Roti Roti J L
Natl Cancer Inst Monogr. 1982 Jun;61:3-10.
Although several lines of evidence suggest that the cellular membrane plays a role in heat-induced cell death, a basic question remains unanswered. Namely, how does membrane damage lead to reproductive death which is traditionally thought to reflect DNA damage? Recent results suggest that membrane damage in the absence of heat can cause an increase in chromatin protein content similar to that induced by hyperthermia. The increased protein content in chromatin could cause structural alterations that lead to inhibition of enzyme-mediated DNA function. These alterations appear to play a major role in heat-induced radiosensitization by inhibiting the repair of X-ray-induced DNA strand breaks and thymine damage. The correlation between cell killing by heat alone and the increase in chromatin content imply that structural alterations in chromatin are part of the killing mechanism. Recently, heat-induced DNA damage has been observed. Therefore, the molecular mechanism by which hyperthermia kills cells could involve DNA damage resulting from alterations in chromatin structure.
尽管有几条证据表明细胞膜在热诱导的细胞死亡中起作用，但一个基本问题仍未得到解答。也就是说，膜损伤是如何导致传统上认为反映DNA损伤的生殖死亡的？最近的结果表明，在无热情况下的膜损伤可导致染色质蛋白含量增加，类似于热疗诱导的增加。染色质中蛋白质含量的增加可能导致结构改变，从而导致酶介导的DNA功能受到抑制。这些改变似乎通过抑制X射线诱导的DNA链断裂和胸腺嘧啶损伤的修复，在热诱导的放射增敏中起主要作用。仅热诱导的细胞杀伤与染色质含量增加之间的相关性意味着染色质的结构改变是杀伤机制的一部分。最近，已经观察到热诱导的DNA损伤。因此，热疗杀死细胞的分子机制可能涉及染色质结构改变导致的DNA损伤。
