Griffiths T D, Dahle D B, Meechan P J, Carpenter J G
Biochim Biophys Acta. 1981 Nov 27;656(1):55-61. doi: 10.1016/0005-2787(81)90026-5.
Chinese hamster V-79 cells were treated with metabolic inhibitors o DNA or protein synthesis for various intervals of time after exposure of 3.0 or 5.0 J m-2. After removal of the metabolic block(s) the rate of DNA synthesis was followed by measuring the incorporation of [14C]thymidine into acid-insoluble material. A 2.5 or 5.0 h incubation with cycloheximide or hydroxyurea was effective in delaying the onset of the recovery in the rate of DNA synthesis that normally becomes evident several hours after exposure to ultraviolet light. By using concentrations of cycloheximide or hydroxyurea that inhibit DNA synthesis by a similar amount (70%), but protein synthesis by vastly different amounts (95% for cycloheximide; 0% for hydroxyurea), it was apparent that the delay in recovery caused by the treatment of cells with cycloheximide could be accounted for entirely by its inhibitory effect on DNA synthesis. This suggests that the recovery in DNA synthetic rates following exposure of V-79 cells to ultraviolet light does not appear to require de novo protein synthesis, and therefore does not appear to require the involvement of an inducible DNA repair process.
中国仓鼠V - 79细胞在暴露于3.0或5.0 J m-2的紫外线后,在不同时间段用DNA或蛋白质合成的代谢抑制剂进行处理。去除代谢阻断后,通过测量[14C]胸苷掺入酸不溶性物质的量来跟踪DNA合成速率。用环己酰亚胺或羟基脲孵育2.5或5.0小时可有效延迟DNA合成速率恢复的起始时间,这种恢复通常在暴露于紫外线数小时后变得明显。通过使用抑制DNA合成量相似(70%)但抑制蛋白质合成量差异很大(环己酰亚胺为95%;羟基脲为0%)的环己酰亚胺或羟基脲浓度,很明显,用环己酰亚胺处理细胞导致的恢复延迟完全可以由其对DNA合成的抑制作用来解释。这表明V - 79细胞暴露于紫外线后DNA合成速率的恢复似乎不需要从头合成蛋白质,因此似乎不需要诱导性DNA修复过程的参与。