Sitaramam V, Rao N M
Department of Zoology, University of Pune, Ganeshkhind.
Indian J Biochem Biophys. 1992 Apr;29(2):103-14.
Metabolically-induced (spontaneous) high amplitude swelling of mitochondria has been shown to be due to a serial disruption of the mitochondrial membranes [D. Sambasivarao & V. Sitaramam (1985), Biochim Biophys Acta, 806, 195-209]. Phosphate- and arsenate-induced swelling was investigated in mitochondria to evaluate the role of phosphate transport in the instability created in the mitochondrial membranes. Phosphate-induced swelling in respiring mitochondria was similar to spontaneous swelling. Both represent essentially colloidal swelling due to the variable porosity induced in the inner membrane to polyols by respiration. Swelling of non-respiring mitochondria at high ammonium phosphate concentrations was, on the other hand, primarily due to high permeability to phosphate. This membrane instability created by phosphate transport in the surrounding lipid involves neither the endogenous nor the exogenous Ca2+.
代谢诱导（自发）的线粒体高振幅肿胀已被证明是由于线粒体膜的一系列破坏[D. Sambasivarao和V. Sitaramam（1985年），《生物化学与生物物理学报》，806，195 - 209]。研究了磷酸盐和砷酸盐诱导的线粒体肿胀，以评估磷酸盐转运在造成线粒体膜不稳定中的作用。呼吸状态下的线粒体中磷酸盐诱导的肿胀与自发肿胀相似。两者本质上都代表由于呼吸作用在内膜中诱导出对多元醇的可变孔隙率而导致的胶体肿胀。另一方面，在高磷酸铵浓度下非呼吸状态的线粒体肿胀主要是由于对磷酸盐的高通透性。由周围脂质中的磷酸盐转运造成的这种膜不稳定既不涉及内源性Ca2+也不涉及外源性Ca2+。
