Bedoukian   RussellIPM   RussellIPM   Piezoelectric Micro-Sprayer


Home
Animal Taxa
Plant Taxa
Semiochemicals
Floral Compounds
Semiochemical Detail
Semiochemicals & Taxa
Synthesis
Control
Invasive spp.
References

Abstract

Guide

Alphascents
Pherobio
InsectScience
E-Econex
Counterpart-Semiochemicals
Print
Email to a Friend
Kindly Donate for The Pherobase

« Previous AbstractInduced responses in clover to an herbaceous mite    Next AbstractN-acylhomoserine-lactone-mediated communication between Pseudomonas aeruginosa and Burkholderia cepacia in mixed biofilms »

GMS Curr Top Otorhinolaryngol Head Neck Surg


Title:Cellular and molecular mechanisms in environmental and occupational inhalation toxicology
Author(s):Riechelmann H;
Address:"Department of Otorhinolaryngology, University of Ulm, Germany"
Journal Title:GMS Curr Top Otorhinolaryngol Head Neck Surg
Year:2004
Volume:20041228
Issue:
Page Number:Doc02 -
DOI:
ISSN/ISBN:1865-1011 (Print) 1865-1011 (Electronic) 1865-1011 (Linking)
Abstract:"The central issue of this review are inflammatory changes that take place in the mucous membranes of the respiratory tract as a result of inhaled pollutants. Of particular relevance are dusts, SO(2), ozone, aldehydes und volatile organic compounds. Bioorganic pollutants, especially fragments of bacteria and fungi, occur predominantly in indoor dusts. They activate the toll-like/IL-1 receptor and lead to the activation of the transcription factor NF-kappaB for the release of numerous proinflammatory cytokines. Metals are predominant in ambient air dust particles. They induce the release of reactive oxygen species that cause damage to lipids, proteins and the DNA of the cell. As well as NF-kappaB, transcription factors that foster proliferation are activated via stress activated protein kinases. Organic compounds such as polycyclic aromatic hydrocarbons and nitroso-compounds of incomplete combustion processes activate additional via the cytosolic arylhydrocarbon receptor for detoxification enzymes. Sulphur dioxide leads to acid stress, and ozone to oxidative stress of the cell. This is accompanied by the release of proinflammatory cytokines via stress activated protein kinases. Aldehydes and volatile organic compounds activate the vanilloid receptor of trigeminal nerve fibres and induce a hyperreactivity of the mucous membrane via the release of nerve growth factors. The mechanisms described work synergistically and lead to a chronic inflammatory reaction of the mucous membranes of the upper respiratory tract that is regularly demonstrable in inhabitants of western industrial nations. It is unclear whether we are dealing here with a physiological inflammation or with an at least partially avoidable result of chronic pollutant exposure"
Keywords:cell membrane receptors endotoxins metals nitrogen monoxide polycyclic aromatic hydrocarbons reactive oxygen species respiratory mucous membrane signal transduction toxicology transcription factors;
Notes:"PubMed-not-MEDLINERiechelmann, Herbert eng Germany 2004/01/01 GMS Curr Top Otorhinolaryngol Head Neck Surg. 2004; 3:Doc02. Epub 2004 Dec 28"

 
Back to top
 
Citation: El-Sayed AM 2024. The Pherobase: Database of Pheromones and Semiochemicals. <http://www.pherobase.com>.
© 2003-2024 The Pherobase - Extensive Database of Pheromones and Semiochemicals. Ashraf M. El-Sayed.
Page created on 22-11-2024