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Toxicologic Pathology
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Journal Article

Phenotyping Cytochromes P450 with Monoclonal Antibodies

Fred K. Friedman

Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20205

Sang Shin Park

Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20205

Tadahiko Fujino

Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20205

Byung-Joon Song

Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20205

Richard C. Robinson

Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20205

Donna West

Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20205

Allen K. Radkowsky

Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20205

Haruko Miller

Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20205

Harry V. Gelboin

Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20205

Monoclonal antibodies (MAbs) to cytochrome P-450 isozymes can be used to phenotype tissues for epitope-specific cytochrome P-450 content. MAbs that inhibit specific cytochrome P-450 dependent drug or carcinogen reactions are useful tools for quantitative measurement of the individual or classes of cytochromes P-450 that catalyze these reactions. This method has been applied successfully to animal as well as human tissues. Radioimmunoassays based on MAbs have been developed and provide a rapid and efficient means for detecting cytochromes P-450 independent of functional enzyme activity. In addition, MAbs coupled to a Sepharose support can be used to immunopurify cytochromes P-450 in a procedure that is more rapid and efficient than conventional purification schemes. MAbs add a new dimension to analyses of cytochrome P-450 multiplicity and will find numerous applications in elucidation of the relationship between cytochrome P-450 phenotype and carcinogen or drug metabolism.

Toxicologic Pathology, Vol. 12, No. 2, 155-161 (1984)
DOI: 10.1177/019262338401200207
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