medigraphic.com

2005, Number 3

<< Back Next >>

Bioquimia 2005; 30 (3)

Mitochondrial role in the development of oxidative stress in obesity

Martínez-Abundis E, Sánchez-Rodríguez MA, Hafidi-Bentlakder ME

Language: Spanish
References: 52
Page: 82-89
PDF size: 87.07 Kb.


ABSTRACT

Obesity is a risk factor for the development of hypertension, diabetes, atherosclerosis, etc., which are associated with high levels of oxidative damage markers, due to possible metabolic alterations in mitochondria. During oxidative phosphorylation, a small amount of reactive oxygen species (ROS) is physiologically formed. However, under some pathological conditions such as in the presence of high levels of O2 or decreased adenosine diphosphate (ADP) concentrations, elevated levels of free fatty acids (FFA) and other abnormalities, the formation of ROS increases in the mitochondrial electron transport chain, which induces damage to biomolecules such as lipids, proteins and DNA. This review attempts to present some recent evidence in relation to some metabolic disorders in obesity such as high levels of FFA or triglycerides and their effect on the mitochondria which contribute to generate ROS and to increase oxidative stress.


REFERENCES

  1. Knight JA. Free radicals, antioxidants, aging & disease. Washington: AACC Press; 1999: 21-43.

  2. Beckman K, Ames B. The free radical theory of aging matures. Physiol Rev 1998; 78: 547-581.

  3. Chow CK, Ibrahim W, Wei Z, Chan AC. Vitamin E regulates mitochondrial hidrogen peroxide generation. Free Radic Biol Med 1999; 27: 580-587.

  4. Turrens JF. Mitochondrial formation of reactive oxygen species. J Physiol 2003; 552: 335-344.

  5. Staniek K, Nohl H. Are a mitochondria a permanent source of reactive oxygen species? Biochim Biophys Acta 2000; 1460: 268-275.

  6. St-Pierre J, Buckingham J, Roebuck SJ, Brand MD. Topology of superoxide production from different sites in the mitochondrial electron transport chain. J Biol Chem 2002; 277: 44784-44790.

  7. Kushnareva Y, Murphy AN, Andreyev A. Complex I-mediated reactive oxygen species generation: modulation by cytocrome c and NAD(P)+ oxidation-reduction state. Biochem J 2002; 368: 545-553.

  8. Ide T, Tsutsui H, Kinugawa S, Usumi H, Kang D, Hattori N, el al. Mitochondrial electron transport complex I is a potential source of oxygen free radicals in the failing myocardium. Circ Res 1999; 85: 357-363.

  9. Davidson J, Schiestl R. Mitochondrial respiratory electron carriers are involved in oxidative stress during heat stress in Saccharomyces cerevisiae. Mol Cell Biol 2001; 21: 8483-8489.

  10. Piña-Garza E, Huberman A, Chávez R, Lascurain R, Zenteno E, Piña E, et al. Radicales libres. Beneficios y problemas. Gac Med Mex 1996; 132: 183-203.

  11. Burczynski J, Southard S, Haynes JR, Longhust PA, Colby HD. Changes in mitochondrial and microsomal lipid peroxidation and fatty acid profiles in adrenal glands, testes and livers from a-tocopherol-deficient rats. Free Radic Biol Med 2001; 30: 1029-1035.

  12. Boveris A, Cardenas E, Stoppani A. Role of ubiquinone in the mitochondrial generation of hydrogen peroxide. Biochem J 1976; 156: 435-444.

  13. Hsiao G, Teng CM, Sheu JR, Cheng YW, Lam KK, Lee YM, et al. Cinnamophilin as a novel antiperoxidative cytoprotectan and free radical scavenger. Biochim Biophys Acta 2001; 1525: 77-88.

