Lenton L M, Behm C A, Bygrave F L
Division of Biochemistry and Molecular Biology, School of Life Sciences, Australian National University, Canberra.
Biochim Biophys Acta. 1994 Jul 29;1186(3):237-42. doi: 10.1016/0005-2728(94)90183-x.
The F1F0-ATPase activity of liver mitochondria isolated from rats infected with Fasciola hepatica at 3 and 4 weeks post-infection showed a marked loss of sensitivity to oligomycin and to N,N'-dicyclohexylcarbodiimide. A loss of sensitivity to diethylstilbestrol was also demonstrated at 4 weeks post-infection. Recovery was apparent in most cases by 6 weeks post-infection. No significant difference in latent ATPase activity was observed between mitochondria from control and infected livers at any stage of the infection. The mitochondria from infected livers were therefore considered to have a full complement of the F1 moiety of the F1F0-ATPase complex. Purification of the mitochondrial ATPase from 4-week infected livers resulted in a very low yield of an oligomycin-insensitive complex. This was due to a failure to enrich specific activity during purification. The evidence presented indicates that infection with Fasciola hepatica gives rise to alterations in the function of the host liver mitochondrial ATPase, namely loss of inhibitor sensitivity and apparent structural alterations of the ATPase complex.
感染肝片吸虫3周和4周后从大鼠分离的肝线粒体的F1F0 - ATP酶活性对寡霉素和N,N'-二环己基碳二亚胺的敏感性显著丧失。在感染后4周也表现出对己烯雌酚敏感性的丧失。在大多数情况下，感染后6周恢复明显。在感染的任何阶段，对照肝脏和感染肝脏的线粒体之间未观察到潜在ATP酶活性的显著差异。因此，感染肝脏的线粒体被认为具有F1F0 - ATP酶复合物F1部分的完整成分。从感染4周的肝脏中纯化线粒体ATP酶导致寡霉素不敏感复合物的产量非常低。这是由于在纯化过程中未能提高比活性。所提供的证据表明，感染肝片吸虫会导致宿主肝脏线粒体ATP酶功能的改变，即抑制剂敏感性丧失和ATP酶复合物明显的结构改变。
