Adler S G, Lachant N A, Anderson P S, Cohen A H, Davidson W D, Glassock R J
Department of Medicine, Harbor-UCLA Medical Center, Torrance.
Miner Electrolyte Metab. 1991;17(1):52-7.
The effect of dimethyl sulfoxide (DMSO) on the rate of glucose oxidation by cultured rat glomerular mesangial cells, human erythrocytes and peritoneal exudate cells was studied. Mesangial cells, erythrocytes and peritoneal exudate cells incubated with DMSO showed enhancement of 14CO2 production from D-[1-14C] glucose but not from D-[6-14C] glucose. The concentration of DMSO required to stimulate respiratory burst activity was lowest for erythrocytes and highest for peritoneal exudate cells. Studies utilizing tritiated deoxyglucose revealed that the increased glucose oxidation associated with DMSO exposure was not due to increased transmembrane glucose movement at low concentrations of DMSO, and only partially responsible at high concentrations of DMSO. This study documents the ability of DMSO to specifically enhance the activity of the hexose monophosphate shunt pathway in all cells studied. The precise mechanism whereby DMSO stimulates shunt activity remains unknown.
研究了二甲基亚砜(DMSO)对培养的大鼠肾小球系膜细胞、人红细胞和腹腔渗出细胞葡萄糖氧化速率的影响。用DMSO孵育的系膜细胞、红细胞和腹腔渗出细胞显示,D-[1-¹⁴C]葡萄糖产生¹⁴CO₂的量增加,而D-[6-¹⁴C]葡萄糖产生¹⁴CO₂的量未增加。刺激呼吸爆发活性所需的DMSO浓度,红细胞最低,腹腔渗出细胞最高。利用氚标记的脱氧葡萄糖进行的研究表明,低浓度DMSO时,与DMSO暴露相关的葡萄糖氧化增加并非由于跨膜葡萄糖转运增加,高浓度DMSO时也只是部分原因。本研究证明了DMSO能够特异性增强所研究的所有细胞中磷酸己糖旁路途径的活性。DMSO刺激旁路活性的确切机制尚不清楚。