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Direct and transgenerational effect of benzpyrene treatment at adolescent age on the uterine estrogen receptor and thymic glucocorticoid receptor of the adult rat.

Hormonal imprinting develops perinatally at the first encounter between the maturing receptor and the target hormone, helping the normal accomplishment of receptor maturation. In the presence of hormone excess or foreign molecules able to bind to the maturing receptor, faulty imprinting takes place, which disturbs the normal receptor function for life. Earlier experiments demonstrated that the effect of faulty perinatal benzpyrene imprinting of the steroid hormone receptors is transmitted to the progeny generations. In certain organs which are maturing later (such as the uterus) imprinting can be executed at adolescence. In the present experiments pubertal benzpyrene imprinting caused a durable decrease in female's estrogen receptor density. The transgenerational effect of this type of imprinting was also studied. The pubertal imprinting of the parents was transgenerationally transmitted to the offspring generation in which--without further treatment--the density (Bmax) of the uterine estrogen receptors was significantly higher than that in the controls. There were measurable effects neither in the affinity (Kd) of uterine estrogen receptors nor in the Kd and Bmax of the male thymus glucocorticoid receptors. The experiments call attention to the profound and comprehensive imprinting effect of the environmental pollutant benzpyrene.