FIELD: medicine. SUBSTANCE: method involves determining the number of T-lymphocyte mutant with respect to hypoxanthine-guanine phosphoribozyltransferase in cell culture in the presence of 6-thioguanine. Hypoxanthine-guanine phosphoribozyltransferase deficiency is developed as a result of gene mutation. Point mutations or small deletions manifest themselves in the long X-chromosome arm. Microclones of T-lymphocytes deficient with respect to hypoxanthine-guanine phosphoribozyltransferase are detected. Mutant cells only remain living under such conditions. The normal cells with respect to hypoxanthine- guanine phosphoribozyltransferase contain toxic analog of guanine and die. The number of mutant cells being 1.5-5 times higher when compared to control, high risk of ecological nephropathy is to be predicted. EFFECT: enhanced effectiveness in protecting children against risk of nephropathy in regions contaminated with heavy metals. 1 tbl
Authors
Dates
2000-12-10—Published
1999-09-14—Filed