Sensitivity of Hyperthermia-Treated Human Cells to Killing by Ultraviolet or γ Radiation

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Abstract
Human xeroderma pigmentosum (XP) or Fanconi anemia (FA) fibroblasts displayed shouldered 45.degree. C heat survival curves not significantly different from normal fibroblasts, a result similar to that previously found for ataxia telangiectasia (AT) cells, indicating heat resistance is not linked to either uv or low-LET ionizing radiation resistance. Hyperthermia (45.degree. C) sensitized normal and XP fibroblasts to killing by .gamma. irradiation but failed to sensitize the cells to the lethal effects of 254 nm uv irradiation. Thermal inhibition of repair of ionizing radiation lesions but not uv-induced lesions appears to contribute synergistically to cell death. The thermal enhancement ratio (TER) for the synergistic interaction of hyperthermia (45.degree. C, 30 min) and .gamma. radiation was significantly lower in one FA and two XP strains (TER = 1.7-1.8) than that reported previously for three normal strains (TER = 2.5-3.0). These XP and FA strains may be more .gamma. sensitive than normal human fibroblasts. Since hyperthermia treatment only slightly increases the .gamma.-radiation sensitivity of ataxia telangiectasia (AT) fibroblasts compared to normal strains, it is possible that the degree of thermal enhancement attainable reflects the genetically inherent ionizing radiation repair capacity of the cells. The data indicate that both repair inhibition and particular lesion types are required for lethal synergism between heat and radiation. We therefore postulate that the transient thermal inhibition of repair results in the conversion of .gamma.-induced lesions to irrepairable lethal damage, while uv-type damage can remain unaltered during this period.

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