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首页> 外文期刊>Journal of biochemical and molecular toxicology >Effect of subchronic acrylamide exposure on the expression of neuronal and inducible nitric oxide synthase in rat brain.
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Effect of subchronic acrylamide exposure on the expression of neuronal and inducible nitric oxide synthase in rat brain.

机译：亚慢性丙烯酰胺暴露对大鼠脑神经元和诱导型一氧化氮合酶表达的影响。

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摘要

Acrylamide (ACR) is a known industrial neurotoxic chemical. Evidence suggests that ACR neurotoxic effect is related to brain neurotransmission disturbances. Since nitric oxide (NO) acts as a neurotransmission modulator and is produced by nitric oxide synthase (NOS), the neuronal NOS (nNOS) and inducible NOS (iNOS) expression pattern were determined in rat cerebral cortex and striatum after subchronic exposure to ACR. Using immunocytochemistry, the neuronal count of nNOS or optical density of iNOS from sections at three coronal levels, bregma 1.0, -0.4, and -2.3 mm, were compared between ACR-treated and control rats. At all three levels, nNOS expressions were uniformly decreased in most of the neocortical subregions following the treatment of ACR. At bregma level 1.0 mm, total numbers of nNOS expressing neurons were significantly decreased to 58.7% and 64.7% of the control in the cortex and striatum of ACR-treated rats, respectively. However, at the bregma level -2.3 mm, ACR treatment did not produce a significant difference in the numbers of nNOS expressing neurons both in the cortex and striatum. Contrary to nNOS, iNOS expressions were consistently increased to approximately 32% in the neocortex and 25% in the striatum, following the subchronic ACR treatment. These data suggest that subchronic ACR exposure involves compensatory mechanism on nNOS and iNOS expression to maintain the homeostasis of NO at the rostral part of the neocortex and the striatum. However, in the caudal brain, increased iNOS expression did not suppress nNOS expression. Therefore, the present study is consistent with the hypothesis that ACR toxicity is mediated through the disturbance to the NO signaling pathway and exhibits a rostrocaudal difference through the differential expressions of nNOS and iNOS in the neocortex and the striatum.
机译：丙烯酰胺（ACR）是一种已知的工业神经毒性化学品。有证据表明，ACR神经毒性作用与脑神经传递障碍有关。由于一氧化氮（NO）充当神经传递调节剂并由一氧化氮合酶（NOS）产生，因此在亚慢性暴露于ACR后，在大鼠大脑皮层和纹状体中确定了神经元NOS（nNOS）和诱导型NOS（iNOS）表达模式。使用免疫细胞化学方法，比较了ACR治疗组和对照组大鼠的三个冠状水平（前reg 1.0，-0.4和-2.3 mm）的nNOS的神经元计数或iNOS的光密度。在所有三个水平上，治疗ACR后，大多数新皮层次区域nNOS表达均一下降。在前reg水平1.0 mm处，ACR处理的大鼠皮层和纹状体中表达nNOS的神经元总数分别显着减少至对照组​​的58.7％和64.7％。但是，在前reg水平-2.3 mm处，ACR处理在皮层和纹状体中表达nNOS的神经元数量均未产生显着差异。与nNOS相反，在亚慢性ACR治疗后，新皮层中iNOS的表达一直增加到大约32％，纹状体中增加了25％。这些数据表明，亚慢性ACR暴露涉及nNOS和iNOS表达的补偿机制，以维持新皮​​层和纹状体的鼻端部分NO的稳态。但是，在尾脑中，iNOS表达的增加并未抑制nNOS表达。因此，本研究与以下假设相一致：ACR毒性是通过对NO信号通路的干扰来介导的，并且通过新皮层和纹状体中nNOS和iNOS的差异表达而表现出了尾脑尾状差异。

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