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Article: The involvement of serotonin metabolism in cigarette smoke-induced oxidative stress in rat lung in vivo

TitleThe involvement of serotonin metabolism in cigarette smoke-induced oxidative stress in rat lung in vivo
Authors
Issue Date2012
Citation
Free Radic. Res., 2012, v. 46, p. 1413-1419 How to Cite?
AbstractRecently, we have reported the dysregulation of circulating serotonin (5-hydroxytryptamine, 5-HT) homeostasis in patients with chronic obstructive pulmonary disease (COPD). An increase in metabolism of 5-HT has been reported to induce oxidative stress via monoamine oxidase (MAO)-dependent pathway. The present study aimed at investigating the effect of cigarette smoke exposure on the systemic circulation and local airway 5-HT levels as well as MAO-mediated oxidative pathway using a cigarette smoke-exposed rat model. Male Sprague-Dawley rats (150–200 g) were exposed to either sham air or 4% (v/v, smoke/air) cigarette smoke for 1 hour daily for 56 consecutive days. Sera, bronchoalveolar larvage (BAL) and lung tissues were collected 24 hours after the last exposure. We found a significant reduction in the reduced glutathione (rGSH) and an elevation in advanced oxidation protein products (AOPP), a protein oxidation marker, in the lung of cigarette smoke-exposed group (p < 0.05). A significant increase in 5-HT was found in serum (p < 0.05), but not in the BAL or lung, after cigarette smoke exposure. MAO-A activity was significantly elevated in the lung of cigarette smoke-exposed group (p < 0.05). Furthermore, increased superoxide anion levels were found in lung homogenates of cigarette smoke-exposed rats after incubation with 5-HT (p < 0.05), which was positively associated with the increase in MAO-A activity (r = 0.639, p < 0.05). Our findings supported the presence of GSH disruption and protein oxidation in the lung after cigarette smoke exposure. The metabolism of 5-HT by MAO-A in the lung enhanced cigarette smoke-induced superoxides, which might contribute to the pathogenesis of COPD. Read More: http://informahealthcare.com/doi/abs/10.3109/10715762.2012.721928
Persistent Identifierhttp://hdl.handle.net/10722/186064
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLAU, KWen_US
dc.contributor.authorLI, Xen_US
dc.contributor.authorYeung, SCen_US
dc.contributor.authorCHAN, KHen_US
dc.contributor.authorIp, MSMen_US
dc.contributor.authorMak, JCWen_US
dc.date.accessioned2013-08-20T11:50:27Z-
dc.date.available2013-08-20T11:50:27Z-
dc.date.issued2012en_US
dc.identifier.citationFree Radic. Res., 2012, v. 46, p. 1413-1419en_US
dc.identifier.urihttp://hdl.handle.net/10722/186064-
dc.description.abstractRecently, we have reported the dysregulation of circulating serotonin (5-hydroxytryptamine, 5-HT) homeostasis in patients with chronic obstructive pulmonary disease (COPD). An increase in metabolism of 5-HT has been reported to induce oxidative stress via monoamine oxidase (MAO)-dependent pathway. The present study aimed at investigating the effect of cigarette smoke exposure on the systemic circulation and local airway 5-HT levels as well as MAO-mediated oxidative pathway using a cigarette smoke-exposed rat model. Male Sprague-Dawley rats (150–200 g) were exposed to either sham air or 4% (v/v, smoke/air) cigarette smoke for 1 hour daily for 56 consecutive days. Sera, bronchoalveolar larvage (BAL) and lung tissues were collected 24 hours after the last exposure. We found a significant reduction in the reduced glutathione (rGSH) and an elevation in advanced oxidation protein products (AOPP), a protein oxidation marker, in the lung of cigarette smoke-exposed group (p < 0.05). A significant increase in 5-HT was found in serum (p < 0.05), but not in the BAL or lung, after cigarette smoke exposure. MAO-A activity was significantly elevated in the lung of cigarette smoke-exposed group (p < 0.05). Furthermore, increased superoxide anion levels were found in lung homogenates of cigarette smoke-exposed rats after incubation with 5-HT (p < 0.05), which was positively associated with the increase in MAO-A activity (r = 0.639, p < 0.05). Our findings supported the presence of GSH disruption and protein oxidation in the lung after cigarette smoke exposure. The metabolism of 5-HT by MAO-A in the lung enhanced cigarette smoke-induced superoxides, which might contribute to the pathogenesis of COPD. Read More: http://informahealthcare.com/doi/abs/10.3109/10715762.2012.721928-
dc.languageengen_US
dc.relation.ispartofFree Radic. Res.en_US
dc.titleThe involvement of serotonin metabolism in cigarette smoke-induced oxidative stress in rat lung in vivoen_US
dc.typeArticleen_US
dc.identifier.emailYeung, SC: flag@hkucc.hku.hken_US
dc.identifier.emailIp, MSM: msmip@hku.hken_US
dc.identifier.emailMak, JCW: judymak@hku.hken_US
dc.identifier.authorityIp, MSM=rp00347en_US
dc.identifier.authorityMak, JCW=rp00352en_US
dc.identifier.doi10.3109/10715762.2012.721928-
dc.identifier.pmid22900927-
dc.identifier.hkuros220856en_US
dc.identifier.volume46en_US
dc.identifier.spage1413en_US
dc.identifier.epage1419en_US
dc.identifier.isiWOS:000309937700011-

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