Respiratory effects of hexachlorocyclopentadiene on intact rainbow trout (Salmo gairdneri) and on oxidative phosphorylation of isolated trout heart mitochondria.
Acclimated normal rainbow trout were exposed to 130 ppb hexachlorocyclopentadiene (HEX) in a flow-through well water circuit which was designed to permit measurements of oxygen consumption by the fish. Compared to preHEX values, HEX increased oxygen consumption rates by 186 +/- 24% (means +/- SEM), with maximum oxygen consumption rates being reached in approximately 84 min after HEX exposure. Oxygen consumption subsequently decreased, and all HEX-exposed fish died within 6.5 hr of exposure. Fish exposed to HEX-free vehicle (acetone) showed no changes of oxygen consumption. When added to normal isolated trout heart mitochondria, HEX appeared to uncouple oxidative phosphorylation, with calculated respiratory control ratios being decreased 50% from control values at a HEX concentration of 0.41 microM. We postulate that one important mechanism of HEX intoxication in the intact animal may be due to increased oxygen consumption and impaired oxidative ATP synthesis due to the mitochondrial uncoupling action of the toxicant.
D000818:Animals; D004305:Dose-Response Relationship, Drug; D006843:Hydrocarbons, Chlorinated / Q000494:pharmacology* / Q000633:toxicity; D066298:In Vitro Techniques; D008929:Mitochondria, Heart / Q000378:metabolism*; D010085:Oxidative Phosphorylation / Q000187:drug effects*; D010101:Oxygen Consumption / Q000187:drug effects; D011048:Polarography; D012119:Respiration / Q000187:drug effects*; D012487:Salmonidae / Q000502:physiology*; D014337:Trout / Q000502:physiology*; D014874:Water Pollutants, Chemical / Q000633:toxicity
D006843:Hydrocarbons, Chlorinated; D014874:Water Pollutants, Chemical; C016488:hexachlorocyclopentadiene