|
Sign In to gain access to subscriptions and/or personal tools.
|
Blood β-glucuronidase as a suitable biomarker at acute exposure of severe organophosphorus poisoning in human
K Soltaninejad
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
References
- 1 Milatovic DGupta RCAschner M. Anticholinesterase toxicity and oxidative stress. Scientific World Journal 2006; 6: 295 – 310 .[Medline]
[Order article via Infotrieve]
- 2 Abdollahi MRanjbar AShadnia SNikfar SRezaiee A. Pesticides and oxidative stress: a review. Med Sci Monit 2004; 10: RA144–RA147.
- 3 Khurana DPrabhakar S. Organophosphorous intoxication. Arch Neurol 2000; 57: 600 – 602 .[Free Full Text]
- 4 Nigg HNKnaak JB. Blood cholinesterase as human biomarkers of organophosphorus pesticide exposure. Rev Environ Contam Toxicol 2000; 163: 29 – 111 .[Web of Science][Medline]
[Order article via Infotrieve]
- 5 Banerjee BDSeth VBhattacharya APasha STChakraborty AK. Biochemical effects of some pesticides on lipid peroxidation and free-radical scavengers. Toxicol Lett 1999; 107: 33 – 47 .[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- 6 Ranjbar APasalar PAbdollahi M. