PMID: 9651539Jul 4, 1998Paper

Random population-wide genetic damage induced in replicating cells treated with methotrexate

Mutation Research
M ChowH Rubin

Abstract

Low lethality treatment of the NIH 3T3 mouse cell line with methotrexate (MTX) during exponential multiplication results in heterogeneous, heritable reduction in growth rate of most if not all the replicatively surviving cells. The effective concentrations of MTX are 10 to 100 times higher in molecular, cellular and developmental biology medium 402 (MCDB 402) than in Dulbecco's modification of Eagle's medium (DMEM) medium because of the folate-sparing presence of adenine, thymidine and, particularly, of folinic acid in MCDB 402 medium. The reduced growth rates are detectable during early passages of surviving populations before the faster growing cells dominate them. The heritable effect is most clearly demonstrated by sequestered cloning of many individual cells immediately after drug treatment, and repeatedly measuring the growth rates of the clones in serial passages. After 7-10 passages of the clones, there is an increase in growth rate of some of the slow growing clones presumably due to the generation and selection of faster growing cells. Evidence from mutagenic studies at a single genetic locus in other cell lines suggests that heritable reductions in growth rate arise from chromosome aberrations although point mutation...Continue Reading

References

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Dec 1, 1990·Proceedings of the National Academy of Sciences of the United States of America·A L RubinH Rubin
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May 23, 1995·Proceedings of the National Academy of Sciences of the United States of America·H RubinM Chow
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Aug 5, 1997·Proceedings of the National Academy of Sciences of the United States of America·M Chow, H Rubin

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Citations

Nov 28, 2012·Cytotechnology·Erman Salih Istifli, Mehmet Topaktaş
Aug 26, 1999·In Vitro Cellular & Developmental Biology. Animal·M Chow, H Rubin
Feb 25, 2014·European Journal of Pharmacology·Hayder Gaeed Oufi, Nada Naji Al-Shawi
Jun 9, 1999·Proceedings of the National Academy of Sciences of the United States of America·M Chow, H Rubin

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