Loven D P
Division of Radiation Biology and Oncology, East Carolina University School of Medicine, Greenville, North Carolina 27858.
Med Hypotheses. 1988 May;26(1):39-50. doi: 10.1016/0306-9877(88)90111-9.
A model suggesting a role for superoxide (O2-) and hydrogen peroxide (H2O2) in heat induced cytotoxicity and development of thermotolerance is proposed: (1) Heat shock increases cellular generation of O2- and H2O2 in proportion to the severity of the heat shock. (2) Heat induced generation of O2- or H2O2 in excess of the ability of the antioxidant enzymes to remove these toxic species causes heat induced cell injury and cytotoxicity. This damage is caused by lipid peroxidation, leading to disruption of the cytoskeleton and calcium metabolism. (3) The flux of O2- and H2O2 generated by heat shock induces the synthesis of additional antioxidant enzymes. Other treatments which induce thermotolerance also cause oxidative stress and induce the antioxidant enzymes. The ability of various agents to modify heat induced cytotoxicity and development of thermotolerance is reviewed in light of this model.
提出了一个关于超氧化物（O2-）和过氧化氢（H2O2）在热诱导细胞毒性和耐热性发展中作用的模型：（1）热休克会使细胞产生的O2-和H2O2与热休克的严重程度成比例增加。（2）热诱导产生的O2-或H2O2超过抗氧化酶清除这些有毒物质的能力会导致热诱导的细胞损伤和细胞毒性。这种损伤是由脂质过氧化引起的，导致细胞骨架和钙代谢的破坏。（3）热休克产生的O2-和H2O2通量诱导额外抗氧化酶的合成。其他诱导耐热性的处理也会引起氧化应激并诱导抗氧化酶。根据该模型对各种试剂改变热诱导细胞毒性和耐热性发展的能力进行了综述。
