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Abstract
Purpose: The goal of this study was to determine whether short-duration (15 s–3 min) high-temperature (50°C) heat shocks inhibit the repair of DNA damage.
Materials and methods: Cultured HeLa cells were used. DNA damage was measured after UV exposure or X-irradiation. Three methods were used to measure DNA damage: alkaline comet assay with the endonuclease, UVDE, for single strand breaks and UV photoproducts, antibodies specific for cyclo-pyrimidine dimers (CPD) or for 6-4 photoproducts (64PP), and the appearance-resolution of γ-H2AX foci for DNA double strand breaks.
Results: Heat shocks of 15–30 s at 50°C inhibited repair of DNA damage after UV exposure or X-irradiation detected by the alkaline comet assay (after UV) or by persistence of γ-H2AX foci (after X-rays). The phosphorylation of histone, H2AX, induced by 1 or 4 Gy of X-rays was inhibited in a time-dependent manner after 15–45 s at 52°C. When the excision of UV-induced PP was measured, heat shocks of more than 60 s at 50°C were required to show measurable inhibition.
Conclusion: Severe (50°C) short-duration (15 s or greater) heat shocks inhibit repair of UV-induced DNA damage. The ability to detect the inhibitory effects of very short, 15–60 s, heat shocks was assay dependent. The comet assay could detect repair inhibition after a 15-s heat shock. Detection of DNA damage by specific antibodies could only detect repair inhibition after 1–3-min heat shocks. Using the γ-H2AX foci method 30 s at 50°C induced a significant delay in the repair of DNA damage after 1 Gy of X-rays.