Effects of Dietary Restriction and Antioxidants on Presbyacusis

Objectives/Hypothesis The premise of this study is that the membrane hypothesis of aging, also known as the mitochondrial clock theory of aging, is the basis for presbyacusis. Furthermore, it is proposed that treatment with antioxidants or dietary restriction can attenuate age‐related hearing loss. Many studies have demonstrated a reduction in blood flow to specific tissues, including the cochlea, with aging. Hypoperfusion leads to the formation of reactive oxygen metabolites (ROM). ROM are highly toxic molecules that directly affect tissues including inner ear structures. In addition, ROM can damage mitochondrial DNA (mtDNA), resulting in the production of specific mtDNA deletions (mtDNA del4977 [human] or mtDNA del4834 [rat]; also known as the common aging deletion]. Previous corroborating data suggest that the common aging deletion mtDNA4834 may be associated not only with aging but also with presbyacusis, thus further strengthening the basis of the current studies. In this study, experiments provide compelling evidence that long‐term treatment with compounds that block or scavenge reactive oxygen metabolites attenuate age‐related hearing loss and reduce the impact of associated deleterious changes at the molecular level.

[1]  M. Heidrick,et al.  Effect of dietary 2-mercaptoethanol on the life span, immune system, tumor incidence and lipid peroxidation damage in spleen lymphocytes of aging BC3F1 mice , 1984, Mechanisms of Ageing and Development.

[2]  Edward Byrne,et al.  DECLINE IN SKELETAL MUSCLE MITOCHONDRIAL RESPIRATORY CHAIN FUNCTION: POSSIBLE FACTOR IN AGEING , 1989, The Lancet.

[3]  Wing Kg Studies of basic cochlear physiology and the energy-metabolism of the cochlear response in the cat. , 1959 .

[4]  Z. Oltvai,et al.  Bcl-2 functions in an antioxidant pathway to prevent apoptosis , 1993, Cell.

[5]  L. Ernster,et al.  [14] Skeletal muscle mitochondria , 1967 .

[6]  I. Zs.-Nagy,et al.  Centrophenoxine increases the rates of total and mRNA synthesis in the brain cortex of old rats: An explanation of its action in terms of the membrane hypothesis of aging , 1984, Experimental Gerontology.

[7]  D. Wood,et al.  Risk of angina pectoris and plasma concentrations of vitamins A, C, and E and carotene , 1991, The Lancet.

[8]  C. Fernández,et al.  Modifications of cochlear responses by oxygen deprivation. , 1958, Het Ziekenhuiswezen.

[9]  D. Harman,et al.  Free radical theory of aging: effect of free radical reaction inhibitors on the mortality rate of male LAF mice. , 1968, Journal of gerontology.

[10]  A. Axelsson The cochlear blood vessels in guinea pigs of different ages. , 1971, Acta oto-laryngologica.

[11]  R. Cutler Redundancy of information content in the genome of mammalian species as a protective mechanism determining aging rate. , 1973, Mechanisms of ageing and development.

[12]  J. Montoya,et al.  [Diseases of mitochondrial DNA]. , 2000, Revista de neurologia.

[13]  U. Rosenhall,et al.  Presbyacusis related to socioeconomic factors and state of health. , 1997, Scandinavian audiology.

[14]  P. Southorn,et al.  Free radicals in medicine. I. Chemical nature and biologic reactions. , 1988, Mayo Clinic proceedings.

[15]  W. J. Meek,et al.  THE FEDERATION OF AMERICAN SOCIETIES FOR EXPERIMENTAL BIOLOGY. , 1938, Science.

[16]  D. Wallace,et al.  Hypoxemia is associated with mitochondrial DNA damage and gene induction. Implications for cardiac disease. , 1991, JAMA.

[17]  R. Kimura,et al.  Extensive venous obstruction of the labyrinth. A. Cochlear changes. , 1956, The Annals of otology, rhinology, and laryngology.

[18]  R. G. Allen,et al.  Relationship between metabolic rate, free radicals, differentiation and aging: a unified theory. , 1985, Basic life sciences.

