“Pull and push back” concepts of longevity and life span extension

被引:0
|
作者
Khachik Muradian
机构
[1] State Institute of Gerontology of National Academy of Medical Sciences of Ukraine,
来源
Biogerontology | 2013年 / 14卷
关键词
Aging; Metabolism; Artificial atmosphere; Life span extension; Extreme longevity;
D O I
暂无
中图分类号
学科分类号
摘要
The negative relation between metabolism and life span is a fundamental gerontological discovery well documented in a variety of ontogenetic and phylogenetic models. But how the long-lived species and populations sustain lower metabolic rate and, in more general terms, what is the efficient way to decline the metabolism? The suggested ‘pull and push back’ hypothesis assumes that decreased Po2 (hypoxia) and/or increased PCO2\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${\text{P}}_{{{\text{CO}}_{ 2} }}$$\end{document} (hypercapnia) may create preconditions for the declined metabolic and aging rates. However, wider implementation of such ideas is compromised because of little advances in modification of the metabolic rate. Artificial atmosphere with controlled PO2\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${\text{P}}_{{\text{O}}_{2}}$$\end{document} and PCO2\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${\text{P}}_{{{\text{CO}}_{2} }}$$\end{document} could be a promising approach because of the minimal external invasions and involvement of the backward and forward loops ensuring physiological self-regulation of the metabolic perturbations. General considerations and existing data indicate that manipulations of PCO2\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${\text{P}}_{{{\text{CO}}_{2} }}$$\end{document} may be more efficient in life span extension than PO2\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${\text{P}}_{{\text{O}}_{2}}$$\end{document}. Thus, maximum life span of mammals positively correlates with the blood PCO2\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${\text{P}}_{{{\text{CO}}_{2} }}$$\end{document} and HCO3− but not with PO2\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${\text{P}}_{{\text{O}}_{2}}$$\end{document}. Yet, proportional decease of the body PO2\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${\text{P}}_{{\text{O}}_{2}}$$\end{document} and increase of PCO2\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${\text{P}}_{{{\text{CO}}_{2} }}$$\end{document} seems the most optimal regime ensuring lower losses of the energy equivalents. Furthermore, especially rewarding results could be expected when such changes are modeled without major external invasions using the animals’ inner capacity to consume O2 and generate CO2, as it is typical for the extreme longevity.
引用
收藏
页码:687 / 691
页数:4
相关论文
共 50 条
  • [31] Life-Span Extension by Caloric Restriction Is Determined by Type and Level of Food Reduction and by Reproductive Mode in Brachionus manjava']javacas (Rotifera)
    Gribble, Kristin E.
    Welch, David B. Mark
    JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES, 2013, 68 (04): : 349 - 358
  • [32] Membrane fatty acid unsaturation, protection against oxidative stress, and maximum life span -: A homeoviscous-longevity adaptation?
    Pamplona, R
    Barja, G
    Portero-Otín, M
    INCREASING HEALTHY LIFE SPAN: CONVENTIONAL MEASURES AND SLOWING THE INNATE AGING PROCESS, 2002, 959 : 475 - 490
  • [33] Alternative pathways for the extension of cellular life span: inactivation of p53/pRb and expression of telomerase
    Homayoun Vaziri
    Samuel Benchimol
    Oncogene, 1999, 18 : 7676 - 7680
  • [34] Molecular mechanisms of life- and health-span extension: role of calorie restriction and exercise intervention
    Carter, Christy S.
    Hofer, Tim
    Seo, Arnold Y.
    Leeuwenburgh, Christian
    APPLIED PHYSIOLOGY NUTRITION AND METABOLISM, 2007, 32 (05) : 954 - 966
  • [35] 20S proteasome activation promotes life span extension and resistance to proteotoxicity in Caenorhabditis elegans
    Chondrogianni, Niki
    Georgila, Konstantina
    Kourtis, Nikos
    Tavernarakis, Nektarios
    Gonos, Efstathios S.
    FASEB JOURNAL, 2015, 29 (02) : 611 - 622
  • [36] A review of methionine dependency and the role of methionine restriction in cancer growth control and life-span extension
    Cavuoto, Paul
    Fenech, Michael F.
    CANCER TREATMENT REVIEWS, 2012, 38 (06) : 726 - 736
  • [37] Inactivation of p53 and life span extension of human diploid fibroblasts by mot-2
    Kaul, SC
    Reddel, RR
    Sugihara, T
    Mitsui, Y
    Wadhwa, R
    FEBS LETTERS, 2000, 474 (2-3) : 159 - 164
  • [38] Alternative pathways for the extension of cellular life span: inactivation of p53/pRb and expression of telomerase
    Vaziri, H
    Benchimol, S
    ONCOGENE, 1999, 18 (53) : 7676 - 7680
  • [39] The Neuronal Overexpression of Gcic in Drosophila melanogaster Induces Life Extension With Longevity-Associated Transcriptomic Changes in the Thorax
    Moskalev, Alexey
    Guvatova, Zulfiya
    Shaposhnikov, Mikhail
    Lashmanova, Ekaterina
    Proshkina, Ekaterina
    Koval, Liubov
    Zhavoronkov, Alex
    Krasnov, George
    Kudryavtseva, Anna
    FRONTIERS IN GENETICS, 2019, 10
  • [40] Circadian clocks govern calorie restriction-mediated life span extension through BMAL1-and IGF-1-dependent mechanisms
    Patel, Sonal A.
    Chaudhari, Amol
    Gupta, Richa
    Velingkaar, Nikkhil
    Kondratov, Roman V.
    FASEB JOURNAL, 2016, 30 (04) : 1634 - 1642