Evidence for separate modes of action in thermal radiosensitization and direct thermal cell death

Mivechi, Nahid F.; Hofer, Kurt G.

doi:10.1002/1097-0142(19830101)51:1<38::aid-cncr2820510110>3.0.co;2-5

Cited by 17 publications

(6 citation statements)

References 19 publications

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“…Many data, based on different heat treatments in one cell line, using altered pH, heat modifying agents or development of thermotolerance have suggested a causal relationship between heat killing and heat radiosensitization (Konings and van der Meer-Kalverkamp 1980, Freeman et al 1981, Djordjevic 1983, Haveman 1983, Raaphorst and Azzam 1983, Dewey 1983, Holahan et al 1984, van Rijn et al 1984 although other data do not show this relationship (Lunec and Parker 1980, Mivechi and Hofer 1983, Nielsen 1983, Hartson-Eaton et al 1984. The different results of these investigations may possibly be explained by the differences in cell lines used and in the different heat schedules employed.…”

Section: Heat Sensitivity Versus the Radiosensitizing Effect Of Heatmentioning

confidence: 99%

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Differences in Heat-induced Cell Killing as Determined in Three Mammalian Cell Lines Do Not Correspond with the Extent of Heat Radiosensitization

Kampinga

Jorritsma

Burgman

et al. 1986

International Journal of Radiation Biology and Related Studies

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Three different cell lines, Ehrlich ascites tumour (EAT) cells, HeLa S3 cells and LM mouse fibroblasts, were used to investigate whether or not the extent of heat killing (44 degrees C) and heat radio-sensitization (44 degrees C before 0-6 Gy X-irradiation) are related. Although HeLa cells were the most heat-resistant cell line and showed the least heat radiosensitization, we found that the most heat-sensitive EAT cells (D0, EAT = 8.0 min; D0, LM = 10.0 min; D0, HeLa = 12.5 min) showed less radiosensitization than the more heat-resistant LM fibroblasts (TERHeLa less than TEREAT less than TERLM). Therefore, it is concluded that the routes leading to heat-induced cell death are not identical to those determining heat radiosensitization. Furthermore the inactivation of DNA polymerase alpha and beta activities by heat seemed not to correlate with heat survival alone but showed a positive relationship to heat radiosensitization. The possibility of these enzymes being a determinant in heat radiosensitization is discussed.

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Section: Heat Sensitivity Versus the Radiosensitizing Effect Of Heatmentioning

confidence: 99%

“…Lunec and Parker (1980) reported no effect of lowering pH on heat radiosensitization, while heat survival levels were markedly reduced. Furthermore, Mivechi and Hofer (1983) showed that 5 per cent glycerol did increase heat resistance but had no effect on heat radiosensitization.…”

Section: Introductionmentioning

confidence: 99%

Differences in Heat-induced Cell Killing as Determined in Three Mammalian Cell Lines Do Not Correspond with the Extent of Heat Radiosensitization

Kampinga

Jorritsma

Burgman

et al. 1986

International Journal of Radiation Biology and Related Studies

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“…In the authors' hands, a series of heatresistant cell lines that over-express hsp 27 (a gift of Dr J. Landry, University of Laval, Quebec) also did not display differences in heat-induced radiosensitization (Laszlo and Davidson, unpublished observations). Glycerol, a chemical heat protector, did not affect heat-induced radiosensitization [42]. The results obtained with transiently thermotolerant cells are equivocal: in some cases there is protection, while in others there is not, even in studies with the same cell line (reviewed in [17]).…”

Section: Discussionmentioning

confidence: 99%

Alterations in heat-induced radiosensitization accompanied by nuclear structure alterations in Chinese hamster cells

