• 1 January 1978
    • journal article
    • research article
    • Vol. 49  (8) , 980-983
Abstract
The effects of hyperbaric O2 tensions on O2 consumption and succinate dehydrogenase (SDH) activity of mouse liver were investigated. Liver homogenates exposed to a PO2 [O2 partial pressure] of 3837 mmHg for 30 min showed a 50.6% reduction in O2 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 mmHg. The effects of glutathione as a protective agent against O2 toxicity were also examined. Mouse liver pretreated with reduced glutathione and exposed to hyperbaric O2 tensions showed higher rates of O2 consumption than untreated controls. Oxidized and reduced glutathione protected SDH against hyperbaric O2 inactivation. Glutathione can stimulate O2 consumption and maintain SDH activity after exposure to hyperbaric O2 by increasing succinate formation through the glutathione-succinate shunt.