McGivney A, Bradley S G
Infect Immun. 1979 Aug;25(2):664-71. doi: 10.1128/iai.25.2.664-671.1979.
Escherichia coli O127:B8 lipopolysaccharide (LPS), prepared by the Westphal procedure, caused a marked decrease in the activities of mitochondrial malate dehydrogenase, succinate dehydrogenase, and adenylate kinase in African green monkey kidney (Vero) cells and primary cultures of mouse liver cells within 2 h after exposure to 10 micrograms of LPS/ml of culture medium. These three enzyme activities leaked into the supernatant fraction, and cytochrome oxidase activity was lost from the mouse liver mitochondrial particulate fraction within 45 min after exposure to 10 micrograms of LPS/mg of protein. Loss malate dehydrogenase activity from isolated mitochondria was also accelerated by LPS from E. coli O26:B6 (Boivin preparation) or Salmonella typhosa O901 (Westphal preparation), and by lipid A from Salmonella minnesota or Shigella sonnei. In addition, LPS and lipid A inhibited state 3 respiration by isolated mitochondria with attendant loss of respiratory control, but adenosine 5'-diphosphate/O ratios were relatively unchanged. Impaired mitochondrial function is an early event after exposure to biologically relevant amounts of LPS or lipid A.
通过韦斯特法尔方法制备的大肠杆菌O127:B8脂多糖（LPS），在非洲绿猴肾（Vero）细胞和小鼠肝细胞原代培养物中，当暴露于每毫升培养基10微克LPS后2小时内，导致线粒体苹果酸脱氢酶、琥珀酸脱氢酶和腺苷酸激酶的活性显著下降。这三种酶的活性泄漏到上清液部分，并且在暴露于每毫克蛋白质10微克LPS后45分钟内，小鼠肝线粒体颗粒部分的细胞色素氧化酶活性丧失。来自大肠杆菌O26:B6（博伊文制剂）或伤寒沙门氏菌O901（韦斯特法尔制剂）的LPS，以及来自明尼苏达沙门氏菌或宋内志贺氏菌的脂多糖A，也加速了分离线粒体中苹果酸脱氢酶活性的丧失。此外，LPS和脂多糖A抑制分离线粒体的状态3呼吸，伴随呼吸控制的丧失，但腺苷5'-二磷酸/氧比值相对不变。线粒体功能受损是暴露于生物学相关量的LPS或脂多糖A后的早期事件。
