Fig. 1. Regulation of mitochondrial sulfide oxidation by glutathione (GSH), ascorbate and dehydroascorbate (DHA). (A–C) Initial rates of ATP production (gray circles) and oxygen consumption in state 3 (black circles) and state 4 (black squares) with sulfide (5–100 µmoll^–1) added as a substrate. (A) Sulfide oxidation in the absence of redox-competent molecules. (B) Sulfide oxidation in the presence of 2.5 mmoll^–1 GSH and 2.5 mmoll^–1 ascorbate. Oxygen consumption rates were identical in the presence and in the absence of ADP. (C) Sulfide oxidation in the presence of 1 mmoll^–1 DHA. ^*Significantly different (P>0.05) from corresponding data points without redox competent molecules. (D–F) Inhibition (%) of mitochondrial respiration (black bars) and ATP production (grey bars) with sulfide added as a substrate by 5 µmoll^–1 myxothiazole, 0.05 mmoll^–1 KCN, 1 mmoll^–1 NaN₃ or 0.5 mmoll^–1 SHAM. (D) Inhibition of oxygen consumption (state 3) and ATP production with 5–10 µmoll^–1 sulfide added as a substrate in the absence of redox-competent molecules. (E) Inhibition of oxygen consumption with 10–100 µmoll^–1 sulfide added as a substrate in the presence of 2.5 mmoll^–1 GSH and 2.5 mmoll^–1 ascorbate. ATP production rates were too low to study the effects of inhibitors. (F) Inhibition of oxygen consumption (state 3) and ATP production with 5–50 µmoll^–1 sulfide added as a substrate in the presence of 1 mmoll^–1 DHA. Data are given as means ± s.d. of the results from 3 to 12 different preparations, each comprising approximately 10–15 animals.