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Current Nutrition & Food Science

Editor-in-Chief

ISSN (Print): 1573-4013
ISSN (Online): 2212-3881

Perspective

Calorie Restriction and Extracellular ATP on Health and Longevity- A Perspective

Author(s): Gopikrishna Agraharam*, Agnishwar Girigoswami and Koyeli Girigoswami

Volume 19, Issue 1, 2023

Published on: 31 May, 2022

Page: [4 - 8] Pages: 5

DOI: 10.2174/1573401318666220531111219

Abstract

Oxidative stress is known to be generated within the organism by endogenous cellular mechanisms and can also be generated by external factors. Oxidative stress is known to be involved in various disease pathologies such as cancer, osteoarthritis, cardiovascular diseases, ageing, etc. The chronic/acute exposure to oxidative stress can easily damage cellular integrity through damaging the cellular DNA, mitochondrial DNA, proteins and other organelles that leads to malfunctioning of organs in the process of ageing. Mitochondrial respiration is one of the causes involved in the production of reactive oxygen species while generating bioenergetics (ATP) that provide energy to the cell for maintaining the cellular integrity through the electron transport chain mechanism, and on the other hand, it generates free-radicals that could cause damage to the cellular organelles and biomolecules. In relation to this context, longevity through the calorie restriction method could be due to the generation of lower reactive oxygen species and age-related diseases in vivo but accelerating loss of brain’s grey matter could be due to the depletion of energy. This is because intracellular ATP is the vital source of energy and extracellular ATP acts as signalling molecules. Using advanced technology such as nanotechnology for the internalization of extracellular ATP, and using it as an external source of energy could maintain cellular integrity and improve the healthy longevity status when combined with the calorie restriction method. In this perspective article, we have presented a brief overview and a hypothesis suggesting that the calorie restriction and extracellular ATP treatment could circumvent the mitochondrial pathway and alleviate oxidative stress, thereby improving health and enhancing longevity.

Keywords: Oxidative stress, calorie restriction, extracellular ATP, healthy ageing, longevity, ROS.