  14. Motchnik PA, Frei B, Ames BN. Measurement of antioxidants in human blood plasma. Methods Enzymol 1994; 234: 269-279.

  15. Nicholls DG. Bioenergética: introducción a la teoría quimiosmótica. Barcelona: Reverté. 1987: 71-135.

  16. Castilho R, Kowaltowski A, Meinicke A, Vercesi A. Oxidative damage of mitochondria induced by Fe(II), citrate or t-butyl hydroperoxide in the presence of Ca2+: effect of coenzyme Q redox state. Free Radic Biol Med 1995; 18: 55-59.

  17. Kowaltowski A, Castilho R, Vercesi A. Ca2+-induced mitochondrial membrane permeabilization: role of coenzyme Q redox state. Am J Physiol 1995; 269: C141-C147.

  18. Schnurr K, Hellwing M, Seidemann B, Jungblut P, Kuhn H, Rapaport SM, et al. Oxygenation of biomembranes by mammalian lypoxygenases: the role of ubiquinone. Free Radic Biol Med 1996; 20: 11-21.

  19. Yang CF, Shen HM, Ong CN. Intracellular thiol depletion causes mitochondrial permeability transition in ebselen-induced apoptosis. Arch Biochem Biophys 2000; 380: 319-330.

  20. Bohr VA. Repair of oxidative DNA damage in nuclear and mitochondrial DNA, and some changes with aging in mammalian cells. Free Radic Biol Med 2002; 32: 804-812.

  21. Young I, Woodside J. Antioxidants in health and disease. J Clin Pathol 2001; 54: 176-186.

  22. Santos A, Naoufal Z, Kroemer G. Mitochondria as regulator apoptosis: doubt no more. Biochim Biophys Acta 1998; 1366: 151-165.

  23. Sánchez-Rodríguez MA, Mendoza-Núñez VM. Envejecimiento, enfermedades crónicas y antioxidantes. México: Facultad de Estudios Superiores Zaragoza, UNAM; 2003: 32-51.

  24. Duchen MR. Roles of mitochondria in health and disease. Diabetes 2004; 53: S96-S102.

  25. Yang S, Zhu H, Li Y, Lin H, Gabrielson K, Trush MA, et al. Mitochondrial adaptations to obesity-related oxidant stress. Arch Biochem Biophys 2000; 378: 259-268.

  26. Dobrian A, Davies M, Schriver S, Lauterio TJ, Prewitt RL. Oxidative stress in a rat model of obesity-induced hypertension. Hypertension 2001; 37: 554-560.

  27. Keaney J, Larson M, Vasan R, Wilson PW, Lipinska I, Corey D. Obesity and systemic oxidative stress. Arterioscler Thromb Vasc Biol 2003; 23: 434-439.

  28. Higdon J, Frei B. Obesity and oxidative stress. A direct link to CVD? Arterioscler Thromb Vasc Biol 2003; 23: 365-367.

  29. Fenster C, Weinsier R, Darley-Usmar V, Patel RP. Obesity, aerobic exercise and vascular disease: the role of oxidant stress. Obes Res 2002; 10: 964-968.

  30. El Hafidi M, Perez I, Zamora J, Soto V, Carvajal-Sandoval G, Banos C. Glycine intake decreases plasma free fatty acids, adipose cell size and blood pressure in sucrose-fed rats. Am J Physiol Reg Integr Comp Physiol 2004; 287: R1387-1393.

  31. McBride AG, Borutaité V, Brown GC. Superoxide dismutase and hydrogen peroxide cause rapid nitric oxide breakdown, peroxinitrite production and subsequent cell death. Biochim Biophys Acta 1999; 1454: 275-288.

  32. Perticone F, Ceravolo R, Candigliota M, Ventura G, Iacopino S, Sinopoli F, et al. Obesity and body fat distribution induce endothelial dysfunction by oxidative stress. Diabetes 2001; 50: 159-165.

  33. Morrow J. Is oxidant stress a connection between obesity and atherosclerosis? Arterioscler Thromb Vasc Biol 2003; 23: 368-370.

