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Effect of Cigarette Smoking on the Oxidant/Antioxidant Balance in Healthy Subjects

Chávez, Jennifier MD1; Cano, Clímaco PhD2*; Souki, Aida MgSc2; Bermúdez, Valmore MD2; Medina, Mayerlim MD2; Ciszek, Ana MD2; Amell, Anilsa MD2; Vargas, Maria E MD2; Reyna, Nadia MgSc2; Toledo, Abdon MD2; Cano, Raquel MD2; Suárez, Gustavo MD1; Contreras, Freddy MD3; Israili, Zafar H PhD4; Hernández-Hernández, Rafael MD5; Valasco, Manuel MD3

American Journal of Therapeutics: March-April 2007 - Volume 14 - Issue 2 - p 189-193
doi: 10.1097/01.psp.0000249918.19016.f6
Original Article

Background and Purpose: Cigarette smoking has been associated with the development of cardiovascular disease and cancer. Even though the molecular mechanism(s) are not clear, the pathology has been related to oxygen free radicals present in cigarette smoke. Thus, the main objective of this study was to establish the changes in the oxidation/antioxidation balance induced by cigarette smoking.

Methods: Thirty healthy subjects (15 smokers and 15 nonsmokers) of both sexes were studied. The smokers group had smoked a mean of 14 cigarettes per day for an average of 4.5 years. Fasting serum levels of malondialdehyde (MDA), a marker of oxidative stress, nitric oxide (NO), reduced glutathione (GSH), and vitamin C (ascorbic and dehydroascorbic acids) were measured.

Results: Fasting NO concentration was significantly higher in smokers (51.3 ± 5.3 μM) than in nonsmokers (35.2 ± 4.8 μM, P < 0.05). The smokers had significantly higher serum dehydroascorbic acid levels (2.4 ± 0.5 mg/dL, P < 0.03) than the nonsmokers (1.08 ± 0.08 mg/dL). No significant differences were observed in the levels of ascorbic acid, MDA, and GSH between the smokers and nonsmokers.

Conclusions: Our results suggest that exposure to cigarette smoke increases NO synthesis, such that NO may act in a compensatory way as an inhibitor of lipid peroxidation. Smoking also activates other antioxidative mechanisms such as involving vitamin C. These protective mechanisms appear to be enough in preventing accumulation of oxidative products such as MDA and avoiding oxidative damage.

From the 1Physiology Department, School of Medicine, University of Zulia, Maracaibo, Venezuela; 2Center of Endocrine and Metabolic Research, University of Zulia. School of Medicine, Maracaibo, Venezuela; 3Unidad de Farmacología Clínica, Escuela de Medicina Vargas, La Universidad Central de Venezuela, Caracas, Venezuela; 4Department of Medicine, Emory University School of Medicine, Atlanta, GA; and 5Clinical Pharmacology Unit and Hypertension Clinic, School of Medicine, Universidad Centroccidental “Lisandro Alvarado,” Barquisimeto, Estado Lara, Venezuela.

*Address for correspondence: Facultad de Medicina, Universidad del Zulia, Centro Endocrino-Metabólico (1er piso Frente a la Biblioteca). E-mail:

© 2007 Lippincott Williams & Wilkins, Inc.