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1 Cellular and Molecular Biology Graduate Program, University of Michigan School of Medicine, Ann Arbor, MI, USA
2 Department of Biochemistry and Molecular Biology, University of Louisville, Louisville, KY, USA
3 Departments of Internal Medicine and Physiology, Geriatrics Research, Southern Illinois University, School of Medicine, Springfield, IL, USA
4 Edison Biotechnology Institute and Department of Biomedical Sciences, Ohio University, Athens, OH, USA
5 Department of Pathology, University of Michigan School of Medicine, Ann Arbor, MI, USA
6 Cellular and Molecular Biology Graduate Program, University of Michigan School of Medicine, Ann Arbor, MI, USA; Department of Pathology, University of Michigan School of Medicine, Ann Arbor, MI, USA; Geriatrics Center and Institute of Gerontology and the Ann Arbor DVA Medical Center, University of Michigan, Ann Arbor, MI, USA
* To whom correspondence should be addressed. E-mail: asalmon{at}umich.edu.
Previous studies have shown that dermal fibroblast cell lines derived from young adult mice of the long-lived Snell dwarf mutant stock are resistant, in vitro, to the cytotoxic effects of hydrogen peroxide, cadmium, ultraviolet light, paraquat, and heat. We show here that similar resistance profiles are seen in fibroblast cells derived from a related mutant, the Ames dwarf mouse, and that cells from growth hormone receptor null mice are resistant to hydrogen peroxide, paraquat, and UV but not to cadmium. Resistance to UV, cadmium, and hydrogen peroxide are similar in cells derived from one-week old Snell dwarf or normal mice, and thus the resistance of cell lines derived from young adult donors reflects developmental processes, presumably hormone-dependent, that take place in the first few months of life. The resistance of cells from Snell dwarf mice to these stresses does not reflect merely anti-oxidant defenses: dwarf-derived cells are also resistant to the DNA-alklyating agent methyl methanesulfonate. Furthermore, inhibitor studies show that fibroblast resistance to UV light is unaffected by anti-oxidants ascorbic acid and N-acetyl-L-cysteine. These data suggest that postnatal exposure to altered levels of pituitary hormones leads to development of cellular resistance to oxidative and nonoxidative stressors which are stable through many rounds of in vitro cell division and could contribute to the remarkable disease resistance of long-lived mutant mice.
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