Skip to main content
SpringerLink
Log in

Does Oxidative Stress Limit Mouse Life Span?

  • Chapter
Oxidative Stress in Aging

Part of the book series: Aging Medicine ((AGME))

  • 1313 Accesses

Summary

The free radical theory of aging, in its strongest form, holds that oxidative stress is the determinant of animal life span. However, evolutionary studies suggest that it is highly unlikely that life span is determined by a single biochemical process. Rather, one can restate the free radical radical theory in a more modest form, i.e., that oxidative stress is one of several biochemical processes that limit life span. An obvious prediction of this hypothesis is that knocking out antioxidant genes should result in shortened life span (assuming that knocking-out these genes in fact result in increased oxidative stress). In the best-case scenario, one would expect a segmental progeroid syndrome. In this chapter, I summarize recent studies examining the life span, pathology, and oxidative stress status of antioxidant and oxidative damage repair knockout mice (Sod1, Sod2, Sod3, Gpx1, Prdx1, Prdx2, and MsrA). Data from these studies indicate that whether or not oxidative stress is limiting to life span depends on what markers of oxidative stress are assayed. Specifically, the DNA damage product, 8-oxodeoxyguanosine (8-oxo-dG), is elevated in several antioxidant knockout mice that show no life span reduction. Whether elevations in 8-oxo-dG genuinely represent increased in situ oxidative DNA damage or arise during sample preparation is debatable. Other markers that suffer from minimal isolation artifacts, such as F2-isoprostanes, are only elevated in antioxidant knockout mice that actually have a shortened life span (the Sod1 −/− to be precise). I suggest that measuring the expression of genes responsive to oxidative damage circumvents the issue of isolation artifacts that one way or another affects all biochemical assays of oxidative damage. By these criteria, Sod1 −/− but not Gpx1 −/−, Sod2 +/−, or Gpx4 +/−, mice show an elevation in oxidative stress. If one takes as reference the standard set by DNA repair deficient mice, a strong case can be made that Sod1 −/−, exhibit “accelerated aging.” Thus, I conclude that the present data do not disprove the hypothesis that oxidative stress is limiting to life span in mice.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Log in via an institution
Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 89.00
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 119.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 169.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

References

  1. Beckman KB, Ames BN. The free radical theory of aging matures. Physiol Rev 1998;78(2):547–81.

    PubMed  CAS  Google Scholar 

  2. Austad SN. Is aging programed? Aging Cell 2004;3(5):249–51.

    PubMed  CAS  Google Scholar 

  3. Martin GM, Austad SN, Johnson TE. Genetic analysis of ageing: role of oxidative damage and environmental stresses. Nat Genet 1996;13(1):25–34.

    PubMed  CAS  Google Scholar 

  4. Shmookler Reis RJ. Model systems for aging research: syncretic concepts and diversity of mechanisms. Genome 1989;31(1):406–12.

    PubMed  CAS  Google Scholar 

  5. Rudolph KL, Chang S, Lee HW et al. Longevity, stress response, and cancer in aging telomerase-deficient mice. Cell 1999;96(5):701–12.

    PubMed  CAS  Google Scholar 

  6. Lee HW, Blasco MA, Gottlieb GJ, Horner JW 2nd, Greider CW, DePinho RA. Essential role of mouse telomerase in highly proliferative organs. Nature 1998;392(6676):569–74.

    PubMed  CAS  Google Scholar 

  7. Blasco MA, Lee HW, Hande MP et al. Telomere shortening and tumor formation by mouse cells lacking telomerase RNA. Cell 1997;91(1):25–34.

    PubMed  CAS  Google Scholar 

  8. Vermulst M, Bielas JH, Kujoth GC et al. Mitochondrial point mutations do not limit the natural lifespan of mice. Nat Genet 2007;39(4):540–3.

    PubMed  CAS  Google Scholar 

  9. Peters LL, Robledo RF, Bult CJ, Churchill GA, Paigen BJ, Svenson KL. The mouse as a model for human biology: a resource guide for complex trait analysis. Nat Rev Genet 2007;8(1):58–69.

    PubMed  CAS  Google Scholar 

  10. Beck MA, Esworthy RS, Ho YS, Chu FF. Glutathione peroxidase protects mice from viralinduced myocarditis. FASEB J 1998;12(12):1143–9.

