Antioxidant cellular protection and adaptive response induced by chronic oxidative stimuli

Authors

  • Gloria A. Santa-González Universidad de Antioquia
  • Mauricio Camargo Universidad de Antioquia

DOI:

https://doi.org/10.17533/udea.acbi.328979

Keywords:

adaptation, antioxidant defense, chronic oxidative stress, homeostasis

Abstract

Adaptation is an important mechanism in cells and organisms that allow them to respond to environmental challenges and changing functional demands. To accomplish these requirements, cells integrate modifications at different levels such as gene expression, metabolic activity, cellular functionality and phenotype. The orderly coordination of these changes is fundamental for cells to maintain viability despite a variety of harmful stimuli, such as the case of exceedingly concentrations of reactive oxygen species (ROS). In this study, we tested the hypothesis that chronic and repetitive stimuli with a mild concentration of hydrogen peroxide (H2O2) would activate cellular responses, resulting in adaptation. This was done confronting cell cultures to prolonged exposures of H2O2 obtained with glucose oxydase (GlucOx) added to the medium to generate a constant concentration of the oxidant (≈ 50 μM); this treatment protocol (1h/d) was extended during seven continuous consecutive days after which the following parameters were evaluated: cell morphology and viability, mitochondrial DNA content, mitochondrial ROS accumulation and antioxidant defense gene expression. These data further support the idea that exposure to continuous and low concentrations of ROS, could act as signaling molecules inducing cellular processes that converged toward adaptation to chronic oxidative stress.

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Author Biographies

Gloria A. Santa-González, Universidad de Antioquia

Grupo Genética, Regeneración y Cáncer, SIU-UdeA, Lab. # 432. Universidad de Antioquia. A. A. 1226. Medellín (Antioquia), Colombia.

Mauricio Camargo, Universidad de Antioquia

Grupo Genética, Regeneración y Cáncer, SIU-UdeA, Lab. # 432. Universidad de Antioquia. A. A. 1226. Medellín (Antioquia), Colombia.

Docente, Instituto de Biología, Universidad de Antioquia. A. A. 1226. Medellín (Antioquia), Colombia.

References

Bar-Shai M, Carmeli E, Ljubuncic P, Reznick AZ. 2008. Exercise and immobilization in aging animals: the involvement of oxidative stress and NF-kappaB activation. Free Radical Biology and Medicine, 44: 202-214.

Barzilai A, Yamamoto KI. 2004. DNA damage responses to oxidative stress. DNA Repair, 3: 1109-1115. Boveris A, Cadenas E. 2000. Mitochondrial production of hydrogen peroxide regulation by nitric oxide and the role of ubisemiquinone. International Union of Biochemistry and Molecular Biology Life, 50: 245-250.

Braunersreuther V, Pellieux C, Pelli G, Burger F, Steffens S, Montessuit C, Weber C, Proudfoot A, Mach F, Arnaud C. 2010. Chemokine CCL5/RANTES inhibition reduces myocardial reperfusion injury in atherosclerotic mice. Journal of Molecular and Cellular Cardiology, 48: 789-798.

Burk RF, Olson GE, Winfrey VP, Hill KE, Yin D. 2011. Glutathione peroxidase-3 produced by the kidney binds to a population of basement membranes in the gastrointestinal tract and in other tissues. American Journal of Physiology-Gastrointestinal and Liver Physiology, 301 (1): G32-38.

Cai H. 2005. Hydrogen peroxide regulation of endothelial function: Origins, mechanisms, and consequences. Cardiovascular Research, 68: 26-36.

Calabrese EJ. 2015. Hormesis: principles and applications. Homeopathy, 104: 69-82.

Calabre EJ, Baldwin LA. 2003. Hormesis: the dose-response revolution. Annual Review of Pharmacology and Toxicology, 43: 175-197.

Chance B, Sies H, Boveris A. 1979. Hydroperoxide metabolism in mammalian organs. Physiological Reviews, 59: 527-605.

Crawford DR, Davies KJ. 1994. Adaptive response and oxidative stress. Environmental Health Perspectives, 102 (Suppl 10): 25-28.

D’Autréaux B, Toledano MB. 2007. ROS as signalling molecules: mechanisms that generate specificity in ROS homeostasis. Nature Reviews Molecular Cell Biology, 8: 813-824.

Evans AR, Limp-Foster M, Kelley MR. 2000. Going APE over ref-1. Mutation Research, 461: 83-108.

Evans JL, Goldfine ID, Maddux BA, Grodsky GM. 2003. Are oxidative stress-activated signaling pathways mediators of insulin resistance and beta-cell dysfunction? Diabetes, 52: 1-8.

