The effects of glutathione depletion on thermotolerance and heat stress protein synthesis.
The effects of glutathione depletion on thermotolerance and heat stress protein synthesis.
复制标题
DOI：
10.1038/bjc.1984.118
复制
发表时间：
1984-06
影响因子：
8.8
通讯作者：
McPherson S
中科院分区：
文献类型：
--
作者：
Russo A;Mitchell JB;McPherson S
研究了丁硫酰亚胺耗竭细胞谷胱甘肽对耐热性形成和热应激蛋白合成的影响。发现细胞谷胱甘肽水平在45.5摄氏度下12分钟或43摄氏度下1小时的急性热处理后迅速增加，并长时间保持升高。谷胱苷肽耗尽和谷胱甘肽合成的预防丁硫氨酸亚砜亚胺导致抑制的发展的耐热性和减少总蛋白以及特定的热应激蛋白。虽然两种谷胱甘肽耗竭方案对耐热性的抑制程度相似，但在加热前谷胱甘肽耗竭至低水平时，热应激蛋白合成的抑制作用更大。讨论了谷胱甘肽和细胞氧化还原状态对热耐受性和热应激蛋白合成的可能作用。
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.