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Department of Occupational Health, University of Hamburg, Hamburg [G. L.]; Unit of Toxicogenetics, [H. W. R., U. S., E. S., M. S., T. K.] and Center for Pulmonary Diseases and Thoracic Surgery, Grosshansdorf [D. N.], and Department of Toxicology, University of Mainz, Mainz [G. D.], Federal Republic of Germany
The activity of O6-methylguanine-DNA methyltransferase was determined in fibroblast cultures from 45 patients with lung cancer, 39 patients with cutaneous malignant melanoma, and 29 healthy controls. This enzyme is a critical parameter for the capacity to repair O6-methylguanine (O6-mGua) adducts in DNA, and a decreased activity might therefore be responsible for an enhanced susceptibility to cancer. The assay was performed with 8 x 106 fibroblasts which were homogenized and incubated with a known amount of O6-mGua containing DNA. The remaining substrate was determined fluorimetrically after high performance liquid chromatographic separation. O6-mGua repair was significantly reduced in lung cancer patients [6.64 ± 4.32 (SD) pmol O6-methylguanine repaired/8 x 106 cells as compared to healthy controls [10.35 ± 5.42, P < 0.0022] or patients with cutaneous malignant melanoma [10.83 ± 6.66]. The lowest mean values were detected in a subgroup of 16 lung cancer patients with a tumor manifestation below 46 years of age (5.06 ± 3.89). Fibroblasts from 4 patients with lung cancer had no detectable repair. We conclude that a reduced capacity to remove O6-mGua adducts may represent a further mechanism of individually enhanced lung cancer risk.
1 To whom requests for reprints should be addressed, at Universität Hamburg, Ordinariat für Arbeitsmedizin, Arbeitsgruppe Toxikogenetik, Adolph-Schönfelder-Strasse 5, 2000 Hamburg 76, Federal Republic of Germany.
2 This study is part of a thesis for a medical doctorate.
Received 12/16/88. Revised 5/15/89. Accepted 7/13/89.
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