Fritz G, Grösch S, Tomicic M, Kaina B. 2003. APE/Ref-1 and the mammalian response to genotoxic stress. Toxicology, 193: 67-78.

Furda AM, Bess AS, Meyer JN, Van Houten B. 2012. DNA Repair Protocols. Methods in Molecular Biology, 920: 111-132.

Gomez-Cabrera MC, Domenech E, Viña J. 2008. Moderate exercise is an antioxidant: upregulation of antioxidant genes by training. Free Radical Biology and Medicine, 44: 126-131.

Gough DR, Cotter TG. 2011. Hydrogen peroxide: a Jekyll and Hyde signalling molecule. Cell Death and Disease, 2, e213. Doi: 10.1038/cddis.2011.96

Hirota K, Matsui M, Iwata S, Nishiyama A, Mori K, Yodoi J. 1997. AP-1 transcriptional activity is regulated by a direct association between thioredoxin and Ref-1. Proceedings of the National Academy of Sciences of the United States of America, 94: 3633-3638.

Holmstrom KM, Finkel T. 2014. Cellular mechanisms and physiological consequences of redox-dependent signalling. Nature Reviews Molecular Cell Biology, 15: 411-421.

Jain A, Atale N, Kohli S, Bhattacharya S, Sharma M, Rani V. 2015. An assessment of norepinephrine mediated hypertrophy to apoptosis transition in cardiac cells: A signal for cell death. Chemico- Biological Interactions, 225: 54-62.

Ji LL, Gomez-Cabrera MC, Steinhafel N, Viña J. 2004. Acute exercise activates nuclear factor (NF)-kappaB signaling pathway in rat skeletal muscle. Journal of the Federation of American Societies for Experimental Biology, 18: 1499-1506.

Ji LL, Gomez-Cabrera MC, Viña J. 2006. Exercise and hormesis: activation of cellular antioxidant signaling pathway. Annals of the New York Academy of Sciences, 1067: 425-435.

Ji LL, Gomez-Cabrera MC, Viña J. 2007. Role of nuclear factor kappaB and mitogen-activated protein kinase signaling in exercise- induced antioxidant enzyme adaptation. Applied Physiology, Nutrition, and Metabolism, 32: 930-935.

Kefaloyianni E, Gaitanaki C, Beis I. 2006. ERK1/2 and p38-MAPK signalling pathways, through MSK1, are involved in NF-kappaB transactivation during oxidative stress in skeletal myoblasts. Cellular Signalling, 18: 2238-2251.

Kumar V, Abbas AK, Fausto N, Aster JC. 2005. Respuestas celulares ante el estrés y las agresiones por tóxicos: adaptación, lesión y muerte. En: Mitchell RN, editor. Robbins y Cotran. Patología estructural y funcional. 7a. ed. España: Elsevier. p. 3-42.

Kupsco A, Schlenk D. 2015. Chapter One: Oxidative stress, unfolded protein response, and apoptosis in developmental toxicity. En: Jeon KW, editor. International review of cell and molecular biology. San Diego: Academic Press. p. 1-66.

Lee HC, Wei YH. 2005. Mitochondrial biogenesis and mitochondrial DNA maintenance of mammalian cells under oxidative stress. The International Journal of Biochemistry and Cell Biology, 37: 822-834.

Lemon JA, Rollo CD, Boreham DR. 2008. Elevated DNA damage in a mouse model of oxidative stress: impacts of ionizing radiation and a protective dietary supplement. Mutagenesis, 23: 473-482.

Luna-López A, González-Puertos VY, Romero-Ontiveros J, Ventura- Gallegos JL, Zentella A, Gomez-Quiroz LE, Königsberg M. 2013. A noncanonical NF-κB pathway through the p50 subunit regulates Bcl-2 overexpression during an oxidative-conditioning hormesis response. Free Radical Biology and Medicine, 63: 41-50.

Lushchak VI. 2011. Adaptive response to oxidative stress: Bacteria, fungi, plants and animals. Comparative biochemistry and physiology. Toxicology and Pharmacology: CBP, 153: 175-190.

Marinho HS, Real C, Cyrne L, Soares H, Antunes F. 2014. Hydrogen peroxide sensing, signaling and regulation of transcription factors. Redox Biology, 2: 535-562.

Marteijn JA, Lans H, Vermeulen W, Hoeijmakers JH. 2014. Understanding nucleotide excision repair and its roles in cancer and ageing. Nature Reviews Molecular Cell Biology, 15: 465-481.

