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首页> 外文期刊>Biochemical Pharmacology >Gestational dioxin exposure suppresses prolactin-stimulated nursing in lactating dam rats to impair development of postnatal offspring
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Gestational dioxin exposure suppresses prolactin-stimulated nursing in lactating dam rats to impair development of postnatal offspring

机译：妊娠期二恶英暴露抑制哺乳坝大鼠的催乳素刺激的护理，以损害产后后代的发展

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A number of epidemiological studies have implicated environmental chemicals including dioxins in the induction of negative effects on child development. To clarify the underlying mechanisms, almost all toxicologists have concentrated on effects on the offspring themselves. We examined an alternative hypothesis that gestational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a highly-toxic dioxin, targets factors related to maternal childcare to disturb offspring development. Oral administration of TCDD (1 mu g/kg) to pregnant rats on gestational day 15 suppressed maternal licking behavior, a nursing behavior, and mammary gland maturation during the lactational stage, as well as the body weight and short-term memory of postnatal offspring. In support of these findings, maternal production of prolactin, a pituitary hormone essential for nursing including milk production, was decreased during the same period. Intracerebroventricular infusion of prolactin to dioxin-exposed dams restored or tended to restore many of the above defects observed both in mothers and offspring. The TCDD-dependent defects in maternal nursing behaviors can be due to a direct action on aryl hydrocarbon receptor (AHR) of lactating dams, because they did not emerge in AHR-knockout dams or control dams with TCDD-exposed offspring. Further examinations revealed that TCDD induces transforming growth factor beta 1 expression, which suppresses prolactin-producing cell proliferation, in a nursing period-specific manner. In agreement with this, the number of prolactin-positive cells in nursing dams was decreased by TCDD. These results provide novel evidence that gestational dioxin exposure attenuates prolactin-stimulated nursing in lactating dams to impair offspring development, and that immaturity of prolactin-producing cells can contribute to them.
机译：许多流行病学研究具有含有二恶英在诱导儿童发育的负面影响中的环境化学品。为了澄清潜在的机制，几乎所有毒理学家都集中了对后代的影响。我们研究了一种替代假设，即妊娠期暴露于2,3,7,8-四氯二氯胺-P-二恶英（TCDD），一种高度毒性的二恶英，与孕产妇儿童有关的因素，以扰乱后代发展。口服TCDD（1μg/ kg）对妊娠第15天的孕大鼠抑制了泌母爆炸行为，护理行为和乳腺成熟期间的泌乳阶段，以及后期后代的体重和短期记忆。为了支持这些发现，在同一时期下降，母乳酸催化剂，一种垂体激素，包括牛奶产量，包括牛奶产量的垂体激素。在母亲和后代恢复或倾向于恢复上述许多缺陷的催乳素对二恶英暴露的坝体的颅内腔内输注。母体护理行为中的TCDD依赖性缺陷可能是由于哺乳坝芳基烃受体（AHR）的直接作用，因为它们没有出现在具有TCDD暴露后代的AHR敲除坝或控制坝。进一步的考试表明，TCDD诱导转化的生长因子β1表达，其抑制尿球蛋白产生细胞增殖，以护理期特异性方式。同意这一点，TCDD降低了护理水坝中催乳素阳性细胞的数量。这些结果提供了新的证据，即妊娠二恶英暴露在哺乳液体中衰减催乳素刺激的护理，以损害后代的开发，催乳素产生的细胞的不成熟可以为它们提供贡献。

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