[19]  L. Ernster,et al.  A case of severe hypermetabolism of nonthyroid origin with a defect in the maintenance of mitochondrial respiratory control: a correlated clinical, biochemical, and morphological study. , 1962, The Journal of clinical investigation.

[20]  A. Richardson,et al.  Changes in the expression of superoxide dismutase and catalase as a function of age and dietary restriction. , 1989, Biochemical and biophysical research communications.

[21]  S. Dimauro,et al.  Mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes: A distinctive clinical syndrome , 1984, Annals of neurology.

[22]  S. Korsmeyer,et al.  Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell death , 1993, Cell.

[23]  R. Bolli Superoxide dismutase 10 years later: a drug in search of a use. , 1991, Journal of the American College of Cardiology.

[24]  M. Seidman,et al.  Age-related differences in cochlear microcirculation and auditory brain stem response. , 1996, Archives of otolaryngology--head & neck surgery.

[25]  George Perry,et al.  Free radical damage, iron, and Alzheimer's disease , 1995, Journal of the Neurological Sciences.

[26]  D. Brackmann,et al.  Goals and Mechanisms for Training Otolaryngologists in the Area of Geriatric Medicine , 1989, Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery.

[27]  C. Epstein,et al.  Familial mitochondrial encephalomyopathy (MERRF): Genetic, pathophysiological, and biochemical characterization of a mitochondrial DNA disease , 1988, Cell.

[28]  S. Gatehouse,et al.  Whole blood viscosity and red cell filterability as factors in sensorineural hearing impairment in the elderly. , 1990, Acta oto-laryngologica. Supplementum.

[29]  J. E. Hawkins,et al.  Vascular Changes in the Human Inner Ear Associated with Aging , 1972, The Annals of otology, rhinology, and laryngology.

[30]  L. Pikó,et al.  Studies of sequence heterogeneity of mitochondrial DNA from rat and mouse tissues: Evidence for an increased frequency of deletions/additions with aging , 1988, Mechanisms of Ageing and Development.

[31]  T. Takeda,et al.  Audiological findings of sensorineural deafness associated with a mutation in the mitochondrial DNA. , 1997, American Journal of Otology.

[32]  N. Arnheim,et al.  Detection of a specific mitochondrial DNA deletion in tissues of older humans. , 1990, Nucleic acids research.

[33]  S. Dimauro,et al.  Mitochondrial encephalomyopathies. , 1989, Progress in clinical and biological research.

[34]  H. Schuknecht,et al.  Pathology of Presbycusis , 1969 .

[35]  U. Rosenhall,et al.  Effects of presbycusis and other types of hearing loss on auditory brainstem responses. , 1986, Scandinavian audiology.

[36]  D. Wallace,et al.  Assessment of mitochondrial oxidative phosphorylation in patient muscle biopsies, lymphoblasts, and transmitochondrial cell lines. , 1996, Methods in enzymology.

[37]  K. Wing Studies of basic cochlear physiology and the energy-metabolism of the cochlear response in the cat. , 1959, Acta oto-laryngologica. Supplementum.

[38]  D. Bredesen,et al.  Bcl-2 inhibition of neural death: decreased generation of reactive oxygen species. , 1993, Science.

[39]  D. Wallace,et al.  Spontaneous Kearns-Sayre/chronic external ophthalmoplegia plus syndrome associated with a mitochondrial DNA deletion: a slip-replication model and metabolic therapy. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[40]  A. Ryan,et al.  Development of mammalian endocochlear potential: normal ontogeny and effects of anoxia. , 1986, The American journal of physiology.

[41]  R. Cutler,et al.  Superoxide dismutase: correlation with life-span and specific metabolic rate in primate species. , 1980, Proceedings of the National Academy of Sciences of the United States of America.

[42]  K. Helzlsouer,et al.  Prediagnostic serum levels of carotenoids and vitamin E as related to subsequent cancer in Washington County, Maryland. , 1991, The American journal of clinical nutrition.

[43]  A. Davison,et al.  Mitochondrial mutations may increase oxidative stress: implications for carcinogenesis and aging? , 1990, Free radical biology & medicine.

[44]  J. Bartko,et al.  Possible relationship between conditions associated with chronic hypoxia and brain mitochondrial DNA deletions. , 1996, Archives of biochemistry and biophysics.

