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Exposure to acrylamide decreases noradrenergic axons in rat brain.
NeuroToxicology ( IF 3.4 ) Pub Date : 2020-03-05 , DOI: 10.1016/j.neuro.2020.03.001
Lingyi Zhang 1 , Satoshi Hara 2 , Hiroshi Ichinose 2 , Daichi Nagashima 3 , Kyo Morita 1 , Toshihiro Sakurai 1 , Sahoko Ichihara 4 , Gaku Ichihara 1
Affiliation  

PURPOSE Acrylamide is known to induce disorders in the central nervous system in humans and experimental animals. The present study investigated effects of exposure to acrylamide on adult neurogenesis, noradrenergic axons and the level of norepinephrine in the brain of male rats. METHOD Four groups of 12 male Wistar rats each were exposed to acrylamide at 0, 0.2, 2 and 20 mg/kg body weight by gavage for 5 weeks. Six rats of each groups were injected with 5-bromo-2'-deoxy-uridine (BrdU) after five-week exposure to acrylamide to examine proliferative cells in the dentate gyrus using immunostaining. Density of noradrenergic and serotonergic axons in the prefrontal cortex, hippocampus and cortex behind the bregma was quantified. Remaining 6 rats were decapitated after the last exposure and brains were dissected out to measure monoamine level in the hippocampus and prefrontal cortex using high performance liquid chromatography. RESULT Exposure to acrylamide dose-dependently decreased the density of noradrenergic axons in the prefrontal cortex with a significant change at 20 mg/kg. Norepinephrine level decreased in the hippocampus at 20 mg/kg. Exposure to acrylamide at 20 mg/kg or less did not change the number of BrdU positive cells, but the result should be considered preliminary. CONCLUSION The results show that oral exposure to acrylamide induces decrease in noradrenergic axons and norepinephrine level in the brain of rats. Given the similar effects are observed in 1-bromopropane-exposed rats, there may be the common mechanism in the toxicity of soft electrophiles to the central nervous system.

中文翻译:

暴露于丙烯酰胺会降低大鼠脑中的去甲肾上腺素能轴突。

目的已知丙烯酰胺会在人和实验动物中引起中枢神经系统疾病。本研究调查了暴露于丙烯酰胺对成年大鼠神经形成,去甲肾上腺素能轴突和去甲肾上腺素水平的影响。方法4组12只雄性Wistar大鼠,每只分别通过管饲法以0、0.2、2和20 mg / kg体重暴露于丙烯酰胺中5周。在暴露于丙烯酰胺五周后,每组六只大鼠注射5-溴-2'-脱氧尿苷(BrdU),以使用免疫染色检查齿状回中的增殖细胞。量化前额叶皮层,海马区和前reg后皮层中去甲肾上腺素能和血清素能轴突的密度。最后一次暴露后,将剩余的6只大鼠断头,并使用高效液相色谱法解剖脑以测量海马和前额叶皮层中的单胺水平。结果暴露于丙烯酰胺剂量依赖性地降低了额叶前额叶皮质中去甲肾上腺素能轴突的密度,在20 mg / kg时有显着变化。海马中的去甲肾上腺素水平降低,为20 mg / kg。暴露于20 mg / kg或更少的丙烯酰胺溶液不会改变BrdU阳性细胞的数量,但应将结果视为初步结果。结论结果表明,口服丙烯酰胺可导致大鼠脑中去甲肾上腺素能轴突和去甲肾上腺素水平降低。鉴于在暴露有1-溴丙烷的大鼠中观察到了类似的效果,
更新日期:2020-03-05
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