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N-甲基-D-天冬氨酸受体在甲基汞诱导的大鼠额叶皮质DNA损伤中的作用

Participation of N-methyl-D-aspartate receptors on methylmercury-induced DNA damage in rat frontal cortex.

作者信息

Juárez Bertha I, Portillo-Salazar Haydée, González-Amaro Roberto, Mandeville Peter, Aguirre J Rogelio, Jiménez María E

机构信息

Departamento de Bioquímica, Facultad de Medicina, Universidad Autónoma de San Luis Potosí, Av. V. Carranza 2405, 78210 San Luis Potosí, S.L.P., México.

出版信息

Toxicology. 2005 Feb 14;207(2):223-9. doi: 10.1016/j.tox.2004.09.007.

Abstract

Methylmercury (MeHg) inhibits glutamate uptake by astrocytes, which can contribute to neuronal loss through excitotoxicity. We explored the extent at which this phenomenon is involved in MeHg-induced DNA damage in the rat cortex. MeHg amounts that increase extracellular glutamate (1.5, 7.5 and 15 nmol, according to previous reports) were stereotaxically injected in the frontal cortex of adult rats before DNA-damage determination by means of a quantitative TUNEL assay. After either 24 or 48 h, the cortex of all exposed animals showed significant increments of damaged DNA, compared with rats that only received sterile saline. In parallel experiments, we found that the administration of a non competitive NMDA receptor antagonist (MK-801, 10 mg/kg, i.p.) 1 h before MeHg injection, significantly reduced DNA damage. These results demonstrate that activation of NMDA receptors contributes importantly to MeHg neurotoxicity.

摘要

甲基汞(MeHg)会抑制星形胶质细胞对谷氨酸的摄取,这可能通过兴奋性毒性导致神经元损失。我们探究了这种现象在多大程度上参与了MeHg诱导的大鼠皮质DNA损伤。在通过定量TUNEL测定法确定DNA损伤之前,将根据先前报告可增加细胞外谷氨酸的MeHg量(1.5、7.5和15 nmol)立体定向注射到成年大鼠的额叶皮质中。24小时或48小时后,与仅接受无菌生理盐水的大鼠相比,所有暴露动物的皮质均显示出受损DNA的显著增加。在平行实验中,我们发现,在注射MeHg前1小时给予非竞争性NMDA受体拮抗剂(MK-801,10 mg/kg,腹腔注射)可显著减少DNA损伤。这些结果表明,NMDA受体的激活对MeHg神经毒性起重要作用。

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