Effects of environmental tobacco smoke exposure in utero and/or postnatally on brain development
Effects of environmental tobacco smoke exposure in utero and/or postnatally on brain development
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DOI：
10.1203/00006450-199603000-00018
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发表时间：
1996-03-01
影响因子：
3.6
通讯作者：
Pinkerton, KE
中科院分区：
文献类型：
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作者：
Gospe, SM;Zhou, SS;Pinkerton, KE
我们评估是否环境烟草烟雾暴露在子宫内和/或产后影响大脑的生化组成。孕SD大鼠从妊娠第3天开始暴露于过滤空气（FA）或侧流烟雾（SS）中，每天4 h，每周7 d，直至分娩，然后其母鼠出生后暴露于FA或SS中9 wk。这导致了四种暴露条件：子宫内FA随后是出生后FA（FA/FA），子宫内FA随后是出生后SS（FA/SS），子宫内SS随后是出生后FA（SS/FA），以及子宫内SS随后是出生后SS（SS/SS）。暴露完成后，将大脑取出，并在桥脑中脑交界处分为前脑和后脑;然后分析每个标本的DNA、蛋白质和胆固醇浓度。资料以双因子变异数分析进行分析。在子宫内SS对这三个生化指标没有影响。然而，出生后SS降低后脑DNA浓度（细胞密度的指标）4.4%（p = 0.001）。此外，这些动物的后脑蛋白/DNA比（细胞大小指数）增加了8.4%（p = 0.001）。后脑重量不受SS暴露的影响，但体重降低了6.4%（p = 0.016）。这些数据表明，出生后暴露于SS通过减少细胞总数和增加细胞大小影响后脑（出生后显著生长的区域）。后脑细胞肥大可能有助于抵消细胞数量的减少，从而使后脑重量保持不变。尽管保留了后脑重量，出生后暴露于SS的这些影响可能导致神经功能障碍。
We evaluated whether environmental tobacco smoke exposure in utero and/or postnatally affects the biochemical composition of the brain. Pregnant Sprague-Dawley rats were exposed to filtered air (FA) or to sidestream smoke (SS) for 4 h/d, 7 d/wk from d 3 of pregnancy until delivery, then their female pups were exposed to either FA or SS for 9 wk postnatally. This resulted in four exposure conditions: in utero FA followed by postnatal FA (FA/FA), in utero FA followed by postnatal SS (FA/SS), in utero SS followed by postnatal FA (SS/FA), and in utero SS followed by postnatal SS (SS/SS). After completion of the exposures, the brains were removed and divided at the pontomesencephalic junction into forebrain and hindbrain; each specimen was then analyzed for DNA, protein, and cholesterol concentration. Data were analyzed by 2-way analysis of variance. In utero SS had no effect on these three biochemical measurements. However, postnatal SS reduced hindbrain DNA concentration (an indicator of cellular density) by 4.4% (p = 0.001). In addition, the hindbrain protein/DNA ratio (an index of cell size) was increased in these animals by 8.4% (p = 0.001). Hindbrain weight was not affected by SS exposure, but body weight was reduced by 6.4% (p = 0.016). These data suggest that postnatal exposure to SS affects the hindbrain (a region which undergoes significant postnatal growth) by reducing the total number of cells and by increasing cell size. Hindbrain cellular hypertrophy may help offset the decrease in cell number, thereby leaving hindbrain weight unchanged. Despite preserved hindbrain weight, these effects of postnatal exposure to SS may result in neurologic dysfunction.