Mecanismo fisiológico de la Sensibilidad Química Múltiple.


La sensibilidad química múltiple (SQM), inducida por la pérdida de la tolerancia (GIRE), es una enfermedad iniciada por la exposición a químicos tóxicos, dando lugar a una lesión cerebral tóxica. El ciclo NO/ONOO- Citoquinas inflamatorias, óxido nítrico, estrés oxidativo.

“Los estudios epidemiológicos muestran que la SQM es una enfermedad increíblemente común, incluso más que la diabetes.Mi revisión de la literatura y otras investigaciones que he realizado durante los últimos once años muestra que el probable mecanismo central del SQM es un mecanismo bioquímico vicioso, conocido como el ciclo NO/ONOO-“.Martin L. Pall, Ph.D. [Noticia]

Multiple Chemical Sensitivity: Towards the End of Controversy
Martin L. Pall, Ph.D.
Professor of Biochemistry and Basic Medical Sciences
Washington State University
Pullman, WA 99164-4234 USA
509-335-1246
martin_pall@wsu.edu

El reciente estudio realizado por el grupo de investigación de Roma es significativo en lo que respecta a la teoría del ciclo NO/ONOO-, ya que muestra que hay tres elementos superiores en cantidad en pacientes de SQM (De Luca et al, Toxicología y Farmacología Aplicada, 2010, abril 27 Epub ahead of print). Esos elementos son las citoquinas inflamatorias, el óxido nítrico y el estrés oxidativo. Cada una de estas mediciones proporciona una confirmación importante del mecanismo propuesto por Pall para la afección.[Noticia]

Toxicol Appl Pharmacol. 2010 Nov 1;248(3):285-92. Epub 2010 Apr 27.
Biological definition of multiple chemical sensitivity from redox state and cytokine profiling and not from polymorphisms of xenobiotic-metabolizing enzymes.
De Luca C, Scordo MG, Cesareo E, Pastore S, Mariani S, Maiani G, Stancato A, Loreti B, Valacchi G, Lubrano C, Raskovic D, De Padova L, Genovesi G, Korkina LG.
Source

Laboratory of Tissue Engineering & Skin Pathophysiology, Dermatology Institute (IDI IRCCS), Rome, Italy.

Abstract

BACKGROUND:

Multiple chemical sensitivity (MCS) is a poorly clinically and biologically defined environment-associated syndrome. Although dysfunctions of phase I/phase II metabolizing enzymes and redox imbalance have been hypothesized, corresponding genetic and metabolic parameters in MCS have not been systematically examined.

OBJECTIVES:

We sought for genetic, immunological, and metabolic markers in MCS.

METHODS:

We genotyped patients with diagnosis of MCS, suspected MCS and Italian healthy controls for allelic variants of cytochrome P450 isoforms (CYP2C9, CYP2C19, CYP2D6, and CYP3A5), UDP-glucuronosyl transferase (UGT1A1), and glutathione S-transferases (GSTP1, GSTM1, and GSTT1). Erythrocyte membrane fatty acids, antioxidant (catalase, superoxide dismutase (SOD)) and glutathione metabolizing (GST, glutathione peroxidase (Gpx)) enzymes, whole blood chemiluminescence, total antioxidant capacity, levels of nitrites/nitrates, glutathione, HNE-protein adducts, and a wide spectrum of cytokines in the plasma were determined.

RESULTS:

Allele and genotype frequencies of CYPs, UGT, GSTM, GSTT, and GSTP were similar in the Italian MCS patients and in the control populations. The activities of erythrocyte catalase and GST were lower, whereas Gpx was higher than normal. Both reduced and oxidised glutathione were decreased, whereas nitrites/nitrates were increased in the MCS groups. The MCS fatty acid profile was shifted to saturated compartment and IFNgamma, IL-8, IL-10, MCP-1, PDGFbb, and VEGF were increased.

CONCLUSIONS:

Altered redox and cytokine patterns suggest inhibition of expression/activity of metabolizing and antioxidant enzymes in MCS. Metabolic parameters indicating accelerated lipid oxidation, increased nitric oxide production and glutathione depletion in combination with increased plasma inflammatory cytokines should be considered in biological definition and diagnosis of MCS.


Fuente: http://www.ncbi.nlm.nih.gov/pubmed/20430047 

Enlaces externos relacionados:
María José Moya padece SQM y es autora del blog Mi estrella de mar donde ofrece información y recursos ecológicos.

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