  34. Libby P, Ridker P, Maseri A. Inflammation and atherosclerosis. Circulation 2002; 105: 1135-1143.

  35. Pessayre D, Mansouri A, Fromenty B. Nonalcoholic steatosis and steatohepatitis V. Mitochondrial dysfunction in steatohepatitis. Am J Physiol Gastrointest Liver Physiol 2002; 282: G193-G199.

  36. Browning JD, Horton JD. Molecular mediators of hepatic steatosis and liver injury. J Clin Invest 2004; 114: 147-152.

  37. Leon TI, Lim BO, Yu BP, Lim Y, Jeon EJ, Park DK. Effect of dietary restriction on age-related increase of liver susceptibility to peroxidation in rats. Lipids 2001; 36: 589-593.

  38. Férez S, Lupi H. El comportamiento del miocardio en la isquemia y la reperfusión. Madrid: Elsevier; 2004: 118-123.

  39. Cocco T, Di Paola M, Minuto M, Carlino V, Papa S, Lorusso M. Steady-state proton translocation in bovine heart mitochondria bc1 complex reconstituted into liposomes. J Bioenerg Biomembr 1997; 29: 81-87.

  40. Andreyev A, Bondareva TO, Dedukhova VI, Mokhova EN, Skulachev VP, Tsofina LM. The ATP/ADP-antiporter is involved in the uncoupling effect of fatty acids on mitochondria. Eur J Biochem 1989; 182: 585-592.

  41. Samartsev V, Smirnov A, Zeldi IP, Markova OV, Mokhova EN, Skulachev VP. Involvement of aspartate/glutamate antiporter in fatty acid-induced uncopling of liver mitochondria. Biochim Biophys Acta 1997; 1319: 251-257.

  42. Hillered L, Chan PH. Role of arachidonic acid and other free fatty acids in mitochondrial dysfunction in brain ischemia. J Neurosci Res 1988; 20: 451-456.

  43. Cocco T, Di Paola M, Papa S, Lorusso M. Arachidonic acid interaction with the mitochondrial electron transport chain promotes reactive oxygen species generation. Free Radic Biol Med 1999; 27: 51-59.

  44. Koshkin V, Wang X, Scherer PE, Chan CB, Wheeler MB. Mitochondrial functional state in clonal pancreatic B-cells exposed to free fatty acids. J Biol Chem 2003; 278: 19709-19715.

  45. Nicholls DG, Bernson US, Heaton GM. The identification of the component in the inner membrane of brown adipose tissue mitochondria responsible for regulating energy dissipation. Experientia Suppl 1978; 32: 89-93.

  46. Boss O, Hagen T, Lowell BB. Uncoupling proteins 2 and 3 potential regulators of mitochondrial energy metabolism. Diabetes 2000; 49: 143-156.

  47. Boss O, Muzzin P, Giacobino JP. The uncoupling proteins, a review. Eur J Endocrinol 1998; 139: 1-9.

  48. Schrauwen P, Hesselink M. UCP2 and UCP3 in muscle controlling body metabolism. J Exp Biol 2002; 205: 2275-2285.

  49. Schrauwen P, Saris W, Hesselink MK. An alternative function for human uncoupling protein 3: protection of mitochondria against accumulation of nonesterified fatty acids inside the mitochondrial matrix. FASEB J 2001; 15: 2497-2502.

  50. Huppertz C, Fischer B, Kim YB, Kotani K, Vidal-Puig A, Slieker LJ. Uncoupling protein 3 stimulates glucose uptake in muscle cells through a phosphoinositide 3-kinase-dependient mechanism. J Biol Chem 2001; 276: 12520-12529.

  51. Negree-Salvayre A, Hirtz C, Carrera G, Cazenave R, Trolyn M, Salvayre R, et al. A role for uncoupling protein-2 as a regulator of mitochondrial hydrogen peroxide generation. FASEB J 1997; 11: 809-815.

  52. Maassen JA, Hart LM, Van Essen E, Heine RB, Nijpels G, Jahangir RS, et al. Mitochondrial diabetes. Molecular mechanisms and clinical presentation. Diabetes 2004; 53: S103-S109.




2020     |     www.medigraphic.com