Evidence for pleomorphism of estrogen receptor capacity and affinity in liver and thymus of immature BALB/c and (NZBxNZW) F1 mice, a model of systemic lupus erythematosus.

Binding properties of estrogen receptors in liver, thymus and uterus of BALB/c and (NZBxNZW) F1 mice were compared. (NZBxNZW) F1 mice spontaneously develop an autoimmune disease resembling human systemic lupus erythematosus (SLE). It is hypothesized that estradiol, through its receptors, mediates the progression of murine SLE. High-speed cytosols were prepared from liver, thymus and uterus and incubated with the synthetic estrogen 3H-moxestrol (NEN). Scatchard plots were derived from binding isotherms obtained. Rectilinear Scatchard plots were obtained from all tissues, which is consistent with the presence of only one class of binding sites, or of more than one class but with the same affinity. There were, however, strain differences in that the affinity of the binding reaction was significantly higher in cytosols from BALB/c liver in males and females. In thymus, the situation was reversed in that the affinity was significantly higher in cytosols from (NZBxNZW) F1 mice. Thymic cytosols from BALB/c mice contained significantly more estrogen receptors per mg cytosol protein than did those from (NZBxNZW) F1 mice. The exacerbation of murine SLE may be due, at least in part, to these properties of estrogen receptors in liver and thymus.