Cocaine effects on generation of reactive oxygen species and DNA damage: formation of 8-hydroxydeoxyguanosine in active abusers

 
 
 
  • Abstract
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  • References
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  • Abstract


    Cocaine abuse continues to be a major public health problem in the world. An upper numbers of individuals are initiating cocaine use with a stable rate of growth each year with an increasing number of people with cocaine related problems. Following cocaine oxidative pathways a ROS formation are generated. Oxidative stress has been demonstrated to play an important role in cocaine addiction and toxicity due to its oxidized metabolites produced by cytochrome P450 during cocaine biotransformation. The ROS induced genotoxicities include DNA damage, gene mutation, chromosome aberrations and micronuclei formation. 8-Hydroxy-2’-deoxyguanosine (8-OHdG) an oxidative modified DNA product, is the most representative product that may reflect oxidative damage induced by ROS. The present study was designed to investigate whether a systemic cocaine administration and its metabolism increase 8-OHdG production. Our findings clearly showed that cocaine promoted the ROS formation with significant increased of urinary 8-OHdG and MDA with a decreased of total scavenging capacity (TSC).


  • Keywords


    Cocaine Abusers; ROS; DNA Damage; 8-OHdG; MDA.

  • References


      [1] Marx J 2004, Cancer research - Inflammation and cancer: The link grows stronger. Science 306, 966-968. http://dx.doi.org/10.1126/science.306.5698.966.

      [2] Bartsch H, Nair J 2006, chronic inflammation and oxidative stress in the genesis and perpetuation of cancer: role of lipid peroxidation, DNA damage, and repair. Langenbecks Arch Surg 391, 499-510. http://dx.doi.org/10.1007/s00423-006-0073-1.

      [3] Liou GY, Storz P 2010, Reactive oxygen species in cancer. Free Radic Res 44, 479-496. http://dx.doi.org/10.3109/10715761003667554.

      [4] Przybyszewski J, Box HC, Kulesz-Martin M 1998, Induction of reactive oxygen species without 8-hydroxydeoxyguanosine formation in DNA of initiated mouse keratinocytes treated with 12-O-tetradecanoylphorbol-13-acetate. Carcinogenesis 19, 1467-14774. http://dx.doi.org/10.1093/carcin/19.8.1467.

      [5] Arima Y, Nishigori C, Takeuchi T, Oka S, Morimoto K, Utani A, Miyachi Y 2006, 4-Nitroquinoline 1-oxide forms 8-hydroxydeoxyguanosine in human fibroblasts through reactive oxygen species. Toxicol Sci 91, 382-392. http://dx.doi.org/10.1093/toxsci/kfj161.

      [6] Hirahashi M, Koga Y, Kumagai R, Aishima S, Taguchi K, Oda Y 2014, Induced nitric oxide synthetase and peroxiredoxin expression in intramucosal poorly differentiated gastric cancer of young patients. Pathol Int 64, 155-163. http://dx.doi.org/10.1111/pin.12152.

      [7] Soini Y, Haapasaari KM, Vaarala MH, Turpeenniemi-Hujanen T, Karja V, Karihtala P 2011, 8-hydroxydeguanosine and nitrotyrosine are prognostic factors in urinary bladder carcinoma. Int J Clin Exp Pathol 4, 267-275.

      [8] Caliskan-Can E, Firat H, Ardic S, Simsek B, Torun M, Yardim-Akaydin S 2008, Increased levels of 8-hydroxydeoxyguanosine and its relationship with lipid peroxidation and antioxidant vitamins in lung cancer. Clin Chem Lab Med 46, 107-112. http://dx.doi.org/10.1515/CCLM.2008.010.

      [9] Ece H, Cigdem E, Yuksel K, Ahmet D, Hakan E, Oktay TM 2012, Use of oral antidiabetic drugs (metformin and pioglitazone) in diabetic patients with breast cancer: how does it effect serum Hif-1 alpha and 8Ohdg levels? Asian Pac J Cancer Prev 13, 5143-5148. http://dx.doi.org/10.7314/APJCP.2012.13.10.5143.

      [10] Nishida N, Arizumi T, Takita M, Kitai S, Yada N, Hagiwara S, Inoue T, Minami Y, Ueshima K, Sakurai T, Kudo M 2013, Reactive oxygen species induce epigenetic instability through the formation of 8-hydroxydeoxyguanosine in human hepatocarcinogenesis. Dig Dis 31, 459-466. http://dx.doi.org/10.1159/000355245.

      [11] Kim JH, Moon JY, Park EY, Lee KH, Hong YC 2011, Changes in oxidative stress biomarker and gene expression levels in workers exposed to volatile organic compounds. Ind Health 49, 8-14. http://dx.doi.org/10.2486/indhealth.MS1112.