    PubMed  CAS  Google Scholar 

  11. Mewissen DJ, Rust JH, Haren J, Cluten MJ. [Epidemiology of C57 black/6M mouse strain: statistical findings in a control population]. C R Seances Soc Biol Fil 1977;171(5):1140–4.

    PubMed  CAS  Google Scholar 

  12. Kunstyr I, Leuenberger HG. Gerontological data of C57BL/6J mice. I. Sex differences in survival curves. J Gerontol 1975;30(2):157–62.

    PubMed  CAS  Google Scholar 

  13. Storer JB. Longevity and gross pathology at death in 22 inbred mouse strains. J Gerontol 1966;21(3):404–9.

    PubMed  CAS  Google Scholar 

  14. Festing MF, Blackmore DK. Lifespan of specified-pathogen-free (MRC category 4) mice and rats. Lab Anim 1971;5(2):179–92.

    PubMed  CAS  Google Scholar 

  15. Capecchi MR. Gene targeting in mice: functional analysis of the mammalian genome for the twenty-first century. Nat Rev Genet 2005;6(6):507–12.

    PubMed  CAS  Google Scholar 

  16. Jakupoglu C, Przemeck GK, Schneider M et al. Cytoplasmic thioredoxin reductase is essential for embryogenesis but dispensable for cardiac development. Mol Cell Biol 2005;25(5):1980–8.

    PubMed  CAS  Google Scholar 

  17. Conrad M, Jakupoglu C, Moreno SG et al. Essential role for mitochondrial thioredoxin reductase in hematopoiesis, heart development, and heart function. Mol Cell Biol 2004;24(21):9414–23.

    PubMed  CAS  Google Scholar 

  18. Shi ZZ, Osei-Frimpong J, Kala G et al. Glutathione synthesis is essential for mouse development but not for cell growth in culture. Proc Natl Acad Sci U S A 2000;97(10):5101–6.

    PubMed  CAS  Google Scholar 

  19. Fridovich I. Fundamental aspects of reactive oxygen species, or what's the matter with oxygen? Ann N Y Acad Sci 1999;893:13–8.

    PubMed  CAS  Google Scholar 

  20. Okado-Matsumoto A, Fridovich I. Subcellular distribution of superoxide dismutases (sod) in rat liver. Cu,Zn-sod in mitochondria. J Biol Chem 2001;276(42):38388–93.

    PubMed  CAS  Google Scholar 

  21. Sturtz LA, Diekert K, Jensen LT, Lill R, Culotta VC. A fraction of yeast Cu,Zn-superoxide dismutase and its metallochaperone, ccs, localize to the intermembrane space of mitochondria. A physiological role for sod1 in guarding against mitochondrial oxidative damage. J Biol Chem 2001;276(41):38084–9.

    CAS  Google Scholar 

  22. Muller F. The nature and mechanism of superoxide production by the electron transport chain: its relevance to aging. J Am Aging Assoc 2000;23:227–53.

    CAS  Google Scholar 

  23. Han D, Williams E, Cadenas E. Mitochondrial respiratory chain-dependent generation of super-oxide anion and its release into the intermembrane space. Biochem J 2001;353(2):411–6.

    PubMed  CAS  Google Scholar 

  24. Muller FL, Liu Y, Van Remmen H. Complex III Releases superoxide to both sides of the inner mitochondrial membrane. J Biol Chem 2004;279(47):49064–73.

    PubMed  CAS  Google Scholar 

  25. Reaume AG, Elliott JL, Hoffman EK et al. Motor neurons in Cu/Zn superoxide dismutase-deficient mice develop normally but exhibit enhanced cell death after axonal injury. Nat Genet 1996;13(1):43–7.

    PubMed  CAS  Google Scholar 

  26. Muller FL, Lustgarten MS, Jang Y, Richardson A, Van Remmen H. Trends in oxidative aging theories. Free Radic Biol Med 2007;43(4):477–503.

    PubMed  CAS  Google Scholar 

  27. Muller FL, Song W, Liu Y et al. Absence of CuZn superoxide dismutase leads to elevated oxidative stress and acceleration of age-dependent skeletal muscle atrophy. Free Radic Biol Med 2006;40(11):1993–2004.

