Toxicity of dopamine to mouse neuroblastoma x rat glioma hybrid (NG108) cells in vitro
Abstract
AIM: To study toxicity of dopamine to mouse neuroblastoma x rat glioma hybrid (NG108) cells.
METHODS: Cell viability was estimated using 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide (MTT) assay.
RESULTS: 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.
CONCLUSION: Dopamine toxicity to NG108 cells was mainly attributed to the oxidation of dopamine and its toxic by-products, eg, H2O2.
Keywords:
METHODS: Cell viability was estimated using 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide (MTT) assay.
RESULTS: 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.
CONCLUSION: Dopamine toxicity to NG108 cells was mainly attributed to the oxidation of dopamine and its toxic by-products, eg, H2O2.