Uroporphyria development in cultured chick embryo fibroblasts long‐term treated with chloramphenicol and ethidium bromide

Abstract

Long‐term chloramphenicol‐ and ethidium bromide‐treated chick embryo fibroblasts synthesize large amounts of porphyrins from exogenously added σ‐aminolevulinic acid. The porphyrins consist mainly of uro‐ and heptacarboxyporphyrins and are retained within cells. Uroporphyria development is a time‐dependent process which accompanies a step‐wise decrease in the capacity of the mitochondrial respiratory chain. Upon removal of chloramphenicol from the medium, the pattern of porphyrin production readily returns to normal (mainly proto‐ and coproporphyrins found in the medium) while ethidium bromide‐treated cells remain uroporphyric. The results suggest that impairment of mitochondrial functions in chicken by xenobiotics leads to uroporphyria development.