Effects of cigarette smoke exposure on serum 5-HT levels in rats

Abstract

RATIONALE: Chronic obstructive pulmonary disease (COPD) is characterized by airway limitation together with abnormal inflammation in the lung. One of the major causes of this disease is cigarette smoke (CS). Increased systemic serotonin (5-HT) level in non-smokers after inhaling CS (Clin Investig 1992;70:201-204) and the association of the genetic polymorphism of 5-HT transporter with pulmonary hypertension in COPD (Respiration 2010; 79:288-295), point towards a role of serotonin in COPD. This study was to investigate circulating 5-HT levels in comparison to levels of oxidative stress in an in vivo experimental rat model after CS exposure. METHODS: Sprague-Dawley rats were randomly divided into 2 groups, i.e. sham air (SA) and 4% CS for 56 days. Exposure to SA or 4% CS was performed for 1h/day in the ventilated smoking chamber. The animals were sacrificed 24h after last exposure. Serum was collected and analyzed for 5-HT levels by HPLC, markers of oxidative stress such as 8-isoprostane by ELISA and advanced oxidation protein product (AOPP) by kinetic assay. RESULTS: CS exposure elevated serum 5-HT (5.4 ± 1.5 μg/ml versus 10.6 ± 1.3 μg/ml, p = 0.03) and serum 8-isoprostane (507.9 ± 98.4 pg/ml versus 940.8 ± 92.5 pg/ml, p = 0.02) in comparison to SA exposure. In contrast, serum AOPP level was significantly lower in CS-exposed group compared to SA-exposed group (28.2 ± 3.9 μM versus 20.8 ± 2.7 μM, p = 0.04). Conclusion: We revealed that smoking exposure was associated with high levels of 5-HT and 8-isoprostane but low level of AOPP. The present finding may provide evidence of the importance of a causal relationship between smoking and 5-HT concentrations. Further studies will be required to elucidate the mechanism of CS on how 5-HT interfere oxidative stress in circulation and in lung.