Tirmenstein M A, Mathias P I, Snawder J E, Wey H E, Toraason M
Division of Biomedical and Behavioral Science, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Cincinnati, OH 45226, USA.
Toxicology. 1997 May 16;119(3):203-11. doi: 10.1016/s0300-483x(97)03628-7.
Cultured cardiac myocytes were exposed for up to 4 h to 50 and 100 microM potassium antimonyl tartrate (PAT). After 4 h, 50 and 100 microM PAT killed 14 and 33% respectively of the cardiac myocytes. PAT-induced alterations in both protein and nonprotein thiol homeostasis. Transient increases in oxidized glutathione disulfide (GSSG) levels were detected after cells were treated with 100 microM PAT for 2 h. After 4 h, both concentrations of PAT significantly depleted reduced glutathione (GSH) levels. Protein thiols levels were also decreased after a 2-h exposure to 50 and 100 microM PAT. Cells treated with 50 microM and 100 microM PAT had a 15% and 40% reduction respectively in protein thiols after 4 h. PAT also significantly inhibited glutathione peroxidase and pyruvate dehydrogenase activity in cardiac myocytes. Pyruvate dehydrogenase activity levels were inhibited as early as 1 h after cells were treated with both concentrations of PAT. Cardiac myocyte ATP levels were also decreased by PAT, but only after a 4-h exposure to 50 microM and 100 microM PAT. Decreases in cellular ATP levels paralleled PAT toxicity put appeared to be secondary to other cellular changes initiated by PAT exposure.
将培养的心肌细胞暴露于50和100微摩尔的酒石酸锑钾（PAT）中长达4小时。4小时后，50和100微摩尔的PAT分别杀死了14%和33%的心肌细胞。PAT诱导了蛋白质和非蛋白质硫醇稳态的改变。在用100微摩尔PAT处理细胞2小时后，检测到氧化型谷胱甘肽二硫化物（GSSG）水平短暂升高。4小时后，两种浓度的PAT均显著降低了还原型谷胱甘肽（GSH）水平。在暴露于50和100微摩尔PAT 2小时后，蛋白质硫醇水平也降低。在用50微摩尔和100微摩尔PAT处理的细胞中，4小时后蛋白质硫醇分别降低了15%和40%。PAT还显著抑制心肌细胞中的谷胱甘肽过氧化物酶和丙酮酸脱氢酶活性。在用两种浓度的PAT处理细胞后，丙酮酸脱氢酶活性水平早在1小时就受到抑制。心肌细胞ATP水平也因PAT而降低，但仅在暴露于50微摩尔和100微摩尔PAT 4小时后。细胞ATP水平的降低与PAT毒性平行，但似乎是由PAT暴露引发的其他细胞变化的继发结果。
