Formaldehyde is an important chemical used widely by industry in numerous household products. Therefore, when room ventilation is inadequate, formaldehyde may stagnate in rooms and adversely affect the health of inhabitants. Exposure to formaldehyde in living space has been found to be associated with asthma and 'sick house syndrome' (health disturbances induced by chemical contaminants in domestic environments). In addition, formaldehyde exposure among medical students and teachers who dissect cadavers in the gross anatomy laboratory likely causes a health problem. Avoidance of formaldehyde exposure can reduce the incidence and severity of ill-health conditions, although the ability of low concentrations of formaldehyde to trigger mechanisms contributing to them is still debated. Setting appropriate exposure limits for formaldehyde as an indoor environmental pollutant requires further quantitative and predictive evaluation of its health effects.
"Furthermore, formaldehyde has strong carcinogenic effects on human . In the past, formaldehyde was classified mostly as a compound from extraneous contamination . But recent investigations showed that in vivo methylamine can be catalyzed into formaldehyde by semicarbazide-sensitive amine oxidase , . "
[Show abstract][Hide abstract] ABSTRACT: Background
Recent studies suggest that formaldehyde (FA) could be synthesized endogeneously and transient receptor potential (TRP) channel might be the sensor of FA. However, the physiological significance is still unclear.
The present study investigated the FA induced epithelial Cl- secretion by activation of TRPV-1 channel located in the nerve ending fiber. Exogenously applied FA induced an increase of ISC in intact rat trachea tissue but not in the primary cultured epithelial cells. Western blot and immunofluorescence analysis identified TRPV-1 expression in rat tracheal nerve ending. Capsazepine (CAZ), a TRPV-1 specific antagonist significantly blocked the ISC induced by FA. The TRPV-1 agonist capsaicin (Cap) induced an increase of ISC, which was similar to the ISC induced by FA. L-703606, an NK-1 specific inhibitor and propranolol, an adrenalin β receptor inhibitor significantly abolished the ISC induced by FA or Cap. In the ion substitute analysis, FA could not induce ISC in the absence of extracelluar Cl-. The ISC induced by FA could be blocked by the non-specific Cl- channel inhibitor DPC and the CFTR specific inhibitor CFTRi-172, but not by the Ca2+-activated Cl- channel inhibitor DIDS. Furthermore, both forskolin, an agonist of adenylate cyclase (AC) and MDL-12330A, an antagonist of AC could block FA-induced ISC.
Our results suggest that FA-induced epithelial ISC response is mediated by nerve, involving the activation of TRPV-1 and release of adrenalin as well as substance P.
PLoS ONE 01/2013; 8(1):e54494. DOI:10.1371/journal.pone.0054494 · 3.23 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: A literature review was conducted in order to give an update on data regarding the various factors involved in the pathogenesis of allergic rhinitis and asthma. Preventive strategies are also discussed.
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