Hayes A W
Toxicology. 1976 Aug-Sep;6(2):253-61. doi: 10.1016/0300-483x(76)90027-5.
The effect of rubratoxin B on the electron transport system of mouse liver mitochondria was investigated. Oxygen consumption in mitochondria isolated from male mice was measured polarographically in a Gilson Oxygraph Model K-ICC. Oxygen consumption was depressed 73% at a concentration of 1.13 mM rubratoxin. At concentrations as low as 0.08 mM rubratoxin B, 50% inhibition was observed. Rubratoxin B (0.28 mM) depressed oxygen consumption 67% in ADP-coupled mitochondria and 60% in 2,4-dinitrophenol (DNP)-uncoupled mitochondria using either pyridine-nucleotide linked substrates or succinate. By employing the N,N,N',N''-tetramethyl-p-phenylenediamine (TMPD) shunt, it was shown that inhibition was not between cytochrome b and cytochrome C1 or C. It appears, based on these studies and comparison with known inhibitors of specific sites along the electron transport system that the principal site of action of rubratoxin B is between cytochrome C1 or C and the termination of electron flow.
研究了红天精毒素B对小鼠肝脏线粒体电子传递系统的影响。用吉尔森K - ICC型氧电极极谱法测定从雄性小鼠分离的线粒体中的耗氧量。在1.13 mM红天精毒素浓度下，耗氧量降低了73%。在低至0.08 mM红天精毒素B的浓度下，观察到50%的抑制作用。使用吡啶核苷酸连接底物或琥珀酸盐时，0.28 mM红天精毒素B使ADP偶联的线粒体中的耗氧量降低67%，使2,4 - 二硝基苯酚（DNP）解偶联的线粒体中的耗氧量降低60%。通过采用N，N，N'，N'' - 四甲基 - p - 苯二胺（TMPD）分流，表明抑制作用不在细胞色素b与细胞色素C1或C之间。基于这些研究以及与沿电子传递系统特定部位的已知抑制剂的比较，红天精毒素B的主要作用部位似乎在细胞色素C1或C与电子流终止之间。
