The cellular sites for damage in mammalian cells caused by 193-nm radiation from an argon fluoride excimer laser were investigated. The ability of Chinese hamster ovary cells to reduce a tetrazolium dye (MTT) was decreased to 37% of unirradiated control by <tex-math>$2.5\times 10^{3}\ {\rm J}/{\rm m}^{2}$</tex-math> of 193-nm radiation when measured either 4 or 24 h after irradiation. In contrast, inhibition of MTT reduction by 254-nm radiation which primarily causes DNA damage was not measurable using this assay at 4 h after exposure; at <tex-math>$24\ {\rm h}\ 45\ {\rm J}/{\rm m}^{2}$</tex-math> inhibited MTT reduction to 37% of control. An increase in plasma membrane permeability, detected by51 Cr release, was observed within 15 min of exposure to 193-nm radiation, whereas exposure to 254-nm radiation did not cause this immediate release of51 Cr. In control experiments, the mitochondrial poison, carbonyl cyanide m-chlorophenyl hydrazone, did not cause51 Cr release in the dark, indicating that the 193-nm radiation-induced increase in plasma membrane permeability was not subsequent to loss of mitochondrial function. <tex-math>$[{}^{3}{\rm H}]\text{Arachidonic}$</tex-math> acid was released from C3H10T1/2 cells using low 193-nm fluences, whereas release of [3 H]arachidonic acid using UVB (290-32 nm) radiation required cytotoxic fluences. DNA does not appear to be a major site of 193 nm-induced cellular damage because alkali-labile sites were not detected in cells exposed on ice to up to <tex-math>$2\times 10^{4}\ {\rm J}/{\rm m}^{2}$</tex-math> of 193-nm radiation. These results indicate that 193-nm radiation produces primary damage on the level of the plasma membrane.

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