela, Apartado 47114, Caracas-Venezuela, 1041.
Acta Cient Venez. 2002;53(4):297-306.
It is now accepted that mitochondria are endosymbionts, originated in aerobic bacteria which were integrated by the ancestor of eukaryotic cells. A part of the apoptotic machinery could exist in unicellular eukaryotic and some controlling apoptosis components might be present in prokaryotes. It is therefore possible that the mechanism originally involved in the maintenance of the symbiosis between the bacterial ancestor of the mitochondria and the host cell precursor of eukaryotes, provided the basis for the actual mechanism controlling cell survival. Metazoans would have improved this possibility by connecting to the mitochondria as principal effector of cellular death to the pathways of signal transduction. A variety of events appoint to the mitochondria as principal effector of the apoptosis. This including the release caspase activators (cytochrome c), changes in electron transport, loss of mitochondrial transmembrane potential, altered cellular oxidation-reduction, and participation of pro and antiapoptotic Bcl-2 proteins. The different signals that converge on mitochondria for activation or inhibition of these events, delineate several pathways in the physiology of the cellular death.
现在人们普遍认为，线粒体是内共生体，起源于需氧细菌，被真核细胞的祖先整合。凋亡机制的一部分可能存在于单细胞真核生物中，一些控制凋亡的成分可能存在于原核生物中。因此，最初参与维持线粒体细菌祖先与真核生物宿主细胞前体之间共生关系的机制，可能为控制细胞存活的实际机制提供了基础。后生动物可能通过将作为细胞死亡主要效应器的线粒体与信号转导途径相连，提高了这种可能性。多种事件表明线粒体是凋亡的主要效应器。这包括半胱天冬酶激活剂（细胞色素c）的释放、电子传递的变化、线粒体跨膜电位的丧失、细胞氧化还原的改变以及促凋亡和抗凋亡Bcl-2蛋白的参与。汇聚在线粒体上以激活或抑制这些事件的不同信号，描绘了细胞死亡生理学中的几种途径。