    PubMed  CAS  Google Scholar 

  28. Elchuri S, Oberley TD, Qi W et al. CuZnSOD deficiency leads to persistent and widespread oxidative damage and hepatocarcinogenesis later in life. Oncogene 2005;24(3):367–80.

    PubMed  CAS  Google Scholar 

  29. Kessova IG, Ho YS, Thung S, Cederbaum AI. Alcohol-induced liver injury in mice lacking Cu, Zn-superoxide dismutase. Hepatology 2003;38(5):1136–45.

    PubMed  CAS  Google Scholar 

  30. Reddy VN, Kasahara E, Hiraoka M, Lin LR, Ho YS. Effects of variation in superoxide dismutases (SOD) on oxidative stress and apoptosis in lens epithelium. Exp Eye Res 2004;79(6):859–68.

    PubMed  CAS  Google Scholar 

  31. Busuttil RA, Garcia AM, Cabrera C et al. Organ-specific increase in mutation accumulation and apoptosis rate in CuZn-superoxide dismutase-deficient mice. Cancer Res 2005;65(24):11271–5.

    PubMed  CAS  Google Scholar 

  32. Keithley EM, Canto C, Zheng QY, Wang X, Fischel-Ghodsian N, Johnson KR. Cu/Zn super-oxide dismutase and age-related hearing loss. Hear Res 2005;209(1–2):76–85.

    PubMed  CAS  Google Scholar 

  33. Kostrominova TY, Pasyk KA, Van Remmen H, Richardson AG, Faulkner JA. Adaptive changes in structure of skeletal muscles from adult Sod1 homozygous knockout mice. Cell Tissue Res 2006.

    Google Scholar 

  34. Hadjur S, Ung K, Wadsworth L et al. Defective hematopoiesis and hepatic steatosis in mice with combined deficiencies of the genes encoding Fancc and Cu/Zn superoxide dismutase. Blood 2001;98(4):1003–11.

    PubMed  CAS  Google Scholar 

  35. Matzuk MM, Dionne L, Guo Q, Kumar TR, Lebovitz RM. Ovarian function in superoxide dismutase 1 and 2 knockout mice. Endocrinology 1998;139(9):4008–11.

    PubMed  CAS  Google Scholar 

  36. Ho YS, Gargano M, Cao J, Bronson RT, Heimler I, Hutz RJ. Reduced fertility in female mice lacking copper-zinc superoxide dismutase. J Biol Chem 1998;273(13):7765–9.

    PubMed  CAS  Google Scholar 

  37. Martin GM. Genetics and aging; the Werner syndrome as a segmental progeroid syndrome. Adv Exp Med Biol 1985;190:161–70.

    PubMed  CAS  Google Scholar 

  38. Martin GM. Syndromes of accelerated aging. Natl Cancer Inst Monogr 1982;60:241–7.

    PubMed  CAS  Google Scholar 

  39. Hasty P, Vijg J. Accelerating aging by mouse reverse genetics: a rational approach to understanding longevity. Aging Cell 2004;3(2):55–65.

    PubMed  CAS  Google Scholar 

  40. Hasty P, Campisi J, Hoeijmakers J, van Steeg H, Vijg J. Aging and genome maintenance: lessons from the mouse? Science 2003;299(5611):1355–9.

    PubMed  CAS  Google Scholar 

  41. McFadden SL, Ding D, Reaume AG, Flood DG, Salvi RJ. Age-related cochlear hair cell loss is enhanced in mice lacking copper/zinc superoxide dismutase. Neurobiol Aging 1999;20(1):1–8.

    PubMed  CAS  Google Scholar 

  42. McFadden SL, Ding D, Burkard RF et al. Cu/Zn SOD deficiency potentiates hearing loss and cochlear pathology in aged 129,CD-1 mice. J Comp Neurol 1999;413(1):101–12.

    PubMed  CAS  Google Scholar 

  43. Ohlemiller KK, McFadden SL, Ding DL et al. Targeted deletion of the cytosolic Cu/Zn-superoxide dismutase gene (Sod1) increases susceptibility to noise-induced hearing loss. Audiol Neurootol 1999;4(5):237–46.

