Influence of smoking and free radicals on antioxidant defence and on the pathogenesis of certain diseases

Česká verzia

Authors: V. Holeček ¹; R. Rokyta ²
Authors place of work: Oddělení klinické biochemie a hematologie Mulačova nemocnice s. r. o., Plzeň Přednosta: prim. MUDr. Štěpánka Sobotová ¹; Ústav normální, patologické a klinické fyziologie 3. lékařská fakulta UK, Praha Přednosta: prof. MUDr. Richard Rokyta, DrSc. ²
Published in the journal: Prakt. Lék. 2008; 88(1): 22-30
Category: Postgraduální vzdělávání

Summary

Cigarette smoke leads to the production of a large number of different free radicals, especially superoxide, alkoxy- and alkyl- radicals and free hydroxyl radicals. Antioxidant defence must be complex, i.e. a mixture of different substances. Smoking injures intracellular antioxidant balance, decreases the levels of glutathione, ascorbic acid, glutathione peroxidase and catalase. β-carotene, lutein, zeaxanthin and others are decreased in the extracellular fluid. The most dangerous complications of smoking in the respiratory pathways are inflammatory reactions, proliferation of cells, carcinoma cells, emphysema, and chronic obstructive pulmonary disease. Decrease of antioxidants, increase of asymmetric dimethylarginine, of lipoperoxidation, of endothelin and peroxynitrite are the most important laboratory findings of damage. Another complication is endothelial dysfunction. Nitric oxide production is decreased, as is the dilatation of vessels; apoptosis of endothelial cells is increased, and the differentiation and function of endothelial cells is impaired. There are many causes for the acceleration of atherosclerosis, but oxidative stress is one of the most dangerous. Oxidated and altered LDL-cholesterol contributes to the formation of foam cells. Activated myeloperoxidase produces hypochloric acid, the substrate for which is not only hydrogen peroxide, but also thiocyanate from tobacco. Free radicals oxidate and mutate DNA leading to an increased incidence of carcinomas. Free radicals and reactive oxygen species decrease the fertility of spermatozoa, and in pregnancy can damage the development of the foetus, they also encourage the origin of neurological and psychiatric diseases (Parkinson’s disease, Alzheimer’s disease, hemodynamic and inflammatory diseases of the brain, they evoke the pain etc.). Macular degeneration of the eyes, certain dental, gastrointestinal, renal, orthopaedic and skin diseases, and damage to cochlear epithelial cells due to noise are some of other possibilities of damage due to cigarette smoke.

Key words:
smoking, free radicals, antioxidants, oxidative stress, diseases induced by cigarette smoke.

Zdroje

1. Baginski, T.K., Dabbagh, K., Satjawat-charaphong, C. Cigarette smoke synergistically enhance respiratory mucin induction by proinflammatory stimuli. Am. J. Respir. Cell Mol. Biol. 2006, 35, 2, p. 165-174.

2. Baglole, C.J., Bushinsky, S.M., Garcia, T.M. et al. Different induction of apoptosis by cigarette smoke extrakt in primary human lung fibroblast strains: implications for emphysema. Am. J. Physiol. Lung. Cell Mol. Physiol. 2006, 291, 1, p. 19-29.

3. Das, U. A radical approach to cancer. Med. Sci. Monit. 2002, 8, 4, p. 79-92.

4. Fazol, L., Gulian, J.M., Dalmasso, C. et al. Antioxidant status - of neonates exposed in utero to tobacco smoke. Biol. Neonate 2005, 87, 2, p. 121-126.

5. Fracasso, M.E., Doria, D., Franceschettin P. et al. DNA damage and repair capacity by comet assay in lymphocytes of white-collar active smokers and passive smokers (non- and ex-smokers) at workplace. Toxicol. Lett. 2006, 167, 2, p. 131-141.

6. Hanna, S.T. Nicotine effect on cardiovascular system and ion channels. J. Cardiovasc. Pharmacol. 2006, 47, 3, p. 348-358.

7. Hemalatha, A., Venkatesan, A., Bobby, Z. et al. Antioxidant response to oxidative stress induced by smoking. Indian. J. Physiol. Pharmacol. 2006, 50, 4, p. 416-420.

8. Churg, A. Interactions of endogenous or evoked agents and particles: the role of reactive oxygen species. Free Radic. Biol. Med. 2003, 34, 10, p. 1230-1235.

9. Lang, C.A., Mills, B.J., Lang, H.L. High blood glutathione levels accompany excellent physical and mental health in women ages 60-103 years. J. Lab. Clin. Med. 2002, 140, p. 413-417.

10. Orosz, Z., Csiszar, A., Labinsky, N. et al. Cigarette smoke-induced proinflammatory alterations in the endothelial phenotype: role of NAD(P)H oxidase activation. Am. J. Physiol. Heart Circ. Physiol. 2007, 292, 1, p. 130-139.

11. Palozza, P., Serini, S., Trombino, S. et al. Dual role of beta-carotene in combination with cigarette smoke aqueous extract on the formation of mutagenic lipid peroxidation products in lung membrane: dependence on pO2. Carcinogenesis 2006, 27, 12, p. 2383-2391.

12. Rahman, M.M., Elami, S., Chang, T.K. et al. Increased vascular contractility in isolated vessels from cigarette smoking rats is mediated by basal endothelin release. Vascul. Pharmacol. 2007, 46, 1, p. 35-42.

13. Saleh, R.A., Agarwal, A., Sharma, R.K. et al. Effect of cigarette smoking on levels of seminal oxidative stress in infertile men: a prospective study. Fertil. Steril. 2002, 78(3): p. 491-499.

14 Stavrides J.C. Lung carcinogenesis: Pivotal role of metals in tobacco smoke. Free Rad. Biol. Med. 2006, 41, p. 1017-1030.

15. Valavanidis, A., Haralambous, E. A comparative study by electron paramagnetic resonance of free radical species in the mainstream and sidestream smoke of cigarettes with conventional acetate filters and „bio-filters“. Redox Rep. 2001, 6, 3, p. 161-171.

16. Zalba, G., Beloqui, O., San José, G. et al. NADPH oxidase-dependent superoxide production is associated with carotid intima-media thickness in subjects free of clinical atherosclerotic disease. Arterioscler. Tromb. Vasc. Biol. 2005, 25, 7, p. 1452-1457.

17. Zhang, W.Z., Venardos, K., Chin-Dusting, J. et al. Adverse effects of cigarette smoke on NO bioavailability: role of arginine metabolism and oxidative stress. Hypertension 2006, 48, 2, p. 278-285.

18. Zheng, J.Y., Cao, Y.X., Xu, C.B. et al. Lipid-soluble smoke particles damage endothelial cells and redukce endothelium-dependent dilatation in rat and man. BMC Cardiovasc. Disorders. 2006, 19, 6, p. 3.