Wang R G, Zhu X Z
Department of Pharmacology I, Shanghai Institute of Materia Medica, Chinese Academy of Sciences.
Zhongguo Yao Li Xue Bao. 1995 Jul;16(4):294-6.
To study toxicity of dopamine to mouse neuroblastoma x rat glioma hybrid (NG108) cells.
Cell viability was estimated using 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide (MTT) assay.
Dopamine at 100 mumol L-1 was toxic when added to cultures 24 h after plating. The cell viability was about 1/4 of control. Toxicity did not seem to be mediated by dopaminergic receptors because the dopaminergic antagonists sulpiride and Sch-23390 did not block the toxic effect of dopamine. Catalase 50 kU L-1, superoxide dismutase 50 kU L-1 and l-ascorbic acid 200 mumol L-1 blocked the dopamine (125 mumol L-1) toxicity and elevated the cell viability from 25.9 +/- 11.0% to 74.8 +/- 4.4%, 72.3 +/- 4.5% and 71.4 +/- 2.3%, respectively.
Dopamine toxicity to NG108 cells was mainly attributed to the oxidation of dopamine and its toxic by-products, eg, H2O2.
研究多巴胺对小鼠神经母细胞瘤×大鼠胶质瘤杂交瘤（NG108）细胞的毒性。
采用3-[4,5-二甲基噻唑-2-基]-2,5-二苯基四氮唑溴盐（MTT）法评估细胞活力。
接种24小时后向培养物中添加100μmol L-1的多巴胺具有毒性。细胞活力约为对照组的1/4。毒性似乎不是由多巴胺能受体介导的，因为多巴胺能拮抗剂舒必利和Sch-23390不能阻断多巴胺的毒性作用。50 kU L-1的过氧化氢酶、50 kU L-1的超氧化物歧化酶和200μmol L-1的L-抗坏血酸可阻断多巴胺（125μmol L-1）的毒性，并将细胞活力分别从25.9±11.0%提高到74.8±4.4%、72.3±4.5%和71.4±2.3%。
多巴胺对NG108细胞的毒性主要归因于多巴胺及其毒性副产物（如H2O2）的氧化作用。