    PubMed  CAS  Google Scholar 

  44. Imamura Y, Noda S, Hashizume K et al. Drusen, choroidal neovascularization, and retinal pigment epithelium dysfunction in SOD1-deficient mice: a model of age-related macular degeneration. Proc Natl Acad Sci U S A 2006;103(30):11282–7.

    PubMed  CAS  Google Scholar 

  45. Flood DG, Reaume AG, Gruner JA et al. Hindlimb motor neurons require Cu/Zn superoxide dismutase for maintenance of neuromuscular junctions. Am J Pathol 1999;155(2):663–72.

    PubMed  CAS  Google Scholar 

  46. Shefner JM, Reaume AG, Flood DG et al. Mice lacking cytosolic copper/zinc superoxide dismutase display a distinctive motor axonopathy. Neurology 1999;53(6):1239–46.

    PubMed  CAS  Google Scholar 

  47. Muller FL, Song W, Jang Y et al. Denervation-Induced skeletal muscle atrophy is associated with increased mitochondrial ROS production. Am J Physiol 2007; 293: R1159–1168.

    CAS  Google Scholar 

  48. Iuchi Y, Okada F, Onuma K et al. Elevated oxidative stress in erythrocytes due to a SOD1 deficiency causes anaemia and triggers autoantibody production. Biochem J 2007;402(2):219–27.

    PubMed  CAS  Google Scholar 

  49. Mitchell WA, Meng I, Nicholson SA, Aspinall R. Thymic output, ageing and zinc. Biogerontology 2006;7(5–6):461–70.

    PubMed  CAS  Google Scholar 

  50. Miller RA. “Accelerated aging”: a primrose path to insight? Aging Cell 2004;3(2):47–51.

    PubMed  CAS  Google Scholar 

  51. Cabiscol E, Levine RL. Carbonic anhydrase III. Oxidative modification in vivo and loss of phosphatase activity during aging. J Biol Chem 1995;270(24):14742–7.

    PubMed  CAS  Google Scholar 

  52. Huang TT, Carlson EJ, Kozy HM et al. Genetic modification of prenatal lethality and dilated cardiomyopathy in Mn superoxide dismutase mutant mice. Free Radic Biol Med 2001;31(9):1101–10.

    PubMed  CAS  Google Scholar 

  53. Li Y, Huang TT, Carlson EJ et al. Dilated cardiomyopathy and neonatal lethality in mutant mice lacking manganese superoxide dismutase. Nat Genet 1995;11(4):376–81.

    PubMed  CAS  Google Scholar 

  54. Lebovitz RM, Zhang H, Vogel H et al. Neurodegeneration, myocardial injury, and perinatal death in mitochondrial superoxide dismutase-deficient mice. Proc Natl Acad Sci USA 1996;93(18):9782–7.

    PubMed  CAS  Google Scholar 

  55. Melov S, Coskun P, Patel M et al. Mitochondrial disease in superoxide dismutase 2 mutant mice. Proc Natl Acad Sci U S A 1999;96(3):846–51.

    PubMed  CAS  Google Scholar 

  56. Williams MD, Van Remmen H, Conrad CC, Huang TT, Epstein CJ, Richardson A. Increased oxidative damage is correlated to altered mitochondrial function in heterozygous manganese superoxide dismutase knockout mice. J Biol Chem 1998;273(43):28510–5.

    PubMed  CAS  Google Scholar 

  57. Van Remmen H, Salvador C, Yang H, Huang TT, Epstein CJ, Richardson A. Characterization of the antioxidant status of the heterozygous manganese superoxide dismutase knockout mouse. Arch Biochem Biophys 1999;363(1):91–7.

    PubMed  Google Scholar 

  58. Van Remmen H, Williams MD, Guo Z et al. Knockout mice heterozygous for Sod2 show alterations in cardiac mitochondrial function and apoptosis. Am J Physiol 2001;281(3): H1422–32.

    Google Scholar 

  59. Van Remmen H, Ikeno Y, Hamilton M et al. Life-long reduction in MnSOD activity results in increased DNA damage and higher incidence of cancer but does not accelerate aging. Physiol Genomics 2003;16(1):29–37.

