Peroxidase activity as a marker for estrogenicity: studies in uterus and mammary tumors.
We examined the possibility that peroxidase activity might be a marker for estrogen activity in established estrogen-dependent tissues: dimethylbenz[a]anthracene (DMBA)-induced rat mammary tumors and human breast cancer. In DMBA-induced tumors undergoing regression after ovariectomy or tamoxifen treatment, tumor size decreased by 50%, estradiol receptors (ER) and progesterone receptors (PgR) decreased by 25 and 20%, respectively, but peroxidase activity paradoxically increased six- to sevenfold. In DMBA tumors stimulated by estradiol treatment or by the cessation of tamoxifen administration in intact rats, tumor size increased threefold. ER and PgR increased two- and threefold, respectively, while peroxidase activity decreased 50%. These data indicate an inverse relation between tumor growth, ER and PgR on the one hand, and peroxidase activity on the other. In the human breast cancers there was a significant negative relation between the presence of ER and peroxidase activity. By using a calibrated Sephadex G-100 column it was shown that uterine peroxidase differs in molecular weight from the peroxidase of rat mammary tumors and that of human breast cancer.
D000818:Animals; D001943:Breast Neoplasms / Q000201:enzymology*; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D006801:Humans; D008325:Mammary Neoplasms, Experimental / Q000201:enzymology*; D009376:Neoplasms, Hormone-Dependent; D010544:Peroxidases / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D011960:Receptors, Estrogen / Q000032:analysis; D011980:Receptors, Progesterone / Q000032:analysis; D014599:Uterus / Q000201:enzymology*
D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D004958:Estradiol; D010544:Peroxidases