THERMOTOLERANCE INDUCED BY HEAT, SODIUM ARSENITE, OR PUROMYCIN - ITS INHIBITION AND DIFFERENCES BETWEEN 43-DEGREES-C AND 45-DEGREES-C
THERMOTOLERANCE INDUCED BY HEAT, SODIUM ARSENITE, OR PUROMYCIN - ITS INHIBITION AND DIFFERENCES BETWEEN 43-DEGREES-C AND 45-DEGREES-C
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DOI：
10.1002/jcp.1041350306
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发表时间：
1988-06-01
影响因子：
5.6
通讯作者：
DEWEY, WC
中科院分区：
文献类型：
--
作者：
LEE, YJ;DEWEY, WC
When CHO cells were treated either for 10 min at 45-45.5.degree. C or for 1 hr with 100 .mu.M sodium arsenite (ARS) or for 2 hr with 20 .mu.g/ml puromycin (PUR-20), they became thermotolerant to a heat treatment at 45-45.5.degree. C administered 4-14 hr later, with thermotolerance ratios at 10-3 isosurvival of 4-6, 2-3.2, and 1.7, respectively. These treatments caused an increase in synthesis of HSP families (70, 87, and 110 kDa) relative to total protein synthesis. However, for a given amount of thermotolerance, the ARS and PUR-20 treatments induced 4 times more synthesis than the heat treatment. This decreased effectiveness of the ARS treatment may occur because ARS has been reported to stimulate minimal redistribution of HSP-70 to the nucleus and nucleolus. Inhibiting protein synthesis with cycloheximide (CHM, 10 .mu.g/ml) or PUR (100 .mu.g/ml) after the initial treatments greatly inhibited thermotolerance to 45-45.5.degree. C in all cases. However, for a challenge at 43.degree. C, thermotolerance was inhibited only for the ARS and PUR-20 treatments. CHM did not suppress heat-induced thermotolerance to 43.degree. C, which was the same as heat protection observed when CHM was added before and during heating at 43.degree. C without the initial heat treatment. These differences between the initial treatments and between 43 and 45.degree. C may possibly be explained by reports that show that heat causes more redistribution of HSP-70 to the nucleus and nucleolus than ARS and that redistribution of HSP-70 can occur during heating at 42.degree. C with or without the presence of CHM. Heating cells at 43.degree. C for 5 hr after thermotolerance had developed induced additional thermotolerance, as measured with a challenge at 45.degree. C immediately after heating at 43.degree. C. Compared to the nonthermotolerant cells, thermotolerance ratios were 10 for the ARS treatment and 8.5 for the initial heat treatment. Adding CHM (10 .mu.g/ml) or PUR (100 .mu.g/ml) to inhibit protein synthesis during heating at 43.degree. C did not greatly reduce this additional thermotolerance. If, however, protein synthesis was inhibited between the initial heat treatment and heating at 43.degree. C, protein synthesis was required during 43.degree. C for the development of additional thermotolerance to 45.degree. C. These data suggest that if a considerable amount of synthesis of HSP families occurred after the initial treatment before heating at 43.degree. C, redistribution during 43.degree. C of the previously synthesized HSP families could lead to the additional thermotolerance to 45.degree. C.
