作者: L DeFrancesco , I E Scheffler , M J Bissell
DOI: 10.1016/S0021-9258(17)33242-8
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摘要: We have recently described a Chinese hamster cell line with greatly reduced rate of respiration. In this report we conclude that the defects is in NADH-coenzyme Q reductase (NADH oxidase), first part electron transport chain. The conclusion based on following observations. (a) and earlier determined relevant enzymes Krebs cycle are present active. (b) Oxygen consumption by isolated mitochondria normal when driven succinate alpha-glycerolphosphate. (c) Difference spectra between oxidized forms indicate all cytochromes functional. (d) contrast, substrates such as malate, glutamate, alpha-ketoglutarate, isocitrate which generate NADH do not stimulate oxygen mutant mitochondria. (e) A direct assay rotenone-sensitive oxidase Lubrol-treated from cells revealed less than one-tenth activity compared wild type (f) treatment rotenone, specific inhibitor NADH-CoQ reductase, yielded an exact phenocopy several criteria. This respiration-deficient mammalian tissue culture.