Prenatal exposure to ozone disrupts cerebellar monoamine contents in newborn rats
Prenatal exposure to ozone disrupts cerebellar monoamine contents in newborn rats
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DOI：
10.1007/s11064-007-9534-3
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发表时间：
2008-05-01
影响因子：
4.4
通讯作者：
Gonzalez-Maciel, Angelica
中科院分区：
文献类型：
--
作者：
Gonzalez-Pina, Rigoberto;Escalante-Membrillo, Carmen;Gonzalez-Maciel, Angelica
臭氧（O3）广泛分布在空气污染严重的环境中。由于产前接触 O3 会导致小脑形态破坏，因此 O3 可能对某些神经递质系统（例如单胺）产生影响。为了检验这一假设，我们使用了 60 只雄性大鼠，这些大鼠要么来自在整个怀孕期间暴露于 1 ppm O3 的母亲，要么来自在怀孕期间呼吸过滤和清洁空气的母亲。在出生后0、5和10天提取小脑。对组织进行处理，以便通过 HPLC 分析多巴胺 (DA) 水平、3,4 二羟基苯乙酸 (DOPAC) 和高香草酸 (HVA)、去甲肾上腺素 (NA)、血清素和 5-羟基吲哚乙酸 (5-HIAA) 含量。结果显示，DA、NA、DOPAC 和 HVA 的下降主要发生在产后 0 天和 5 天。 5-HT 水平没有变化，5-HIAA 在出生后 10 天后出现增加。 DOPAC + HVA/DA 比值在出生后 0 天和 10 天出现变化，而 5-HIAA/5-HT 比值在出生后 0 天略有下降。数据表明，产前接触氧气会破坏小脑儿茶酚胺系统，而不是吲哚胺系统。小脑神经元的紊乱可能会导致共济失调症状，也可能会限制成人皮质脑损伤后的恢复。鉴于在动物中观察到的恢复机制也在人类中观察到，这些发现很重要。
Ozone (O3) is widely distributed in environments with high levels of air pollution. Since cerebellar morphologic disruptions have been reported with prenatal O3 exposure, O3 may have an effect on some neurotransmitter systems, such as monoamines. In order to test this hypothesis, we used 60 male rats taken from either, mothers exposed to 1 ppm of O3 during the entire pregnancy, or from mothers breathing filtered and clean air during pregnancy. The cerebellum was extracted at 0, 5, and 10 postnatal days. Tissues were processed in order to analyze by HPLC, dopamine (DA) levels, 3,4 dihydroxyphenilacetic acid (DOPAC) and homovanillic acid (HVA), norepinephrine (NA), serotonin, and 5-hydroxy-indole-acetic acid (5-HIAA) contents. Results showed a decrease of DA, NA, DOPAC and HVA mainly in 0 and 5 postnatal days. There were no changes in 5-HT levels, and 5-HIAA showed an increase after 10 postnatal days. DOPAC + HVA/DA ratio showed changes in 0 and 10 postnatal days, while 5-HIAA/5-HT ratio showed a slight decrease in 0 days. The data suggest that prenatal O3 exposure disrupts the cerebellar catecholamine system rather than the indole-amine system. Disruptions in cerebellar NA could lead to ataxic symptoms and also could limit recovery after cortical brain damage in adults. These finding are important given that recovery mechanisms observed in animals are also observed in humans.