MECHANISM FOR 193-NM LASER RADIATION-INDUCED EFFECTS ON MAMMALIAN-CELLS
MECHANISM FOR 193-NM LASER RADIATION-INDUCED EFFECTS ON MAMMALIAN-CELLS
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DOI:
10.2307/3577598
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发表时间:
1990-05-01
影响因子:
3.4
通讯作者:
MIRRO, J
中科院分区:
文献类型:
--
作者:
KOCHEVAR, IE;WALSH, AA;MIRRO, J
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 2.5 .times. 103 J/m2 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 24 h 45 J/m2 inhibited MTT reduction to 37% of control. An increase in plasma membrane permeability, detected by 51Cr release, was observed within 15 min of exposure to 193-nm radiation, whereas exposure to 254-nm radiation did not cause this immediate release of 51Cr. In control experiments, the mitochondrial poison, carbonyl cyanide m-chlorophenyl hydrazone, did not cause 51Cr release in the dark, indicating that the 193-nm radiation-induced increase in plasma membrane permeability was not subsequent to loss of mitochondrial function. [3H]-Arachidonic acid was released from C4H10T1/2 cells using low 193-nm fluences, whereas release of [3H]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 2 .times. 104 J/m2 of 193-nm radiation. These results indicate that 193-nm radiation produces primary damage on the level of the plasma membrane.