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Abstract
1H-NMR metabolomics was used to investigate the changes of metabolites in the lungs of mice with and without being exposed to a controlled amount of cigarette smoke. It was found that the concentrations of adenosine derivatives (i.e. ATP, ADP and AMP), inosine and uridine were significantly changed in the lungs of mice exposed to cigarette smoke when compared with controls regardless the mice were obese or of regular weight. The decreased ATP, ADP, AMP and elevated inosine suggested that the deaminases in charge of adenosine derivatives to inosine derivatives conversion would be significantly changed in the lungs of mice exposed to cigarette smoke. Indeed, transcriptional study confirmed that the concentrations of adenosine monophosphate deaminase 2 and adenosine deaminase 2 were significantly changed in the lungs of mice exposed to cigarette smoke. We also found that the ratio of glycerophosphocholine (GPC) to phosphocholine (PC) was significantly increased in the lungs of obese mice compared with those of the regular weight mice. The GPC/PC ratio was further elevated in the lungs of obese group exposed to cigarette smoke.
Highlights
Exposure to cigarette smoke is one of the major risk factors inducing pulmonary and bronchial injury either through direct toxic effects or indirectly by initiating inflammatory responses [1]
Stimulated by the metabolomics findings from this work, we re-evaluated the trascriptomics data by focusing on the purine metabolism pathway, we found that the concentrations corresponding to adenosine deaminase (Adat2) and adenosine monophosphate deaminase 2 (Ampd2) were significantly altered in the lungs of mice exposed to smoke
The decreased ATP, ADP, adenosine monophosphate (AMP) and elevated inosine found in this study predicted that the deaminases in charge of adenosine derivatives to inosine derivatives conversion were altered in the lungs of mice exposed to cigarette smoke
Summary
Exposure to cigarette smoke is one of the major risk factors inducing pulmonary and bronchial injury either through direct toxic effects or indirectly by initiating inflammatory responses [1]. Smoke increases the risk of infections, including structural changes in the respiratory tract such as mucosal permeability and decrease in immune response, and is a substantial risk factor for important bacterial and viral infections, which is believed to pivotal to progressions of cancer, heart disease, and chronic obstructive pulmonary disease (COPD), etc [5,6]. Obesity is a metabolic disorder associating with the development of metabolic syndrome, including hyperlipidemia, insulin resistance and type 2 diabetes, that affects one third of adults and one fifth of children in the United States, as well as 300 million adults worldwide according to the World Health Organization's report [7,8].
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