The role of pentachlorophenol in causing mitochondrial derangement in hexachlorobenzene induced experimental porphyria

Hexachlorobenzene feeding to rats for 60 days to induce experimental porphyria resulted in partial and constant uncoupling of oxidative phosphorylation of liver mitochondria from the early phase (i.e. 20 days) of treatment. Direct experimental evidence has been presented that this uncoupling is completely due to the action of pentachlorophenol endogenously formed by metabolism of hexachlorobenzene. The complete restoration of membrane potential by albumin under these conditions indicates that no irreversible damage occurs in the mitochondrial membrane. No appreciable correlation between concentrations of pentachlorophenol and the degree of porphyria has been observed