Biotransformations of Cyclodienes and Their Photoisomers and Hexachlorocyclopentadiene in Mammals and Fish

Khan, Mohammad Zafar; Sudershan, P.; Feroz, M.; Podowski, A. A.

doi:10.1016/b978-0-08-027530-7.50026-1

Cited by 6 publications

(1 citation statement)

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“…Our studies of the respiratory effects of HEX were prompted by earlier work which revealed pulmonary damage in terrestrial animals and gill damage in aquatic species exposed to HEX, and accumulation of [14C]HEX in respiratory structures (Khan et al, 1981;Lawrence and Dorough, 1981;Sinhaseni, 1982). These observations suggested that a primary target of damage by HEX might be the respiratory tract, with toxicity being manifest as respiratory depression leading to hypoxia, possibly due to impaired gas transport into the systemic circulation, ultimately leading to the organism's death.…”

Section: Discussionmentioning

confidence: 99%

Respiratory effects of hexachlorocyclopentadiene on intact rainbow trout (Salmo gairdneri) and on oxidative phosphorylation of isolated trout heart mitochondria

Sinhaseni

DʼAlecy

Hartung

et al. 1983

Toxicology and Applied Pharmacology

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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.

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Section: Discussionmentioning

confidence: 99%