Moreno A J, Madeira V M
Departamento de Zoologia, Universidade de Coimbra, Portugal.
Biochim Biophys Acta. 1991 Oct 18;1060(2):166-74. doi: 10.1016/s0005-2728(09)91004-0.
The organochloride insecticide DDT (2,2-bis(p-chlorophenyl)-1,1-trichloroethane) depresses the phosphorylation efficiency of mitochondria as inferred from the decrease of respiratory control ratio (RCR) and P/O ratio, perturbations of transmembrane potential (delta psi) fluctuations associated with mitochondrial energization and phosphorylative cycle induced by ADP. DDT depresses the delta psi developed by energized mitochondria and prevents complete repolarization, that is delayed and resumed at a lower rate. The inhibitory action of DDT on phosphorylation efficiency may result from: (1) a direct effect on the ubiquinol-cytochrome c segment of the redox chain; (2) direct action on the ATP-synthetase complex; (3) partial inhibition of the phosphate transporter. DDT preferentially interacts with phosphorylation process in relation to respiration. High concentrations of DDT induce destruction of the structural integrity of mitochondria.
有机氯杀虫剂滴滴涕(2,2-双(对氯苯基)-1,1,1-三氯乙烷)会降低线粒体的磷酸化效率,这可从呼吸控制率(RCR)和P/O比值的降低、与线粒体能量化相关的跨膜电位(δψ)波动的扰动以及由ADP诱导的磷酸化循环中推断出来。滴滴涕会降低由活跃线粒体产生的δψ,并阻止完全复极化,即复极化会延迟且以较低速率恢复。滴滴涕对磷酸化效率的抑制作用可能源于:(1)对氧化还原链中泛醇-细胞色素c部分的直接作用;(2)对ATP合成酶复合体的直接作用;(3)对磷酸转运体的部分抑制。相对于呼吸作用,滴滴涕优先与磷酸化过程相互作用。高浓度的滴滴涕会导致线粒体结构完整性的破坏。