Implications of nitrocathecholamines in Parkinson's disease

研究了6-硝基肾上腺素是否增加过氧化氢的产生。6-硝基去甲肾上腺素可使大鼠血管内皮细胞Fas表达增加，在0μM时，0~0.2nmol/60min/10^5细胞，在0.3μM时，1~2nmol/60min/10^5细胞。进一步增加胺的浓度是不合适的，因为胺的颜色干扰了过氧化氢的测定。用SH-SY5Y细胞检测了6-硝基肾上腺素可能的诱导凋亡活性。通过从核小体中释放组蛋白来评估细胞的凋亡。浓度为30 0μM的胺诱导细胞凋亡。6-1OHDA作为对照化合物，在30和300μM浓度下诱导细胞凋亡。神经毒性农药草甘膦铵能刺激大鼠脑内一氧化氮的产生，并引起惊厥。HMDA受体拮抗剂可抑制这些反应。

It was investigated whether or not 6-nitronorepinephrine increased hydrogen peroxide production. 6-Nitronorepinephrine increased it in rat vascular endothelial cells ; at 0 μM, 0-0.2 nmol/60 min/10^5 cells ; 0.3μM, 1-2 nmol/60 min/10^5 cells. Further inceases in the amine concentration was inappropriate because the color of the amine interfered the hydrogen peroxide assay.Possible apoptosis-eliciting activities of 6-nitronorepinephrine was tested with use of SH-SY5Y cells. Apoptosis was evaluated by released histone from mucleosomes. The amine at a concentration of 300 μM induced apoptosis. 6-1OHDA, a control compound, induced apoptosis at concentrations of 30 and 300 μM.A neurotoxic pesticide, glufosinate ammonium, was found to be able to stimulate nitric oxide production in rat brain and to induce convulsion. HMDA receptor antagonists inhibited those response.