Effects of hyperbaric oxygen and glutathione on mammalian liver metabolism.
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.
D000255:Adenosine Triphosphate / Q000096:biosynthesis; D000818:Animals; D001274:Atmospheric Pressure; D005260:Female; D005978:Glutathione / Q000494:pharmacology*; D008099:Liver / Q000201:enzymology / Q000378:metabolism*; D051379:Mice; D010100:Oxygen / Q000494:pharmacology*; D010101:Oxygen Consumption / Q000187:drug effects*; D013385:Succinate Dehydrogenase / Q000378:metabolism*
D000255:Adenosine Triphosphate; D013385:Succinate Dehydrogenase; D005978:Glutathione; D010100:Oxygen