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[Cancer Research 47, 410-413, January 15, 1987]
© 1987 American Association for Cancer Research

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Cytotoxicity and Mutagenicity of Low Intensity, 248 and 193 nm Excimer Laser Radiation in Mammalian Cells1

Howard Green, James Boll, John A. Parrish, Irene E. Kochevar and Allan R. Oseroff2

Department of Dermatology, Harvard Medical School, Massachusetts General Hospital, Boston, Massachusetts 02114

The cytotoxicity of 193 and 248 nm excimer laser radiation was compared to that produced by a germicidal lamp (predominantly 254 nm) using Chinese hamster ovary cells (CHO), and a human diploid fibroblast line, AG-1522A. Excimer laser radiation at 248 nm (3.5 x 102 w/m2) and germicidal radiation (5.3 x 10-5 w/m2) caused toxicity in both cell lines, with the AG-1522A cells (D37 = 7-8 J/m2) being slightly more sensitive than the CHO cells (D37 = 11 J/m2). Incident 193 nm radiation was less cytotoxic than 248 nm to AG-1522A and CHO cells with D37 values of 18 and 85 J/m2, respectively. The mutagenic potential of UV excimer radiation at 193 and 248 nm was evaluated using the hypoxanthine guanine phosphoribosyl transfer assay system with CHO cells. Excimer laser radiation at 248 nm induced mutation in proportion to dose (1.7 x 10-5 resistant colonies per survivor per J/m2 incident radiation) up to 14 J/m2, similar to results reported for 254 nm light. However, excimer laser radiation at 193 nm did not cause mutation greater than the dark control. The decreased cytotoxicity and mutagenicity of 193 nm radiation may be due to the shielding of the nucleus by cytoplasmic and membrane components or to the formation of different DNA photoproducts. These differences between 193 and 248 nm radiation may be important in choosing an excimer wavelength for ablation in biological systems.

1 This work was supported in part by a grant from the Arthur O. and Gullan M. Wellman Medical Foundation and NIH Grant AM 35092-08.

2 Present address: Department of Dermatology, New England Medical Center, Boston, MA 02111. To whom requests for reprints should be addressed.

Received 2/ 4/86. Revised 9/ 2/86. Accepted 10/14/86.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1987 by the American Association for Cancer Research.