SISTER CHROMATID EXCHANGES AND CELL-DIVISION DELAYS INDUCED BY DIETHYLSTILBESTROL, ESTRADIOL, AND ESTRIOL IN HUMAN-LYMPHOCYTES

  • 1 January 1983
    • journal article
    • research article
    • Vol. 43  (9) , 4114-4118
Abstract
Exposure of human lymphocytes in vitro to diethylstilbestrol (DES), a synthetic estrogen and known human carcinogen, led to the induction of sister chromatid exchanges. More sister chromatid exchanges were induced in cells from pregnant women than from men. To see if the effects of DES could be induced by other estrogens, lymphocytes from a man and a pregnant woman were treated in vitro with the natural estrogens estradiol and estriol. These did not induce sister chromatid exchanges. To see if the presence of exogenous female hormones might be responsible for the increase in DES-induced sister chromatid exchanges seen in cells from pregnant women, lymphocytes from a man and a pregnant woman were also treated in vitro simultaneously with DES, estradiol, estriol and progesterone. Treatments with these exogenous hormones did not alter the number of DES-induced sister chromatid exchanges. DES also inhibits in vitro proliferation of lymphocytes. Estradiol also strongly inhibits this proliferation but that estriol is only a weak inhibitor. The cause of delayed cell proliferation induced by DES and estradiol was 2-fold: some of the cells were delayed in phytohemagglutinin-mediated blast cell transformation but additionally, most cells had a porlonged cell cycle because of an extended G2 phase. DES, but not estradiol or estriol, induced a low level of polyploidy in human lymphocytes.