Matsumura A, Emoto MC, Suzuki S, Iwahara N, Hisahara S, Kawamata J, Suzuki H, Yamauchi A, Sato-Akaba H, Fujii HG, Shimohama S. 2015. Evaluation of oxidative stress in the brain of a transgenic mouse model of Alzheimer’s disease by in vivo electron paramagnetic resonance imaging. Free Radical Biology and Medicine, 85: 165-73. Doi: 10.1016/j.freeradbiomed.2015.04.013

Mittal M, Siddiqui MR, Tran K, Reddy SP, Malik AB. 2014. Reactive oxygen species in inflammation and tissue injury. Antioxidants and Redox Signaling, 20: 1126-1167.

Muñoz-Espín D, Serrano M. 2014. Cellular senescence: from physiology to pathology. Nature Reviews Molecular Cell Biology, 15: 482-496.

Nam E, Cortez D. 2011. ATR signalling: more than meeting at the fork. Biochemical Journal, 436, 527-36.

Orozco E, Santa G, Camargo M. 2010. NAC and L-Carnitine antioxidant action in a chronic oxidative stress model in C2C12 myoblast cell line. Revista de la Asocación Colombiana de Ciencias Biológicas, 22: 31-54.

Osburn WO, Kensler TW. 2008. Nrf2 signaling: an adaptive response pathway for protection against environmental toxic insults. Mutation Research, 659: 31-39.

Palikaras K, Tavernarakis N. 2014. Mitochondrial homeostasis: The interplay between mitophagy and mitochondrial biogenesis. Experimental Gerontology, 56: 182-188.

Phoa N, Epe B. 2002. Influence of nitric oxide on the generation and repair of oxidative DNA damage in mammalian cells Carcinogenesis, 23: 469-475.

Pickering AM, Vojtovich L, Tower J, Davies KJ. 2013. Oxidative stress adaptation with acute, chronic, and repeated stress. Free Radical Biology and Medicine, 55: 109-118.

Pluskota-Karwatka D. 2008. Modifications of nucleosides by endogenous mutagens-DNA adducts arising from cellular processes. Bioorganic Chemistry, 36: 198-213.

Powers SK, Duarte J, Kavazis AN, Talbert EE. 2010. Reactive oxygen species are signalling molecules for skeletal muscle adaptation. Experimental Physiology, 95: 1-9.

Radak Z, Naito H, Kaneko T, Tahara S, Nakamoto H, Takahashi R, Cardozo-Pelaez F, Goto S. 2002. Exercise training decreases DNA damage and increases DNA repair and resistance against oxidative stress of proteins in aged rat skeletal muscle. Pflügers Archiv European Journal of Physiology, 445, 273-278.

Radak Z, Chung HY, Goto S. 2005. Exercise and hormesis: oxidative stress- related adaptation for successful aging. Biogerontology, 6: 71-75.

Radak Z, Chung HY, Goto S. 2008. Systemic adaptation to oxidative challenge induced by regular exercise. Free Radical Biology and Medicine, 44: 153-159.

Rooney JP, Ryde IT, Sanders LH, Howlett EH, Colton MD, Germ KE, Mayer GD, Greenamyre JT, Meyer JN. 2015. PCR based determination of mitochondrial DNA copy number in multiple species. Methods in Molecular Biology, 1241: 23-38.

Sabri A, Hughie HH, Lucchesi PA. 2003. Regulation of hypertrophic and apoptotic signaling pathways by reactive oxygen species in cardiac myocytes. Antioxidants and Redox Signaling, 5: 731-740.

Takahashi K, Cohen HJ. 1986. Selenium-dependent glutathione peroxidase protein and activity: Immunological investigations on cellular and plasma enzymes. Blood, 68: 640-645.

Wiese AG, Pacifici RE, Davies KJ. 1995. Transient adaptation of oxidative stress in mammalian cells. Archives of Biochemistry and Biophysics, 318: 231-240.

Wink DA, Cook JA, Pacelli R, Liebmann J, Mitchell JB, Murali C. 1995. Nitric oxide (NO) protects against cellular damage by reactive oxygen species. Toxicology Letters, 82/83: 221-226.

Yu BP. 2004. Hormesis and intervention of aging. Geriatrics and Gerontology International, 4: S81-S83.

Zhang Y. 2004. Reactive Oxygen Species (ROS), troublemakers between Nuclear Factor-B (NF- B) and c-Jun NH2-terminal Kinase (JNK). Cancer Research, 64: 1902-1905.

Published

2017-10-02

How to Cite

Santa-González, G. A., & Camargo, M. (2017). Antioxidant cellular protection and adaptive response induced by chronic oxidative stimuli. Actualidades Biológicas, 38(104), 71–80. https://doi.org/10.17533/udea.acbi.328979

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