Uyemura S A, Albuquerque S, Curti C
Departamento de Análises Clínicas, Bromatológicas e Toxicológicas, Faculdade de Ciências Farmacêuticas--USP, Ribeirão Preto, Brazil.
Int J Biochem Cell Biol. 1995 Nov;27(11):1183-9. doi: 10.1016/1357-2725(95)00073-x.
The energetics of heart mitochondria was studied in the acute phase of Trypanosoma cruzi infection in rats. Wistar rats were infected with 2 x 10(5) trypomastigote forms of the Y strain of T. cruzi, and heart mitochondria and submitochondrial particles isolated after 7 and 25 days of infection. Ultrastructure of mitochondria seemed to be preserved, but cytochrome c levels were significantly depressed. Respiratory control ratios (RCR) were decreased for glutamate and succinate oxidations, as a consequence of inhibition of respiration in state 3 and/or of stimulation of respiration in state 4. Stimulation of hydrolytic activity of FoF1-ATPase by energization of mitochondria was approx. 2-fold higher in relation to controls. Mitochondrial ATP concentration remained constant. In conclusion, during the acute phase of T. cruzi infection in rats there is an energy impairment at the level of heart mitochondria, but their ultrastructure and ATP concentration seem to be preserved; the maintenance of ATP may be due to an adaptative mechanism of the cell which includes inhibition of the hydrolytic activity of FoF1-ATPase.
在大鼠克氏锥虫感染的急性期，对心脏线粒体的能量代谢进行了研究。将Wistar大鼠感染2×10⁵个克氏锥虫Y株的锥鞭毛体形式，在感染7天和25天后分离心脏线粒体和亚线粒体颗粒。线粒体的超微结构似乎得以保留，但细胞色素c水平显著降低。由于状态3呼吸受到抑制和/或状态4呼吸受到刺激，谷氨酸和琥珀酸氧化的呼吸控制率（RCR）降低。线粒体通电刺激F₀F₁ - ATP酶的水解活性比对照高约2倍。线粒体ATP浓度保持恒定。总之，在大鼠克氏锥虫感染的急性期，心脏线粒体水平存在能量损伤，但其超微结构和ATP浓度似乎得以保留；ATP的维持可能归因于细胞的一种适应性机制，其中包括对F₀F₁ - ATP酶水解活性的抑制。