Graphical Abstract

[1]
Available from: https://www.who.int/news-room/fact-sheets/detail/ ageing-and-health (Accessed on 2022 May 18).
[2]
Jaul E, Barron J. Age-related diseases and clinical and public health implications for the 85 years old and over population. Front Public Health 2017; 5: 335.
[http://dx.doi.org/10.3389/fpubh.2017.00335] [PMID: 29312916]
[3]
López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. The hallmarks of aging. Cell 2013; 153(6): 1194-217.
[http://dx.doi.org/10.1016/j.cell.2013.05.039] [PMID: 23746838]
[4]
Phaniendra A, Jestadi DB, Periyasamy L. Free radicals: Properties, sources, targets, and their implication in various diseases. Indian J Clin Biochem 2015; 30(1): 11-26.
[http://dx.doi.org/10.1007/s12291-014-0446-0] [PMID: 25646037]
[5]
Thomson GJ, Hernon C, Austriaco N, Shapiro RS, Belenky P, Bennett RJ. Metabolism-induced oxidative stress and DNA damage selectively trigger genome instability in polyploid fungal cells. EMBO J 2019; 38(19): e101597.
[http://dx.doi.org/10.15252/embj.2019101597] [PMID: 31448850]
[6]
Doudican NA, Song B, Shadel GS, Doetsch PW. Oxidative DNA damage causes mitochondrial genomic instability in Saccharomyces cerevisiae. Mol Cell Biol 2005; 25(12): 5196-204.
[http://dx.doi.org/10.1128/MCB.25.12.5196-5204.2005] [PMID: 15923634]
[7]
Korovila I, Hugo M, Castro JP, et al. Proteostasis, oxidative stress and aging. Redox Biol 2017; 13: 550-67.
[http://dx.doi.org/10.1016/j.redox.2017.07.008] [PMID: 28763764]
[8]
Shinmura K. Effects of caloric restriction on cardiac oxidative stress and mitochondrial bioenergetics: Potential role of cardiac sirtuins. Oxid Med Cell Longev 2013; 2013: 528935.
[http://dx.doi.org/10.1155/2013/528935] [PMID: 23577224]
[9]
Dunn J, Grider MH. Physiology, adenosine triphosphate StatPearls. Treasure Island, FL: StatPearls Publishing 2021.
[10]
Rodwell VW, Bender DA, Botham KM, Kennelly PJ, Weil PA. Harper’s illustrated biochemistry-bioenergetics: the role of ATP. New York, NY, USA: McGraw-Hill Education 2018.
[11]
Bose Girigoswami K, Bhaumik G, Ghosh R. Induced resistance in cells exposed to repeated low doses of H2O2 involves enhanced activity of antioxidant enzymes. Cell Biol Int 2005; 29(9): 761-7.
[http://dx.doi.org/10.1016/j.cellbi.2005.05.001] [PMID: 16087365]
[12]
Bose Girigoswami K, Ghosh R. Response to gamma-irradiation in V79 cells conditioned by repeated treatment with low doses of hydrogen peroxide. Radiat Environ Biophys 2005; 44(2): 131-7.
[http://dx.doi.org/10.1007/s00411-005-0009-0] [PMID: 16136317]
[13]
Ghosh R, Girigoswami K. NADH dehydrogenase subunits are overexpressed in cells exposed repeatedly to H2O2. Mutat Res 2008; 638(1-2): 210-5.
[http://dx.doi.org/10.1016/j.mrfmmm.2007.08.008] [PMID: 17905312]
[14]
Heo SJ, Hwang JY, Choi JI, et al. Protective effect of diphlorethohydroxycarmalol isolated from Ishige okamurae against high glucose-induced-oxidative stress in human umbilical vein endothelial cells. Food Chem Toxicol 2010; 48(6): 1448-54.
[http://dx.doi.org/10.1016/j.fct.2010.02.025] [PMID: 20176069]
[15]
Khazim K, Gorin Y, Cavaglieri RC, Abboud HE, Fanti P. The antioxidant silybin prevents high glucose-induced oxidative stress and podocyte injury in vitro and in vivo. Am J Physiol Renal Physiol 2013; 305(5): F691-700.
[http://dx.doi.org/10.1152/ajprenal.00028.2013] [PMID: 23804455]
[16]
Cheng X, Ni B, Zhang F, Hu Y, Zhao J. High glucose-induced oxidative stress mediates apoptosis and extracellular matrix metabolic imbalances possibly via p38 MAPK activation in rat nucleus pulposus cells. J Diabetes Res 2016; 2016: 3765173.
[http://dx.doi.org/10.1155/2016/3765173] [PMID: 27635402]
[17]
Żebrowska E, Maciejczyk M, Żendzian-Piotrowska M, Zalewska A, Chabowski A. High protein diet induces oxidative stress in rat cerebral cortex and hypothalamus. Int J Mol Sci 2019; 20(7): 1547.
[http://dx.doi.org/10.3390/ijms20071547] [PMID: 30925663]
[18]
Meurer F, Do HT, Sadowski G, Held C. Standard Gibbs energy of metabolic reactions: II. Glucose-6-phosphatase reaction and ATP hydrolysis. Biophys Chem 2017; 223: 30-8.
[http://dx.doi.org/10.1016/j.bpc.2017.02.005] [PMID: 28282626]
[19]
Wang C, Geng B, Cui Q, Guan Y, Yang J. Intracellular and extracellular adenosine triphosphate in regulation of insulin secretion from pancreatic β cells (β). J Diabetes 2014; 6(2): 113-9.
[http://dx.doi.org/10.1111/1753-0407.12098]
[20]
Zumerle S, Calì B, Munari F, et al. Intercellular calcium signaling induced by ATP potentiates macrophage phagocytosis. Cell Rep 2019; 27(1): 1-10.e4.
[http://dx.doi.org/10.1016/j.celrep.2019.03.011] [PMID: 30943393]
[21]
Solini A, Usuelli V, Fiorina P. The dark side of extracellular ATP in kidney diseases. J Am Soc Nephrol 2015; 26(5): 1007-16.
[http://dx.doi.org/10.1681/ASN.2014070721] [PMID: 25452669]
[22]
Stachon P, Geis S, Peikert A, et al. Extracellular ATP induces vascular inflammation and atherosclerosis via purinergic receptor Y2 in mice. Arterioscler Thromb Vasc Biol 2016; 36(8): 1577-86.
[http://dx.doi.org/10.1161/ATVBAHA.115.307397] [PMID: 27339459]
[23]
Wang X, Li Y, Qian Y, et al. Extracellular ATP, as an energy and phosphorylating molecule, induces different types of drug resistances in cancer cells through ATP internalization and intracellular ATP level increase. Oncotarget 2017; 8(50): 87860-77.
[http://dx.doi.org/10.18632/oncotarget.21231] [PMID: 29152126]
[24]
Villa-Bellosta R. ATP-based therapy prevents vascular calcification and extends longevity in a mouse model of Hutchinson-Gilford progeria syndrome. Proc Natl Acad Sci USA 2019; 116(47): 23698-704.
[http://dx.doi.org/10.1073/pnas.1910972116] [PMID: 31690656]
[25]
Xu C, Hwang W, Jeong DE, et al. Genetic inhibition of an ATP synthase subunit extends lifespan in C. elegans. Sci Rep 2018; 8(1): 14836.
[http://dx.doi.org/10.1038/s41598-018-32025-w] [PMID: 30287841]
[26]
Zheng J, Mutcherson RII, Helfand SL. Calorie restriction delays lipid oxidative damage in Drosophila melanogaster. Aging Cell 2005; 4(4): 209-16.
[http://dx.doi.org/10.1111/j.1474-9726.2005.00159.x] [PMID: 16026335]
[27]
Zhang S, Zhang M, Sun S, et al. Moderate calorie restriction ameliorates reproduction via attenuating oxidative stress-induced apoptosis through SIRT1 signaling in obese mice. Ann Transl Med 2021; 9(11): 933.
[http://dx.doi.org/10.21037/atm-21-2458] [PMID: 34350248]
[28]
Kanikowska D, Kanikowska A, Swora-Cwynar E, et al. Moderate caloric restriction partially improved oxidative stress markers in obese humans. Antioxidants 2021; 10(7): 1018.
[http://dx.doi.org/10.3390/antiox10071018] [PMID: 34202775]
[29]
Ji Z, Liu GH, Qu J. Mitochondrial sirtuins, metabolism, and aging. J Genet Genomics 2021; S1673-8527(21): 00358-1.
[http://dx.doi.org/10.1016/j.jgg.2021.11.005]
[30]
Weiss EP, Fontana L. Caloric restriction: Powerful protection for the aging heart and vasculature. Am J Physiol Heart Circ Physiol 2011; 301(4): H1205-19.
[http://dx.doi.org/10.1152/ajpheart.00685.2011]
[31]
Pifferi F, Terrien J, Marchal J, et al. Caloric restriction increases lifespan but affects brain integrity in grey mouse lemur primates. Commun Biol 2018; 1(1): 30.
[http://dx.doi.org/10.1038/s42003-018-0024-8] [PMID: 30271916]

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