INTRACELLULAR STIMULATION OF BIOCHEMICAL CONTROL MECHANISMS BY LOW-DOSE, LOW-LET IRRADIATION
INTRACELLULAR STIMULATION OF BIOCHEMICAL CONTROL MECHANISMS BY LOW-DOSE, LOW-LET IRRADIATION
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DOI：
10.1097/00004032-198705000-00020
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发表时间：
1987-05-01
期刊：
影响因子：
2.2
通讯作者：
SONDHAUS, CA
中科院分区：
文献类型：
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作者：
FEINENDEGEN, LE;MUHLENSIEPEN, H;SONDHAUS, CA
细胞内自由基的非特异性产生超过正常水平，例如由于细胞中的急性辐射吸收事件，导致了胸苷激酶的延迟和暂时的抑制。即使在低水平暴露后，酶活性也在4h达到最低值，并在此后不久完全恢复。这一过程似乎代表了对初始物理事件的生化反应，但必须与DNA修复酶系统的反应区分开来。细胞胸苷激酶活性的降低预计会导致DNA合成的暂时减少，并可能对细胞有利。这种反应可以被认为是辐射兴奋的一个例子，因为这种对辐射刺激的补偿反应可以提供保护，防止自由基浓度的反复增加，无论是通过重新辐射暴露还是通过一般的新陈代谢。修复效率的提高或自由基解毒水平的提高对单个细胞和整个生物体都是有益的。
Non-specific generation of intracellular free radicals in excess of normal levels, eg by the acute radiation absorption event in cells, has led to a delayed and temporary inhibition of thymidine kinase. The enzyme activity reaches a minimum at 4 h even after a low-level exposure with full recovery soon thereafter. This process appears to represent a biochemical response to an initial physical event, but must be distinguished from the response of the DNA repair enzyme system. A reduction of cellular thymidine kinase activity is expected to cause a temporary reduction of DNA synthesis and may be of advantage to the cell. Such a response may be regarded as an instance of radiation hormesis in the sense that such a compensatory response to the stimulus of irradiation may confer protection against a repeated increase in free radical concentration whether by renewed radiation exposure or by metabolism in general. An improvement of the efficiency of repair or an increased level of free radical detoxification should be of benefit to both the individual cell and to the organism as a whole.