23-May-2013
09:03:07 IST
|
NISCAIR ONLINE PERIODICALS REPOSITORY (NOPR) >
NISCAIR PUBLICATIONS >
Research Journals >
Indian Journal of Experimental Biology (IJEB) >
IJEB Vol.48 [2010] >
IJEB Vol.48(07) [July 2010] >
| Title: | Idiopathic environmental intolerances (IEI): From molecular epidemiology to molecular medicine |
| Authors: | Luca, C De
Scordo, G
Cesareo, E
Raskovic, D
Genovesi, G
Korkina, L |
| Keywords: | Antioxidants
Chelators
Genetic polymorphism
Idiopathic environmental intolerances
Redox imbalance |
| Issue Date: | Jul-2010 |
| Publisher: | CSIR |
| Abstract: | Inherited or acquired impairment of
xenobiotics metabolism is a postulated mechanism underlying
environment-associated pathologies such as multiple chemical sensitivity,
fibromyalgia, chronic fatigue syndrome, dental amalgam disease, and others,
also collectively named idiopathic environmental intolerances (IEI). In view of
the poor current knowledge of their etiology and pathogenesis, and the absence
of recognised genetic and metabolic markers of the diseases. They are often
considered “medically unexplained syndromes”,. These disabling conditions share
the features of poly-symptomatic multi-organ syndromes, considered by part of
the medical community to be aberrant responses triggered by exposure to
low-dose organic and inorganic chemicals and metals, in concentrations far below
average reference levels admitted for environmental toxicants. A genetic
predisposition to altered biotransformation of environmental chemicals, drugs,
and metals, and of endogenous low-molecular weight metabolites, caused by
polymorphisms of genes coding for xenobiotic metabolizing enzymes, their
receptors and transcription factors appears to be involved in the
susceptibility to these environment-associated pathologies, along with
epigenetic factors. Free radical/antioxidant homeostasis may also be heavily
implicated, indirectly by affecting the regulation of xenobiotic metabolizing
enzymes, and directly by causing increased levels of oxidative products,
implicated in the chronic damage of cells and tissues, which is in part
correlated with clinical symptoms. More systematic studies of molecular
epidemiology, toxico- and pharmaco-genomics, elucidating the mechanisms of
regulation, expression, induction, and activity of antioxidant/detoxifying
enzymes, and the possible role of inflammatory mediators, promise a better
understanding of this pathologically increased sensitivity to low-level
chemical stimuli, and a solid basis for effective individualized antioxidant-
and/or chelator-based treatments. |
| Page(s): | 625-635 |
| ISSN: | 0975-1009 (Online); 0019-5189 (Print) |
| Source: | IJEB Vol.48(07) [July 2010]
|
|
