Rate of heating as a determinant of hyperthermic cytotoxicity

T. S. Herman, E. W. Gerner, B. E. Magun, D. Stickney, C. C. Sweets, D. M. White

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Abstract

In Chinese hamster ovary cells and in normal and transformed rat embryonic fibroblasts, survival as a function of time at 42.4° was dependent upon the rate of heating from 37° to 42.4°. Unexpectedly, the untransformed rat fibroblasts were more heat sensitive than were the transformed cells, and the protective effect of slow rates of heating upon survival at 42.4° was also more pronounced in the normal cells than in the transformed cells. In Chinese hamster ovary cells, total cellular cholesterol content and cell volume were found to change significantly with time at 42.4° when cells were heated immediately (37 to 42.4° within 3 min) but did not vary significantly during 6 hr at 42.4° in cells heated from 37 to 42.4° over 3 hr. Chinese hamster ovary cells heated immediately to 42.4° also showed a significant drop in the protein content of the particulate fraction with time at 42.4°. In contrast, cells heated over 3 hr showed a significant increase in the protein content of the particulate fraction with time at 42.4°. These data suggest that, if cells are heated to hyperthermic temperatures over sufficiently long intervals, mechanisms have time to develop which protect the cell membrane against changes associated with cell death in rapidly heated cells. The protective effect of slow rates of heating may partially explain the relative lack of success thus far observed with the use of whole-body hyperthermia in which heating from 37° to 42° often requires 2 to 3 hr.

Original languageEnglish (US)
Pages (from-to)3519-3523
Number of pages5
JournalCancer Research
Volume41
Issue number9 I
StatePublished - 1981
Externally publishedYes

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Heating
Cricetulus
Ovary
Fibroblasts
Cell Size
Proteins
Cell Death
Fever
Hot Temperature
Cholesterol
Cell Membrane
Temperature

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Herman, T. S., Gerner, E. W., Magun, B. E., Stickney, D., Sweets, C. C., & White, D. M. (1981). Rate of heating as a determinant of hyperthermic cytotoxicity. Cancer Research, 41(9 I), 3519-3523.

Rate of heating as a determinant of hyperthermic cytotoxicity. / Herman, T. S.; Gerner, E. W.; Magun, B. E.; Stickney, D.; Sweets, C. C.; White, D. M.

In: Cancer Research, Vol. 41, No. 9 I, 1981, p. 3519-3523.

Research output: Contribution to journalArticle

Herman, TS, Gerner, EW, Magun, BE, Stickney, D, Sweets, CC & White, DM 1981, 'Rate of heating as a determinant of hyperthermic cytotoxicity', Cancer Research, vol. 41, no. 9 I, pp. 3519-3523.
Herman TS, Gerner EW, Magun BE, Stickney D, Sweets CC, White DM. Rate of heating as a determinant of hyperthermic cytotoxicity. Cancer Research. 1981;41(9 I):3519-3523.
Herman, T. S. ; Gerner, E. W. ; Magun, B. E. ; Stickney, D. ; Sweets, C. C. ; White, D. M. / Rate of heating as a determinant of hyperthermic cytotoxicity. In: Cancer Research. 1981 ; Vol. 41, No. 9 I. pp. 3519-3523.
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N2 - In Chinese hamster ovary cells and in normal and transformed rat embryonic fibroblasts, survival as a function of time at 42.4° was dependent upon the rate of heating from 37° to 42.4°. Unexpectedly, the untransformed rat fibroblasts were more heat sensitive than were the transformed cells, and the protective effect of slow rates of heating upon survival at 42.4° was also more pronounced in the normal cells than in the transformed cells. In Chinese hamster ovary cells, total cellular cholesterol content and cell volume were found to change significantly with time at 42.4° when cells were heated immediately (37 to 42.4° within 3 min) but did not vary significantly during 6 hr at 42.4° in cells heated from 37 to 42.4° over 3 hr. Chinese hamster ovary cells heated immediately to 42.4° also showed a significant drop in the protein content of the particulate fraction with time at 42.4°. In contrast, cells heated over 3 hr showed a significant increase in the protein content of the particulate fraction with time at 42.4°. These data suggest that, if cells are heated to hyperthermic temperatures over sufficiently long intervals, mechanisms have time to develop which protect the cell membrane against changes associated with cell death in rapidly heated cells. The protective effect of slow rates of heating may partially explain the relative lack of success thus far observed with the use of whole-body hyperthermia in which heating from 37° to 42° often requires 2 to 3 hr.

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