Russo A, Mitchell J B, McPherson S
Br J Cancer. 1984 Jun;49(6):753-8. doi: 10.1038/bjc.1984.118.
The effects of cellular glutathione depletion by buthionine sulfoximine on the development of thermotolerance and synthesis of heat stress protein was studied. Cellular glutathione levels were found to increase rapidly following an acute heat treatment of either 12 min at 45.5 degrees C or 1 h at 43 degrees C and remain elevated for prolonged periods. Glutathione depletion and prevention of glutathione synthesis by buthionine sulfoximine resulted in inhibition of the development of thermotolerance and a decrease in total protein as well as specific heat stress proteins. While the degree of inhibition of thermotolerance was similar for both glutathione depletion protocols, inhibition in heat stress protein synthesis was greater when glutathione was depleted to low levels prior to heating. The possible role of glutathione and the cellular redox state to thermotolerance and synthesis of heat stress protein is discussed.
研究了丁硫氨酸亚砜胺使细胞内谷胱甘肽耗竭对耐热性发展和热应激蛋白合成的影响。发现细胞经45.5℃12分钟或43℃1小时的急性热处理后，谷胱甘肽水平迅速升高，并在较长时间内保持升高。丁硫氨酸亚砜胺导致的谷胱甘肽耗竭及谷胱甘肽合成的抑制，会抑制耐热性的发展，并使总蛋白以及特定热应激蛋白减少。虽然两种谷胱甘肽耗竭方案对耐热性的抑制程度相似，但在加热前将谷胱甘肽耗竭至低水平时，对热应激蛋白合成的抑制作用更大。文中讨论了谷胱甘肽和细胞氧化还原状态对耐热性及热应激蛋白合成的可能作用。