      [12] Lin MH, Liou SH, Chang CW, Huang IH, Strickland PT, Lai CH 2011, An engineering intervention resulting in improvement in lung function and change in urinary 8-hydroxydeoxyguanosine among foundry workers in Taiwan. International Archives of Occupational and Environmental Health 84, 175-183. http://dx.doi.org/10.1007/s00420-010-0580-9.

      [13] Wen S, Yang FX, Gong Y, Zhang XL, Hui Y, Li JG, Liu AL, Wu YN, Lu WQ, Xu Y 2008, Elevated levels of urinary 8-hydroxy-2'-deoxyguanosine in male electrical and electronic equipment dismantling workers exposed to high concentrations of polychlorinated dibenzo-p-dioxins and dibenzofurans, polybrominated diphenyl ethers, and polychlorinated biphenyls. Environmental Science & Technology 42, 4202-4207. http://dx.doi.org/10.1021/es800044m.

      [14] Zhang YT, Zheng QS, Pan J, Zheng RL 2004, Oxidative damage of biomolecules in mouse liver induced by morphine and protected by antioxidants. Basic & Clinical Pharmacology & Toxicology 95, 53-58. http://dx.doi.org/10.1111/j.1742-7843.2004.950202.x.

      [15] Karreman G, Isenberg I, Szent-Gyorgyi A 1959, on the mechanism of action of chlorpromazine. Science 130, 1191-1192. http://dx.doi.org/10.1126/science.130.3383.1191.

      [16] Shi X, Yao D, Gosnell BA, Chen C 2012, Lipidomic profiling reveals protective function of fatty acid oxidation in cocaine-induced hepatotoxicity. J Lipid Res 53, 2318-2330. http://dx.doi.org/10.1194/jlr.M027656.

      [17] Cunha-Oliveira T, Silva L, Silva AM, Moreno AJ, Oliveira CR, Santos MS 2013, Acute effects of cocaine, morphine and their combination on bioenergetic function and susceptibility to oxidative stress of rat liver mitochondria. Life Sci 92, 1157-1164. http://dx.doi.org/10.1016/j.lfs.2013.04.016.

      [18] Oztezcan S, Dogru-Abbasoglu S, Mutlu-Turkoglu U, Calay Z, Aykac-Toker G, Uysal M 2000, the role of stimulated lipid peroxidation and impaired calcium sequestration in the enhancement of cocaine induced hepatotoxicity by ethanol. Drug Alcohol Depend 58, 77-83. http://dx.doi.org/10.1016/S0376-8716(99)00061-7.

      [19] Vitcheva V 2012, Cocaine toxicity and hepatic oxidative stress. Curr Med Chem 19, 5677-5682. http://dx.doi.org/10.2174/092986712803988929.

      [20] Sharan N, Chong VZ, Nair VD, Mishra RK, Hayes RJ, Gardner EL 2003, Cocaine treatment increases expression of a 40 kDa catecholamine-regulated protein in discrete brain regions. Synapse 47, 33-44. http://dx.doi.org/10.1002/syn.10140.

      [21] Moritz F, Monteil C, Isabelle M, Bauer F, Renet S, Mulder P, Richard V, Thuillez C 2003, Role of reactive oxygen species in cocaine-induced cardiac dysfunction. Cardiovasc Res 59, 834-843. http://dx.doi.org/10.1016/S0008-6363(03)00499-1.

      [22] Vergeade A, Mulder P, Vendeville C, Ventura-Clapier R, Thuillez C, Monteil C 2012, Xanthine oxidase contributes to mitochondrial ROS generation in an experimental model of cocaine-induced diastolic dysfunction. J Cardiovasc Pharmacol 60, 538-543. http://dx.doi.org/10.1097/FJC.0b013e318271223c.

      [23] Kovacic P, Sacman A, Wu-Weis M 2002, Nephrotoxins: Widespread role of oxidative stress and electron transfer. Current Medicinal Chemistry 9, 823-847. http://dx.doi.org/10.2174/0929867024606803.

      [24] Valente MJ, Carvalho F, Bastos MD, de Pinho PG, Carvalho M 2012, Contribution of Oxidative Metabolism to Cocaine-Induced Liver and Kidney Damage. Current Medicinal Chemistry 19, 5601-5606. http://dx.doi.org/10.2174/092986712803988938.

      [25] Portugal-Cohen M, Numa R, Yaka R, Kohen R 2010, Cocaine induces oxidative damage to skin via xanthine oxidase and nitric oxide synthase. J Dermatol Sci 58, 105-112. http://dx.doi.org/10.1016/j.jdermsci.2010.03.010.

      [26] Molgo MN, Arriagada CE, Salomone CB, Vera CK, Giesen LF, Solar AG, Gonzalez SB 2014, [Skin necrosis: report of eleven cases]. Rev Med Chil 142, 118-124. http://dx.doi.org/10.4067/S0034-98872014000100019.

      [27] Menick FJ, Salibian A 2014, Primary intranasal lining injury cause, deformities, and treatment plan. Plast Reconstr Surg 134, 1045-1056. http://dx.doi.org/10.1097/PRS.0000000000000694.

