一氧化氮介导的1型人类免疫缺陷病毒包膜蛋白在原代皮质培养物中的神经毒性
Human immunodeficiency virus type 1 coat protein neurotoxicity mediated by nitric oxide in primary cortical cultures.
作者信息
Dawson V L, Dawson T M, Uhl G R, Snyder S H
机构信息
National Institute on Drug Abuse, Addiction Research Center, Baltimore, MD 21224.
出版信息
Proc Natl Acad Sci U S A. 1993 Apr 15;90(8):3256-9. doi: 10.1073/pnas.90.8.3256.
Abstract
The human immunodeficiency virus type 1 coat protein, gp120, kills neurons in primary cortical cultures at low picomolar concentrations. The toxicity requires external glutamate and calcium and is blocked by glutamate receptor antagonists. Nitric oxide (NO) contributes to gp120 toxicity, since nitroarginine, an inhibitor of NO synthase, prevents toxicity as does deletion of arginine from the incubation medium and hemoglobin, which binds NO. Superoxide dismutase also attenuates toxicity, implying a role for superoxide anions.
摘要
1型人类免疫缺陷病毒外壳蛋白gp120在皮摩尔低浓度下可杀死原代皮质培养中的神经元。这种毒性需要细胞外谷氨酸和钙，且可被谷氨酸受体拮抗剂阻断。一氧化氮（NO）促成gp120毒性，因为NO合酶抑制剂硝基精氨酸可防止毒性，从培养基中去除精氨酸以及使用结合NO的血红蛋白也有同样效果。超氧化物歧化酶也可减轻毒性，这表明超氧阴离子起了作用。
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