Abstract
The aryl hydrocarbon (benzo[a]pyrene) hydroxylase activity induced in the eye of the C57BL 6 N (responsive) inbred mouse strain by β-naphthoflavone is two- to more than 10-fold higher than that in the eye of the DBA 2 N (non-responsive) inbred mouse strain. Genetic expression of the hydroxylase induction in the eye appears to be under the same genetic regulation as that in the liver. The hydroxylase activity can be induced in cultured cells of chick embryonic retinal pigmented epithelium by 1,2-benz[a]anthracene. It is proposed that genetically regulated induction of the hydroxylase activity in the retinal pigmented epithelium plays an important role in metabolic potentiation, as well as detoxification, of drugs and other xenobiotic compounds. All known mouse strains which develop retinal degeneration are aromatic hydrocarbon responsive strains. Some of the major products of the aryl hydrocarbon hydroxylase reaction, phenolic benzo[a]pyrene derivatives, have a marked labilizing effect on lysosomal membranes. On the basis of these two observations, a possible involvement of the hydroxylase activity in initiating retinal degeneration is suggested.
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