Zychlinski L, Byczkowski J Z
Department of Toxicology, Academy of Medicine, Gdansk, Poland.
Arch Environ Contam Toxicol. 1990 Jan-Feb;19(1):138-42. doi: 10.1007/BF01059822.
The bioenergetic functions of liver mitochondria were studied following the acute and chronic exposure of rats to vanadium pentoxide via respiratory tract. The mitochondrial respiration with glutamate or succinate as substrate was inhibited significantly when compared to the control animals. No inhibition was found with ascorbate. The same effects were observed in vitro. Vanadium (V) was responsible for these inhibitory effects. It is postulated that significant amounts of vanadate are accumulated in the intermembrane space of liver mitochondria of the exposed rats. The process of "detoxification" by reduction of vanadate in the tissue may be insufficient to prevent the deleterious action of this compound on liver mitochondria.
通过呼吸道对大鼠进行急性和慢性五氧化二钒暴露后,研究了肝线粒体的生物能量功能。与对照动物相比,以谷氨酸或琥珀酸为底物的线粒体呼吸受到显著抑制。抗坏血酸未发现抑制作用。体外也观察到了相同的效果。钒(V)是造成这些抑制作用的原因。据推测,暴露大鼠肝线粒体膜间隙中积累了大量钒酸盐。组织中钒酸盐还原的“解毒”过程可能不足以防止该化合物对肝线粒体的有害作用。