    PubMed  Google Scholar 

  60. Lynn S, Van Remmen H, Epstein CJ, Huang TT. Investigation of mitochondrial DNA deletions in post-mitotic tissues of the heterozygous superoxide dismutase 2 knockout mouse: effect of ageing and genotype on the tissue-specific accumulation. Free Radic Biol Med 2001;31:S58–S.

    Google Scholar 

  61. Stadtman ER, Van Remmen H, Richardson A, Wehr NB, Levine RL. Methionine oxidation and aging. Biochim Biophys Acta 2005;1703(2):135–40.

    PubMed  CAS  Google Scholar 

  62. Kadiiska MB, Gladen BC, Baird DD et al. Biomarkers of oxidative stress study III. Effects of the nonsteroidal anti-inflammatory agents indomethacin and meclofenamic acid on measurements of oxidative products of lipids in CCl4 poisoning. Free Radic Biol Med 2005;38(6):711–8.

    PubMed  CAS  Google Scholar 

  63. Kadiiska MB, Gladen BC, Baird DD et al. Biomarkers of oxidative stress study II: are oxidation products of lipids, proteins, and DNA markers of CCl4 poisoning? Free Radic Biol Med 2005;38(6):698–710.

    PubMed  CAS  Google Scholar 

  64. Chan SH, Higgins E Jr. Uncoupling activity of endogenous free fatty acids in rat liver mitochondria. Can J Biochem 1978;56(2):111–6.

    PubMed  CAS  Google Scholar 

  65. Brewer GJ, Jones TT, Wallimann T, Schlattner U. Higher respiratory rates and improved creatine stimulation in brain mitochondria isolated with anti-oxidants. Mitochondrion 2004;4(1):49–57.

    PubMed  CAS  Google Scholar 

  66. Edwards MG, Sarkar D, Klopp R, Morrow JD, Weindruch R, Prolla TA. Age-related impairment of the transcriptional responses to oxidative stress in the mouse heart. Physiol Genomics 2003;13(2):119–27.

    PubMed  CAS  Google Scholar 

  67. Edwards MG, Anderson RM, Yuan M, Kendziorski CM, Weindruch R, Prolla TA. Gene expression profiling of aging reveals activation of a p53-mediated transcriptional program. BMC Genomics 2007;8:80.

    PubMed  Google Scholar 

  68. Asimakis GK, Lick S, Patterson C. Postischemic recovery of contractile function is impaired in SOD2 but not SOD1 mouse hearts. Circulation 2002;105(8):981–6.

    PubMed  CAS  Google Scholar 

  69. Andreassen OA, Ferrante RJ, Klivenyi P et al. Partial deficiency of manganese superoxide dismutase exacerbates a transgenic mouse model of amyotrophic lateral sclerosis. Ann Neurol 2000;47(4):447–55.

    PubMed  CAS  Google Scholar 

  70. Murakami K, Kondo T, Kawase M et al. Mitochondrial susceptibility to oxidative stress exacerbates cerebral infarction that follows permanent focal cerebral ischemia in mutant mice with manganese superoxide dismutase deficiency. J Neurosci 1998;18(1):205–13.

    PubMed  CAS  Google Scholar 

  71. Lewen A, Matz P, Chan PH. Free radical pathways in CNS injury. J Neurotrauma 2000;17(10):871–90.

    PubMed  CAS  Google Scholar 

  72. Kim GW, Kondo T, Noshita N, Chan PH. Manganese superoxide dismutase deficiency exacerbates cerebral infarction after focal cerebral ischemia/reperfusion in mice: implications for the production and role of superoxide radicals. Stroke 2002;33(3):809–15.

    PubMed  CAS  Google Scholar 

  73. Marklund SL. Human copper-containing superoxide dismutase of high molecular weight. Proc Natl Acad Sci U S A 1982;79(24):7634–8.

    PubMed  CAS  Google Scholar 

  74. Carlsson LM, Jonsson J, Edlund T, Marklund SL. Mice lacking extracellular superoxide dismutase are more sensitive to hyperoxia. Proc Natl Acad Sci U S A 1995;92(14):6264–8.

    PubMed  CAS  Google Scholar 

  75. Sentman ML, Granstrom M, Jakobson H, Reaume A, Basu S, Marklund SL. Phenotypes of mice lacking extracellular superoxide dismutase and copper- and zinc-containing superoxide dismutase. J Biol Chem 2006;281(11):6904–9.

