Implications of nitrocathecholamines in Parkinson's disease

研究了6-硝基肾上腺素是否会增加过氧化氢的产生。6-硝基肾上腺素增加了大鼠血管内皮细胞的表达；在0 μM， 0-0.2 nmol/60 min/10^5个细胞；0.3μM， 1-2 nmol/60 min/10^5个细胞。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6-硝基肾上腺素可能的促凋亡活性。核小体释放组蛋白评价细胞凋亡。300 μM浓度的胺诱导细胞凋亡。对照化合物6-1OHDA在浓度为30 μM和300 μM时诱导细胞凋亡。一种具有神经毒性的农药，草甘膦铵，被发现能够刺激大鼠脑中一氧化氮的产生并引起抽搐。HMDA受体拮抗剂抑制这些反应。

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.