Document Detail


Cumene hydroperoxide debilitates macrophage physiology by inducing oxidative stress: possible protection by alpha-tocopherol.
MedLine Citation:
PMID:  19135433     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Macrophages, the major phagocytes of body, are largely dependent on membrane for their apposite functioning. Cum-OOH, a catalyst used in chemical and pharmaceutical industry, is a peroxidative agent, which may induce oxidative stress in macrophages hampering the integrity of their membrane. Alpha-tocopherol is known to protect the membrane from oxidative modulation and preserve its integrity. In the present study, we investigated the effect of Cum-OOH on physiology of macrophages and evaluated the protective effect of alpha-tocopherol against Cum-OOH-induced functional impairment. An in vitro exposure to 10-200 microM Cum-OOH altered redox balance of murine peritoneal macrophages and led to a severe physiological impairment. It markedly augmented the release of proinflammatory cytokines (tumor necrosis factor-alpha, interleukin-1beta and prostaglandin E(2)), lipopolysaccharide primed nitric oxide release and inducible nitric oxide synthase expression, and lysosomal hydrolases secretion. It mitigated respiratory burst and phagocytosis and intracellular killing of yeast (Saccharomyces cerevisiae). Mannose receptor, a major macrophage phagocytic receptor (also implicated in S. cerevisiae phagocytosis), exhibited a hampered recycling with its number being reduced to about 54% of the untreated, control cells following Cum-OOH exposure. A 24-h pretreatment of macrophages with 25 microM alpha-tocopherol preserved most of the assessed functions close to their corresponding control values. These data suggest that exposure to Cum-OOH may impair the physiology of immune cells such as macrophages and that supplementation with alpha-tocopherol can safeguard these cells against Cum-OOH toxicity.
Authors:
Gurpreet Kaur; M Sarwar Alam; Mohammad Athar
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-12-24
Journal Detail:
Title:  Chemico-biological interactions     Volume:  179     ISSN:  1872-7786     ISO Abbreviation:  Chem. Biol. Interact.     Publication Date:  2009 May 
Date Detail:
Created Date:  2009-03-24     Completed Date:  2009-05-06     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0227276     Medline TA:  Chem Biol Interact     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  94-102     Citation Subset:  IM    
Affiliation:
Department of Medical Elementology & Toxicology, Faculty of Science, Jamia Hamdard, Hamdard Nagar, New Delhi 110062, India.
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MeSH Terms
Descriptor/Qualifier:
Animals
Benzene Derivatives / antagonists & inhibitors,  pharmacology*
Dinoprostone / metabolism
Dose-Response Relationship, Drug
Glucuronidase / metabolism
Glutathione / analysis
Interleukin-1beta / metabolism
Lectins, C-Type / drug effects
Macrophages / drug effects*,  physiology
Male
Mannose-Binding Lectins / drug effects
Muramidase / metabolism
Oxidative Stress / drug effects*
Oxygen / metabolism
Phagocytosis / drug effects
Rats
Rats, Wistar
Receptors, Cell Surface / drug effects
Saccharomyces cerevisiae / drug effects
Tumor Necrosis Factor-alpha / metabolism
alpha-Tocopherol / pharmacology*
Chemical
Reg. No./Substance:
0/Benzene Derivatives; 0/Interleukin-1beta; 0/Lectins, C-Type; 0/Mannose-Binding Lectins; 0/Receptors, Cell Surface; 0/Tumor Necrosis Factor-alpha; 0/mannose receptor; 363-24-6/Dinoprostone; 59-02-9/alpha-Tocopherol; 70-18-8/Glutathione; 7782-44-7/Oxygen; 80-15-9/cumene hydroperoxide; EC 3.2.1.17/Muramidase; EC 3.2.1.31/Glucuronidase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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