    PubMed  CAS  Google Scholar 

  76. Halliwell B, Gutteridge J. Free radicals in biology and medicine. Third ed. New York: Oxford University Press; 1999.

    Google Scholar 

  77. Ho YS, Magnenat JL, Bronson RT et al. Mice deficient in cellular glutathione peroxidase develop normally and show no increased sensitivity to hyperoxia. J Biol Chem 1997;272(26):16644–51.

    PubMed  CAS  Google Scholar 

  78. Wolf N, Penn P, Pendergrass W et al. Age-related cataract progression in five mouse models for anti-oxidant protection or hormonal influence. Exp Eye Res 2005;81(3):276–85.

    PubMed  CAS  Google Scholar 

  79. Reddy VN, Giblin FJ, Lin LR et al. Glutathione peroxidase-1 deficiency leads to increased nuclear light scattering, membrane damage, and cataract formation in gene-knockout mice. Invest Ophthalmol Vis Sci 2001;42(13):3247–55.

    PubMed  CAS  Google Scholar 

  80. Esposito LA, Kokoszka JE, Waymire KG, Cottrell B, MacGregor GR, Wallace DC. Mitochondrial oxidative stress in mice lacking the glutathione peroxidase-1 gene. Free Radic Biol Med 2000;28(5):754–66.

    PubMed  CAS  Google Scholar 

  81. Van Remmen H, Qi W, Sabia M et al. Multiple deficiencies in antioxidant enzymes in mice result in a compound increase in sensitivity to oxidative stress. Free Radic Biol Med 2004;36(12):1625–34.

    PubMed  Google Scholar 

  82. Low FM, Hampton MB, Peskin AV, Winterbourn CC. Peroxiredoxin 2 functions as a non-catalytic scavenger of low level hydrogen peroxide in the erythrocyte. Blood 2006.

    Google Scholar 

  83. Chae HZ, Kim IH, Kim K, Rhee SG. Cloning, sequencing, and mutation of thiol-specific antioxidant gene of Saccharomyces cerevisiae. J Biol Chem 1993;268(22):16815–21.

    PubMed  CAS  Google Scholar 

  84. Wood ZA, Schroder E, Robin Harris J, Poole LB. Structure, mechanism and regulation of peroxiredoxins. Trends Biochem Sci 2003;28(1):32–40.

    PubMed  CAS  Google Scholar 

  85. Dubuisson M, Vander Stricht D, Clippe A et al. Human peroxiredoxin 5 is a peroxynitrite reductase. FEBS Lett 2004;571(1–3):161–5.

    PubMed  CAS  Google Scholar 

  86. Smith S, Hwang JY, Banerjee S, Majeed A, Gupta A, Myung K. Mutator genes for suppression of gross chromosomal rearrangements identified by a genome-wide screening in Saccharomyces cerevisiae. Proc Natl Acad Sci U S A 2004;101(24):9039–44.

    PubMed  CAS  Google Scholar 

  87. Huang ME, Kolodner RD. A biological network in Saccharomyces cerevisiae prevents the deleterious effects of endogenous oxidative DNA damage. Mol Cell 2005;17(5):709–20.

    PubMed  CAS  Google Scholar 

  88. Ragu S, Faye G, Iraqui I, Masurel-Heneman A, Kolodner RD, Huang ME. Oxygen metabolism and reactive oxygen species cause chromosomal rearrangements and cell death. Proc Natl Acad Sci U S A 2007;104(23):9747–52.

    PubMed  CAS  Google Scholar 

  89. Inoue Y, Matsuda T, Sugiyama K, Izawa S, Kimura A. Genetic analysis of glutathione peroxidase in oxidative stress response of Saccharomyces cerevisiae. J Biol Chem 1999;274(38):27002–9.

    PubMed  CAS  Google Scholar 

  90. Wang X, Phelan SA, Forsman-Semb K et al. Mice with targeted mutation of per-oxiredoxin 6 develop normally but are susceptible to oxidative stress. J Biol Chem 2003;278(27):25179–90.

