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Abstract
Chlordecone (CHLO, 14–30 μδ) and chlordecone alcohol (CHLO ALC, 10–23 μδ) altered the permeability of isolated ovine erythrocytes as evidenced by a concentration‐and time‐dependent induction of K+ efflux and hemolysis. Hemolysis, but not K+ efflux, was markedly delayed when the erythrocytes were suspended in isotonic sucrose. CHLO‐induced and CHLO ALC‐induced hemolysis and K+ efflux were dependent on the pH of the external media. Raising the pH from 6.5 to 9.4 inhibited CHLO‐induced K+ efflux and hemolysis, whereas CHLO ALC‐induced K+ efflux and hemolysis were increased. Low concentrations of both compounds (1–4 μδ) protected erythrocytes against hypotonic hemolysis. Neither CHLO (30 μδ) nor CHLO ALC (23 μδ) induced the release of trapped K+ from KSCN‐loaded unilamellar liposomes made from erythrocyte lipids. It is postulated that CHLO and CHLO ALC interact with membrane proteins and increase the permeability of the membrane to cations. This interaction leads to colloid‐osmotic hemolysis.