      [28] Shawwa K, Alraiyes AH, Eisa N, Alraies MC 2013, Cocaine-induced leg ulceration. BMJ Case Rep 2013. http://dx.doi.org/10.1136/bcr-2013-200507.

      [29] Szabo C 2003, multiple pathways of peroxynitrite cytotoxicity. Toxicology Letters 140, 105-112. http://dx.doi.org/10.1016/S0378-4274(02)00507-6.

      [30] Isabelle M, Vergeade A, Moritz F, Dautreaux B, Henry JP, Lallemand F, Richard V, Mulder P, Thuillez C, Monteil C 2007, NADPH oxidase inhibition prevents cocaine-induced up-regulation of xanthine oxidoreductase and cardiac dysfunction. Journal of Molecular and Cellular Cardiology 42, 326-332. http://dx.doi.org/10.1016/j.yjmcc.2006.11.011.

      [31] Aoki K, Ohmori M, Takimoto M, Ota H, Yoshida T 1997, Cocaine-induced liver injury in mice is mediated by nitric oxide and reactive oxygen species. Eur J Pharmacol 336, 43-49. http://dx.doi.org/10.1016/S0014-2999(97)01230-2.

      [32] Ergaz Z, Avgil M, Ornoy A 2005, intrauterine growth restriction-etiology and consequences: what do we know about the human situation and experimental animal models? Reprod Toxicol 20, 301-322. http://dx.doi.org/10.1016/j.reprotox.2005.04.007.

      [33] Harris AL 2002, Hypoxia--a key regulatory factor in tumour growth. Nat Rev Cancer 2, 38-47. http://dx.doi.org/10.1038/nrc704.

      [34] Inaba Y, Koide S, Yokoyama K, Karube I 2011, Development of urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) measurement method combined with SPE. J Chromatogr Sci 49, 303-309. http://dx.doi.org/10.1093/chrsci/49.4.303.

      [35] Benzie IFF, Strain JJ 1996, the ferric reducing ability of plasma (FRAP) as a measure of ''antioxidant power'': The FRAP assay. Analytical Biochemistry 239, 70-76. http://dx.doi.org/10.1006/abio.1996.0292.

      [36] Spickett CM, Wiswedel I, Siems W, Zarkovic K, Zarkovic N 2010, Advances in methods for the determination of biologically relevant lipid peroxidation products. Free Radic Res 44, 1172-1202. http://dx.doi.org/10.3109/10715762.2010.498476.

      [37] Kloss MW, Rosen GM, Rauckman EJ 1984, Biotransformation of norcocaine to norcocaine nitroxide by rat brain microsomes. Psychopharmacology (Berl) 84, 221-224. http://dx.doi.org/10.1007/BF00427449.

      [38] Inoue S, Kawanishi S 1987, Hydroxyl Radical Production and Human DNA Damage Induced by Ferric Nitrilotriacetate and Hydrogen-Peroxide. Cancer Research 47, 6522-6527.

      [39] Devi BG, Chan AWK 1996, Cocaine-induced peroxidative stress in rat liver: Antioxidant enzymes and mitochondria. Journal of Pharmacology and Experimental Therapeutics 279, 359-366.

      [40] Badisa RB, Kumar SS, Mazzio E, Haughbrook RD, Allen JR, Davidson MW, Fitch-Pye CA, Goodman CB 2015, N-acetyl cysteine mitigates the acute effects of cocaine-induced toxicity in astroglia-like cells. PLoS One 10, e0114285. http://dx.doi.org/10.1371/journal.pone.0114285.

      [41] LaRowe SD, Mardikian P, Malcolm R, Myrick H, Kalivas P, McFarland K, Saladin M, McRae A, Brady K 2006, Safety and tolerability of N-acetylcysteine in cocaine-dependent individuals. Am J Addict 15, 105-110. http://dx.doi.org/10.1080/10550490500419169.

      [42] Javaid JI, Fischman MW, Schuster CR, Dekirmenjian H, Davis JM 1978, Cocaine plasma concentration: relation to physiological and subjective effects in humans. Science 202, 227-228. http://dx.doi.org/10.1126/science.694530.

      [43] Siegel RK 1982, Cocaine smoking. J Psychoactive Drugs 14, 271-359. http://dx.doi.org/10.1080/02791072.1982.10471937.

      [44] Yu RC, Lee TC, Wang TC, Li JH 1999, Genetic toxicity of cocaine. Carcinogenesis 20, 1193-1199. http://dx.doi.org/10.1093/carcin/20.7.1193.

      [45] Wieland P, Lauterburg BH 1995, Oxidation of mitochondrial proteins and DNA following administration of ethanol. Biochem Biophys Res Commun 213, 815-819. http://dx.doi.org/10.1006/bbrc.1995.2202.


 

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Article ID: 5970
 
DOI: 10.14419/ijpt.v4i2.5970




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