Baeyens D A, Meier M J
Aviat Space Environ Med. 1978 Aug;49(8):980-3.
The effects of hyperbaric oxygen tensions on oxygen consumption and succinate dehydrogenase (SDH) activity of mouse liver were investigated. Liver homogenates exposed to a PO2 of 3837 mm Hg for 30 min showed a 50.6% reduction in oxygen consumption compared to controls exposed to nitrogen at ambient pressure. The SDH activity was significantly reduced during a 3-h exposure to a PO2 of 3796 mm Hg. The effects of glutathione as a protective agent against oxygen toxicity were also examined. Mouse liver pretreated with reduced glutathione and exposed to hyperbaric oxygen tensions showed higher rates of oxygen consumption than untreated controls. Oxidized and reduced glutathione protected SDH against hyperbaric oxygen inactivation. It is concluded that glutathione can stimulate oxygen consumption and maintain SDH activity after exposure to hyperbaric oxygen by increasing succinate formation through the glutathione-succinate shunt.
研究了高压氧张力对小鼠肝脏耗氧量和琥珀酸脱氢酶(SDH)活性的影响。与在常压下暴露于氮气的对照组相比,暴露于3837 mmHg的PO2 30分钟的肝脏匀浆显示耗氧量降低了50.6%。在暴露于3796 mmHg的PO2 3小时期间,SDH活性显著降低。还研究了谷胱甘肽作为抗氧毒性保护剂的作用。用还原型谷胱甘肽预处理并暴露于高压氧张力下的小鼠肝脏显示出比未处理的对照组更高的耗氧率。氧化型和还原型谷胱甘肽可保护SDH免受高压氧失活。得出的结论是,谷胱甘肽可以通过谷胱甘肽-琥珀酸分流增加琥珀酸的形成,从而在暴露于高压氧后刺激耗氧量并维持SDH活性。