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Housing adult rats on ground corncob bedding impedes male and female mating behavior and causes acyclicity in females. The suppressive effects on ovarian cyclicity are mimicked by a mitogenic agent purified from the ground corncob bedding material (corn mitogen; CM), which stimulates the proliferation of estrogen receptor (ER)-positive (MCF-7 cells) and ER-negative (MDA-MD-231 cells) breast cancer cells. Purified CM does not compete for [(3)H]estradiol binding to ER or nuclear type II sites, and its effects on MCF-7 breast cancer cell proliferation are not blocked by the antiestrogen ICI-182,780. These results suggest that the active component is unlikely to be a phytoestrogen, bioflavonoid, mycotoxin, or other known endocrine-disrupting agent that modifies cell growth via ER or type II [(3)H]estradiol binding sites. CM also stimulates the proliferation of PC-3 human prostatic cancer cells in vitro, and the growth rate of PC-3 cell xenografts is accelerated in nude male mice housed on ground corncob as opposed to pure cellulose bedding. Consequently, this endocrine-disrupting agent in ground corncob bedding may influence behavioral and physiologic reproductive response profiles and malignant cell proliferation in experimental animals. Fresh corn (kernels and cob) or corn tortillas also contain CM, indicating that human exposure is likely; consequently, CM and/or related mitogens in corn products may influence human health and development.

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The effects of TCDD exposure on the developing immune system were investigated in F344 rats. Fetal and neonatal rats were exposed to TCDD through maternal dosing (5 microgram/kg) on day 18 of gestation and on days 0, 7, and 14 of postnatal life (group I). Another group of neonatal rats was exposed to TCDD through maternal dosing on days 0, 7, and 14 of postnatal life only (group II). Body weights and thymus/body weight ratios were found to be suppressed up to 145 days of age in group I, but only up to 39 days of age in group II. Parameters of cell-mediated and humoral immune function were investigated. TCDD suppressed cell-mediated immune function without affecting humoral immune function. Suppression of T-cell function was selective in that "helper" cell function was not suppressed.