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甲基汞中毒小鼠神经组织中假定氨基酸水平的改变及形态学发现。

Alteration of putative amino acid levels and morphological findings in neural tissues of methylmercury-intoxicated mice.

作者信息

Hirayama K, Inouye M, Fujisaki T

出版信息

Arch Toxicol. 1985 Apr;57(1):35-40. doi: 10.1007/BF00286572.

Abstract

Methylmercury chloride was administered PO to male Kud: ddY mice at a dose of 5 mg/kg/day for 20 days. The contents of taurine, aspartate, glutamate, glycine, and gamma-aminobutyric acid were determined in tissue and crude synaptosomal (P2) fraction of cerebellum, cerebral cortex, and spinal cord of methylmercury-treated mice with or without ataxia. In the cerebellum of ataxic mice, increased levels of taurine and glycine were found in the tissue and P2 fraction, and increased levels of glutamate were found in the P2 fraction. In the cerebral cortex, the levels of gamma-aminobutylic acid decreased in the tissue and in the P2 fraction of ataxic mice, but increased levels were found in the tissue of non-ataxic mice. A decreased aspartate level in the cerebral cortex of ataxic mice and an increased taurine level in the cerebral cortex of non-ataxic mice were also found. In the spinal cord of ataxic mice, taurine increased in the tissue and in the P2 fraction. Glutamate level decreased in the spinal cord of ataxic mice, but increased in the P2 fraction of non-ataxic mice. Increased glycine levels in the P2 fraction of the spinal cord were also found in non-ataxic mice. Histologically, some degenerative changes were demonstrated in the cerebral and cerebellar cortices of ataxic mice. Such changes were also present to a mild degree in non-ataxic mice. In conclusion, methylmercury treatment altered the levels of putative neurotransmitter amino acids in neural tissue of mice. These alterations might be caused by specific neural cell dysfunction and could be related to the appearance of ataxia.

摘要

将氯化甲基汞以5毫克/千克/天的剂量经口给予雄性Kud:ddY小鼠,持续20天。测定了甲基汞处理的小鼠(有或无共济失调)小脑、大脑皮层和脊髓的组织及粗制突触体(P2)组分中牛磺酸、天冬氨酸、谷氨酸、甘氨酸和γ-氨基丁酸的含量。在共济失调小鼠的小脑中,组织和P2组分中的牛磺酸和甘氨酸水平升高,P2组分中的谷氨酸水平升高。在大脑皮层中,共济失调小鼠的组织和P2组分中的γ-氨基丁酸水平降低,但未患共济失调小鼠的组织中γ-氨基丁酸水平升高。还发现共济失调小鼠大脑皮层中的天冬氨酸水平降低,未患共济失调小鼠大脑皮层中的牛磺酸水平升高。在共济失调小鼠的脊髓中,组织和P2组分中的牛磺酸增加。共济失调小鼠脊髓中的谷氨酸水平降低,但未患共济失调小鼠的P2组分中的谷氨酸水平升高。在未患共济失调小鼠的脊髓P2组分中也发现甘氨酸水平升高。组织学检查显示,共济失调小鼠的大脑和小脑皮层有一些退行性变化。在未患共济失调的小鼠中也有轻度的此类变化。总之,甲基汞处理改变了小鼠神经组织中假定神经递质氨基酸的水平。这些改变可能是由特定的神经细胞功能障碍引起的,并且可能与共济失调的出现有关。

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