抄録
The ability of 17 β-estradiol (E2) and its nine metabolites to induce apoptosis in Syrian hamster embryo (SHE) cells was investigated. When SHE cells were treated with E2, estron (E1), 2-hydroxyestrone (2-OHE1), 4-hydroxyestrone (4-OHE1), 2-metho-xyestrone (2-MeOE 1), 16 α -hydoroxyestrone (16 α-OHE1), 2-hydroxyestradiol (2-OHE2), 4-hydroxyestradiol (4-OHE2), 2-methoxyestradiol (2-MeOE2) or estriol (E3) at 0.1-10 μ g/mL for 48 h, the abilities of these estrogens to induce apoptosis were ranked as follows: 2-MeOE2>2-OHE1≅2-OHE2>4-OHE1≅4-OHE2>2-MeOE1>E2>>E1, 16α-OHE1≅E3. These results corresponded to the cytotoxicities of these estrogens in SHE cells. Induction of apoptosis by E2 Was not blocked by co-treatment with a pure antiestrogen ICI 182, 780, suggesting that estrogen-induced apoptosis in SHE cells is not medicated by estrogen receptors. Expression of p53 and p21 proteins was enhanced in SHE cells treated with the estrogens that induced apoptosis. In addition, cleavage of Bax protein was observed in SHE cells treated with these estrogens. These results indicate the differential abilities of E1, E2, and their metabolites to induce apoptosis in SHE cells which is medicated through p53 and Bax pathways.
