This Article Free Full Text (Free PDF) Free References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Soltaninejad, K Articles by Abdollahi, M Search for Related Content PubMed PubMed Citation Articles by Soltaninejad, K Articles by Abdollahi, M Social Bookmarking                   What's this?

Blood β-glucuronidase as a suitable biomarker at acute exposure of severe organophosphorus poisoning in human

Laboratory of Forensic Toxicology, Legal Medicine Organization, Tehran, Iran

S Shadnia

Toxicological Research Center, Loqman-Hakim Hospital, School of Medicine, Shaheed Beheshti University of Medical Sciences, Tehran, Iran

M Afkhami-Taghipour

Laboratory of Toxicology, Faculty of Phamacy, and Pharmaceutical Sciences Research Center, Tehran University of Medical Sciences, Tehran, Iran

R Saljooghi

Laboratory of Toxicology, Faculty of Phamacy, and Pharmaceutical Sciences Research Center, Tehran University of Medical Sciences, Tehran, Iran

A Mohammadirad

Laboratory of Toxicology, Faculty of Phamacy, and Pharmaceutical Sciences Research Center, Tehran University of Medical Sciences, Tehran, Iran

M Abdollahi

Laboratory of Toxicology, Faculty of Phamacy, and Pharmaceutical Sciences Research Center, Tehran University of Medical Sciences, Tehran, Iran

Organophosphorus compounds are known to cause the selective release of liver microsomal β-glucuronidase into plasma. Organophophoruses may induce nitrosative stress leading to the generation of nitrogen free radicals and alterations in scavengers of free radicals in many biological systems. In this study, we investigate how acute human organophosphorus intoxication is associated with changes of blood nitric oxide, total thiol molecules, and activities of the acetylcholinesterase and β-glucuronidase. A total of 21 acute organophosphorus-poisoned patients were recruited into study and were divided into two groups of mildly (13) and severely affected (9); 26 age-matched healthy volunteers were recruited as control group. Results indicated that both mildly and severely affected patients had lower acetylcholinesterase activities as compared to controls. The extent of acetylcholinesterase reduction in the severely affected patients was higher than that of mildly affected patients. A significant increase in serum β-glucuronidase was observed only in severely affected patients as compared to controls. Both mildly and severely affected patients had lower plasma total thiol molecules as compared to controls. The extent of reduction of total thiol molecules in the severely affected patients was higher than that of mildly affected patients. No significant difference was observed in plasma total nitric oxide of controls and patients. It is concluded that nitrosative stress has a minor role in toxicity of organophosphorus, whereas blood β-glucuronidase is very sensitive biomarker at high exposure of severe organophosphorus poisoning.

Key Words: β-glucuronidase • acute poisoning • biomarker • organophosphate

Human & Experimental Toxicology, Vol. 26, No. 12, 963-966 (2007)
DOI: 10.1177/0960327107085349


CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?