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Sinclair, P.R. et al.

Sinclair, Gorman, Walton, Bement, Szakacs, Gonzalez, Dalton, Nebert, Sinclair,

Relative roles of CYP2E1 and CYP1A2 in mouse uroporphyria caused by acetone.

Porphyria cutanea tarda is a liver disease characterized by excess production of uroporphyrin. We previously reported that acetone, an inducer of CYP2E1, enhances hepatic uroporphyrin accumulation in mice treated with iron dextran (Fe) and 5-aminolevulinic acid (ALA). Cyp2e1(-/-) mice treated with Fe and ALA were used to investigate whether CYP2E1 is required for the acetone effect. Hepatic uroporphyrin accumulation was stimulated by acetone in Cyp2e1(-/-) mice to the same extent as in wild-type mice. In the absence of acetone, uroporphyrin accumulated in Cyp2e1(-/-) mice treated with Fe and ALA, but less than in wildtype mice. However, in Cypla2(-/-) mice, uroporphyrin accumulation caused by Fe and ALA, with or without acetone, was completely prevented. Acetone was not an inducer of hepatic CYP1A2 in the wild-type mice. Although acetone is an inducer of CYP2E1, CYP1A2 appears to have the essential role in acetone-enhancement of uroporphyria.[1]

References

Relative roles of CYP2E1 and CYP1A2 in mouse uroporphyria caused by acetone. Sinclair, P.R., Gorman, N., Walton, H.S., Bement, W.J., Szakacs, J., Gonzalez, F.J., Dalton, T.P., Nebert, D.W., Sinclair, J.F. Arch. Biochem. Biophys. (2000) [Pubmed]

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