[45]  P. McCabe 10 – PRODUCTION OF SINGLE-STRANDED DNA BY ASYMMETRIC PCR , 1990 .

[46]  E. Flamm,et al.  The free radical pathology and the microcirculation in the major central nervous system disorders. , 1980, Acta physiologica Scandinavica. Supplementum.

[47]  Mitochondrial Inheritance of Acquired Deafness , 1991, Annals of the New York Academy of Sciences.

[48]  J. Maassen,et al.  Mutation in mitochondrial tRNALeu(UUR) gene in a large pedigree with maternally transmitted type II diabetes mellitus and deafness , 1992, Nature Genetics.

[49]  J. Wilberger,et al.  Effects of pegorgotein on neurologic outcome of patients with severe head injury. A multicenter, randomized controlled trial. , 1996, JAMA.

[50]  R. Kimura,et al.  XLIII Experimental Obstruction of Venous Drainage and Arterial Supply of the Inner Ear , 1957, The Annals of otology, rhinology, and laryngology.

[51]  G. Rebillard,et al.  Glutamate neurotoxicity in the cochlea: a possible consequence of ischaemic or anoxic conditions occurring in ageing. , 1990, Acta oto-laryngologica. Supplementum.

[52]  R. Ziegler,et al.  Vegetables, fruits, and carotenoids and the risk of cancer. , 1991, The American journal of clinical nutrition.

[53]  L. Ernster,et al.  Enzymic Activities of Human Skeletal Muscle Mitochondria: A Tool in Clinical Metabolic Research , 1959, Nature.

[54]  T. Ozawa,et al.  Age-dependent increase in deleted mitochondrial DNA in the human heart: possible contributory factor to presbycardia. , 1991, American heart journal.

[55]  D. Hegner,et al.  Do mitochondria produce oxygen radicals in vivo? , 1978, European journal of biochemistry.

[56]  L. Sabatier,et al.  Chromosomal instability and alteration of telomere repeat sequences. , 1995, Biochimie.

[57]  A. Tappel,et al.  Protection of vitamin E, selenium, trolox C, ascorbic acid palmitate, acetylcysteine, coenzyme Q0, coenzyme Q10, beta-carotene, canthaxanthin, and (+)-catechin against oxidative damage to rat blood and tissues in vivo. , 1995, Free radical biology & medicine.

[58]  T. Byers,et al.  Vitamin E supplements and coronary heart disease. , 2009, Nutrition reviews.

[59]  A. Nuttall,et al.  The Protective Effects of Allopurinol and Superoxide Dismutase-Polyethylene Glycol on Ischemic and Reperfusion-Induced Cochlear Damage , 1991, Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery.

[60]  C. Cross,et al.  Free radicals, antioxidants, and human disease: where are we now? , 1992, The Journal of laboratory and clinical medicine.

[61]  C. Olanow,et al.  Oxidative stress and the pathogenesis of Parkinson's disease , 1996, Neurology.

[62]  J. A. V Pritchard,et al.  CANCER DETECTION , 1976, The Lancet.

[63]  V. Honrubia,et al.  MAINTENANCE OF COCHLEAR POTENTIALS DURING ASPHYXIA. , 1965, Acta oto-laryngologica.

[64]  M. Seidman,et al.  Mitochondrial DNA deletions associated with aging and possibly presbycusis: a human archival temporal bone study. , 1997, The American journal of otology.

[65]  M. Raichle The pathophysiology of brain ischemia , 1983, Annals of neurology.

[66]  B. A. Schulte,et al.  Alterations in microvasculature are associated with atrophy of the stria vascularis in quiet-aged gerbils , 1995, Hearing Research.

[67]  D. Wallace,et al.  Maternally transmitted diabetes and deafness associated with a 10.4 kb mitochondrial DNA deletion , 1992, Nature Genetics.

[68]  N. Jones,et al.  Presbyacusis , 2001, The Journal of Laryngology & Otology.

[69]  H. Pillsbury,et al.  Cochlear microcirculation in young and old gerbils. , 1990, Archives of otolaryngology--head & neck surgery.