    PubMed  CAS  Google Scholar 

  91. Lee TH, Kim SU, Yu SL et al. Peroxiredoxin II is essential for sustaining lifespan of erythrocytes in mice. Blood 2003;101(12):5033–8.

    PubMed  CAS  Google Scholar 

  92. Neumann CA, Krause DS, Carman CV et al. Essential role for the peroxiredoxin Prdx1 in erythrocyte antioxidant defence and tumour suppression. Nature 2003;424(6948):561–5.

    PubMed  CAS  Google Scholar 

  93. Egler RA, Fernandes E, Rothermund K et al. Regulation of reactive oxygen species, DNA damage, and c-Myc function by peroxiredoxin 1. Oncogene 2005;24(54):8038–50.

    PubMed  CAS  Google Scholar 

  94. Han YH, Kim HS, Kim JM, Kim SK, Yu DY, Moon EY. Inhibitory role of peroxiredoxin II (Prx II) on cellular senescence. FEBS Lett 2005;579(21):4897–902.

    PubMed  CAS  Google Scholar 

  95. Hansel A, Kuschel L, Hehl S et al. Mitochondrial targeting of the human peptide methionine sulfoxide reductase (MSRA), an enzyme involved in the repair of oxidized proteins. FASEB J 2002;16(8):911–3.

    PubMed  CAS  Google Scholar 

  96. Kim HY, Gladyshev VN. Methionine sulfoxide reduction in mammals: characterization of methionine-R-sulfoxide reductases. Mol Biol Cell 2004;15(3):1055–64.

    PubMed  CAS  Google Scholar 

  97. Ruan H, Tang XD, Chen ML et al. High-quality life extension by the enzyme peptide methionine sulfoxide reductase. Proc Natl Acad Sci U S A 2002;99(5):2748–53.

    PubMed  CAS  Google Scholar 

  98. Koc A, Gasch AP, Rutherford JC, Kim HY, Gladyshev VN. Methionine sulfoxide reductase regulation of yeast lifespan reveals reactive oxygen species-dependent and —independent components of aging. Proc Natl Acad Sci U S A 2004;101(21):7999–8004.

    PubMed  CAS  Google Scholar 

  99. Moskovitz J, Bar-Noy S, Williams WM, Requena J, Berlett BS, Stadtman ER. Methionine sulfoxide reductase (MsrA) is a regulator of antioxidant defense and lifespan in mammals. Proc Natl Acad Sci U S A 2001;98(23):12920–5.

    PubMed  CAS  Google Scholar 

  100. Klungland A, Rosewell I, Hollenbach S et al. Accumulation of premutagenic DNA lesions in mice defective in removal of oxidative base damage. Proc Natl Acad Sci USA 1999;96(23):13300–5.

    PubMed  CAS  Google Scholar 

  101. Osterod M, Hollenbach S, Hengstler JG, Barnes DE, Lindahl T, Epe B. Age-related and tissue-specific accumulation of oxidative DNA base damage in 7,8-dihydro-8-oxoguanine-DNA glycosylase (Ogg1) deficient mice. Carcinogenesis 2001;22(9):1459–63.

    PubMed  CAS  Google Scholar 

  102. Minowa O, Arai T, Hirano M et al. Mmh/Ogg1 gene inactivation results in accumulation of 8-hydroxyguanine in mice. Proc Natl Acad Sci U S A 2000;97(8):4156–61.

    PubMed  CAS  Google Scholar 

  103. de Souza-Pinto NC, Eide L, Hogue BA et al. Repair of 8-oxodeoxyguanosine lesions in mitochondrial DNA depends on the oxoguanine DNA glycosylase (OGG1) gene and 8-oxo-guanine accumulates in the mitochondrial DNA of OGG1-defective mice. Cancer Res 2001;61(14):5378–81.

    PubMed  Google Scholar 

  104. Trapp C, McCullough AK, Epe B. The basal levels of 8-oxoG and other oxidative modifications in intact mitochondrial DNA are low even in repair-deficient (Ogg1−/−/Csb−/−) mice. Mutat Res 2007.

    Google Scholar 

  105. Osterod M, Larsen E, Le Page F et al. A global DNA repair mechanism involving the Cockayne syndrome B (CSB) gene product can prevent the in vivo accumulation of endogenous oxidative DNA base damage. Oncogene 2002;21(54):8232–9.

