Download Advances in Mutagenesis Research by Günter Obe, H.H. Evans, D. Frankenberg, M. PDF

By Günter Obe, H.H. Evans, D. Frankenberg, M. Frankenberg-Schwager, E. Gebhart, W. Köhnlein, R.H. Nussbaum, D.G. Papworth, J.R.K. Savage, R.-D. Wegner

ISBN-10: 3642762344

ISBN-13: 9783642762345

Applied genetic learn, genetic toxicology and mutation study examine the mutagenicity and cancerogenicity of chemical compounds and different brokers. everlasting mutation in genes and chromosomes, could be brought on by way of a plethora of brokers, together with ionizing and nonionizing radiations, chemical substances, and viruses. one of the points mentioned via Advances in Mutagenesis Research are (1) the certainty of the molecular mechanisms resulting in mutations, and (2) the prevention of a inconsiderate creation of mutagenic brokers into the environment.

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1990) than when the target gene is in a heterozygous region (Kronenberg and Little 1989a; Mencl et al. 1989; Geard et al. 1990) or located on a foreign and thus nonessential chromosome (He et al. 1990). 01 Fig. 8. Mutant frequencies induced at the tk locus in mouse lymphoma cells. 0-0 TK+1- heterozygous strain LY-RI6; 0-0 TK+1o hemizygous strain L Y-R83. Mutant frequency is expressed as the number of TK /- mutants per 1 X 103 surviving cells minus the spontaneous mutant frequency. Cells were exposed to radon and its progeny at Battelle Northwest Laboratories, Richland, WA (Menel et al.

Evidence for the identification of unrepaired DNA double-strand breaks as the critical lesion leading to cell death in S. cerevisiae has been presented by Frankenberg et al. (1981) who demonstrated that the oxygen enhancement ratio (OER) and RBE values for a-particles with respect to unrepaired double-strand breaks under different irradiation conditions were similar to the 'corresponding values of OER and RBE for cell killing in the double-strand break repair-deficient rad52 strain of S. cerevisiae.

PER CELL 0. 20. 40. % of Cell s 60 80 100 with Cham. Aberr. Fig. 6A,B. Relationship between cell survival and the induction of chromosomal aberrations by X-radiation and 238pu a-particles. Symbols are the same as in Fig. 5. A Mean number of chromosomal aberrations per cell; B percentage of cells containing aberrations (Nagasawa et al. 07 rings/dicentrics per cell. 005 Gy, a dose which would theoretically result in a-particle traversal of the nucleus in only 3% of the cells. The authors suggest that the induction of SCE therefore occurs by an indirect mechanism (Nagasawa et al.

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