Laszlo

Davidson

Harvey

et al. 2006

International Journal of Hyperthermia

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This paper examined heat-induced radiosensitization in two Chinese hamster heat-resistant cell lines, HR-1 and OC-14, that were isolated from the same wild-type HA-1 cell line. It found a reduction of the magnitude of heat-induced radiosensitization after exposure to 43 degrees C in both HR-1 and OC-14 cells and a similar reduction after exposure to 45 degrees C in HR-1 cells, but not in OC-14 cells. The effect of heat exposure on a class of ionizing radiation-induced DNA damage that inhibits the ability of nuclear DNA to undergo super-coiling changes was also studied using the fluorescent halo assay in these three cell lines. Wild type cells exposed to either 43 or 45 degrees C before irradiation had a DNA rewinding ability that was intermediate between control and unheated cells, a phenomenon previously described as a masking effect. This masking effect was significantly reduced in HR-1 cells exposed to either 43 or 45 degrees C or in OC-14 cells exposed to 43 degrees C under conditions that heat-induced radiosensitization was reduced. In contrast, the masking effect was not altered in OC-14 cells exposed to 45 degrees C, conditions under which heat-induced radiosensitization was similar to that observed in wild-type HA-1 cells. These results suggest that a reduction in the masking effect is associated with a reduction of the magnitude of heat-induced radiosensitization in the HR-1 and OC-14 heat-resistant cell lines. The reduction of the masking effect in the cell lines resistant to heat-induced radiosensitization was associated with neither a reduction in the magnitude of the heat-induced increase in total nuclear protein content nor major differences in the protein profiles of the nucleoids isolated from heated cells.

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“…3) is consistent with studies of hyperthermiainduced radiosensitization, ie., the temporal sequencing of hyperthermia and ionizing i r r a d i a t i~n .~.~.~~ Additionally, the data showing no appreciable difference in the fall of NAD levels for patients heated for 60 to 140 minutes are consistent with in vitro less than 42°C thermal radiosensitization studies of a lymphoid cell line (JM)2h and a sarcoma line (>42"C). 27 This research suggests a working hypothesis: WBH sensitizes cells to DNA-damaging agents by blocking the resynthesis of NAD consumed for ADP-ribose polymer synthesis and thereby limiting polymer synthesis and cellular recovery. Taken collectively, the results presented 2 102 CANCER April 15 199 1 Vol.…”

Section: Fraction Numbermentioning

confidence: 99%

Effect of hyperthermiain vitro andin vivo on adenine and pyridine nucleotide pools in human peripheral lymphocytes

Robins¹,

Jönsson

Jacobson

et al. 1991

Cancer

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Hyperthermia has been shown in vitro and in vivo to potentiate the effects of ionizing irradiation. Previous studies found that hyperthermia alters the metabolism of adenosine diphosphate (ADP)-ribose polymers required for recovery from DNA damage and that poly(ADP-ribose) polymerase activity is very sensitive to cellular nicotinamide-adenine dinucleotide (NAD) levels. Thus, the effect of 41.8"C hyperthermia in vitro and in vivo on NAD and adenosine triphosphate (ATP) levels was studied in human peripheral lymphocytes. In vifro studies showed significant decreases in oxidized NAD (NAD') and ATP levels after heating that simulated a clinical whole-body hyperthermia (WBH) treatment. This nucleotide depletion could not be attributed to nucleotide leakage or increased enzymatic NAD+ consumption. As the reduction of NAD observed was sufficient to decrease poly(ADP4bose)polymerase activity by 5070, the studies were extended to clinical cases. Cellular NAD+ and ATP were measured in previously stored lymphocytes obtained from four patients before and after WBH; a statistically significant decrease in NAD+ was observed after WBH which quantitatively agreed with the in vitro results. Based on these results a prospective study was done in three patients: NAD+ was extracted immediately on sample collection, and the kinetics of WBH-induced NAD depletion were studied. These data, which agree quantitatively with the laboratory results, are presented. Cancer 67:2096-2102,1991. RECLINICAL STUDIES show the potential of temper-P atures as high as 42°C to enhance the effects of ionizing irradiation, chemotherapy, and immunotherapy.'-6 The results of such laboratory work have been extrapolated to the clinical sphere, with promising, but not de

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Evidence for separate modes of action in thermal radiosensitization and direct thermal cell death

Cited by 17 publications

References 19 publications

Differences in Heat-induced Cell Killing as Determined in Three Mammalian Cell Lines Do Not Correspond with the Extent of Heat Radiosensitization

Differences in Heat-induced Cell Killing as Determined in Three Mammalian Cell Lines Do Not Correspond with the Extent of Heat Radiosensitization

Alterations in heat-induced radiosensitization accompanied by nuclear structure alterations in Chinese hamster cells

Effect of hyperthermiain vitro andin vivo on adenine and pyridine nucleotide pools in human peripheral lymphocytes

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