    PubMed  CAS  Google Scholar 

  106. Stevnsner T, Nyaga S, de Souza-Pinto NC et al. Mitochondrial repair of 8-oxoguanine is deficient in Cockayne syndrome group B. Oncogene 2002;21(57):8675–82.

    PubMed  CAS  Google Scholar 

  107. Riis B. Comparison of results from different laboratories in measuring 8-oxo-2~-deoxygua-nosine in synthetic oligonucleotides. Free Radic Res 2002;36(6):649–59.

    PubMed  CAS  Google Scholar 

  108. Collins AR, Cadet J, Moller L, Poulsen HE, Vina J. Are we sure we know how to measure 8-oxo-7,8-dihydroguanine in DNA from human cells? Arch Biochem Biophys 2004;423(1):57–65.

    PubMed  CAS  Google Scholar 

  109. Russo MT, De Luca G, Degan P et al. Accumulation of the oxidative base lesion 8-hydroxy-guanine in DNA of tumor-prone mice defective in both the Myh and Ogg1 DNA glycosy-lases. Cancer Res 2004;64(13):4411–4.

    PubMed  CAS  Google Scholar 

  110. Xie Y, Yang H, Cunanan C et al. Deficiencies in mouse Myh and Ogg1 result in tumor predisposition and G to T mutations in codon 12 of the K-ras oncogene in lung tumors. Cancer Res 2004;64(9):3096–102.

    PubMed  CAS  Google Scholar 

  111. Esworthy RS, Aranda R, Martin MG, Doroshow JH, Binder SW, Chu FF. Mice with combined disruption of Gpx1 and Gpx2 genes have colitis. Am J Physiol Gastrointest Liver Physiol 2001;281(3):G848–55.

    PubMed  CAS  Google Scholar 

  112. Desaint S, Luriau S, Aude JC, Rousselet G, Toledano MB. Mammalian antioxidant defenses are not inducible by H2O2. J Biol Chem 2004;279(30):31157–63.

    PubMed  CAS  Google Scholar 

  113. Zyracka E, Zadrag R, Koziol S, Krzepilko A, Bartosz G, Bilinski T. Yeast as a biosensor for antioxidants: simple growth tests employing a Saccharomyces cerevisiae mutant defective in superoxide dismutase. Acta Biochim Pol 2005;52(3):679–84.

    PubMed  CAS  Google Scholar 

  114. Tamai KT, Gralla EB, Ellerby LM, Valentine JS, Thiele DJ. Yeast and mammalian metal-lothioneins functionally substitute for yeast copper-zinc superoxide dismutase. Proc Natl Acad Sci U S A 1993;90(17):8013–7.

    PubMed  CAS  Google Scholar 

  115. Lynn S, Huang EJ, Elchuri S et al. Selective neuronal vulnerability and inadequate stress response in superoxide dismutase mutant mice. Free Radic Biol Med 2005;38(6):817–28.

    PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, San Antonio, TX

    Florian L. Muller

Authors
  1. Florian L. Muller
    View author publications

    You can also search for this author in PubMed Google Scholar

Editor information

Editors and Affiliations

  1. Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, UK

    Satomi Miwa PhD

  2. Functional Genomics Core, Children's Hospital Oakland Research Institute, Oakland, CA, USA

    Kenneth B. Beckman PhD

  3. Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA

    Florian L. Muller PhD

Rights and permissions

Reprints and permissions

Copyright information

© 2008 Humana Press, a part of Springer Science + Business Media, LLC

About this chapter

Cite this chapter

Muller, F.L. (2008). Does Oxidative Stress Limit Mouse Life Span?. In: Miwa, S., Beckman, K.B., Muller, F.L. (eds) Oxidative Stress in Aging. Aging Medicine. Humana Press. https://doi.org/10.1007/978-1-59745-420-9_8

Download citation

  • DOI: https://doi.org/10.1007/978-1-59745-420-9_8

  • Publisher Name: Humana Press

  • Print ISBN: 978-1-58829-991-8

  • Online ISBN: 978-1-59745-420-9

  • eBook Packages: MedicineMedicine (R0)

Publish with us

Policies and ethics

Search

Navigation