Short-Term Systemic Effects of Nose-Only Cigarette Smoke Exposure in Mice: Role of Oxidative Stress

• Published in: Cellular physiology and biochemistry Vol. 31; no. 1; pp. 15 - 24
• Main Authors: Nemmar, Abderrahim, Raza, Haider, Subramaniyan, Deepa, Yasin, Javed, John, Annie, Ali, Badreldin H., Kazzam, Elsadig E.
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland Cell Physiol Biochem Press GmbH & Co KG 01.01.2013
• Subjects: Alanine Transaminase - blood; Animals; Blood Platelets - cytology; Blood Pressure - physiology; Cigarette smoke; Creatinine - blood; Disease Models, Animal; Erythrocyte Count; Erythrocytes - cytology; gamma-Glutamyltransferase - blood; Kidney - enzymology; Kidney - metabolism; Lipid Peroxidation; Liver - enzymology; Liver - metabolism; Liver enzymes; Mice; Mice, Inbred BALB C; Myocardium - enzymology; Myocardium - metabolism; Nasal Mucosa - metabolism; Nitric Oxide - blood; Nose-only exposure, short-term exposure; Original Paper; Oxidative stress; Oxidative Stress - physiology; Platelet Count; Reactive Oxygen Species - metabolism; Smoking; Superoxide Dismutase - metabolism; Systolic blood pressure; Thrombosis; Thrombosis - metabolism; Thrombosis - pathology; Urea - blood; Systolic blood pressure; Oxidative stress; Liver enzymes; Thrombosis; Cigarette smoke; Nose-only exposure, short-term exposure
• ISSN: 1015-8987; 1421-9778
• DOI: 10.1159/000343345

Background/Aims: Long–term cigarette smoking (CS) is a major risk factor for respiratory and cardiovascular diseases, and is also known to adversely affect other organs. However, data on the systemic effects of short-term CS exposure (STCSE) are scarce. Presently, using a nose-only exposure system, we evaluated the systemic effects of STCSE in mice. Methods: We assessed the effects of CS generated by 9 consecutive cigarettes per day for 4 days in a nose-only exposure system on cardiovascular, hepatic and renal endpoints evaluated on day 5 in mice. Control mice were exposed to air only. Results: CS significantly increased systolic blood pressure and decreased total nitric oxide plasma concentration. Circulating platelets and erythrocyte numbers were also increased. However, STCSE did not significantly increase thrombosis in pial arterioles and venules. STCSE significantly raised plasma alanine aminotransferase and gamma glutamyl transpeptidase activities, but did not affect urea or creatinine concentrations. Interestingly, while STCSE enhanced the production of reactive oxygen species in heart and kidney and lipid peroxidation in heart, liver and kidneys, it also enhanced the antioxidant activity of superoxide dismutase, probably indicating that STCSE causes adaptive reactions to counterbalance the potentially damaging action of oxygen radicals induced by STCSE. Conclusion: These results suggest that STCSE causes blood pressure increase, hepatotoxicity and oxidative stress in the heart, liver and the kidneys. These data provide information on the initial steps leading to the systemic effects of STCSE, a stage at which the diseases may likely be reversed.