Abstract

Hydrogen sulfide (H₂S) could availably regulate electron transport in the inner membrane of mitochondria from bovine heart when succinate as substrate and rotenone as complex I inhibitor at 37°C were used. H₂S increased to a certain extent the respiratory rate of state 4. It also increased first and then decreased the respiratory rate of state 3, respiratory control ratio and ADP/O ratio. In addition, it quicken first and then delayed recovery time from state 3 to state 4. The effects of H₂S as aforementioned in normoxic condition were more obvious than those in hypoxic condition. Experimental results indicated that more than 10 μM H₂S brought about uncoupling of mitochondrial electron transport and the opening of mitochondrial K_ATP channel located in complex III-IV, and less than 10 μM H₂S unexpectedly facilitated this course, which might be via sulfide-quinone oxidoreductase. The finding that H₂S was closely related with sulfide-quinone oxidoreductase, however, requires in depth investigation.

Key words: Respiration, hydrogen sulfide, mitochondria, bovine heart.