de Groot H, Anundi I, Littauer A
Institut für Physiologische Chemie I, Universität Düsseldorf, FRG.
Biomed Biochim Acta. 1989;48(2-3):S11-5.
Reoxygenation following hypoxia enhanced loss of viability of isolated hepatocytes compared to cells maintained under hypoxic conditions. Cell damage due to reoxygenation was not dependent on the conversion of xanthine dehydrogenase to xanthine oxidase which occurred at a time when almost all the hepatocytes had lost their viability. The effect of reoxygenation was critically linked to the duration of the hypoxic period. During the hypoxic period degradation of endogenous glycogen may have provided sufficient substrate for glycolysis to contribute to maintenance of cell integrity by preservation of adenine nucleotides.
与维持在缺氧条件下的细胞相比，缺氧后的复氧增强了分离肝细胞的活力丧失。复氧引起的细胞损伤并不依赖于黄嘌呤脱氢酶向黄嘌呤氧化酶的转化，而这种转化发生在几乎所有肝细胞都丧失活力的时候。复氧的影响与缺氧期的持续时间密切相关。在缺氧期间，内源性糖原的降解可能为糖酵解提供了足够的底物，通过保留腺嘌呤核苷酸来维持细胞完整性。
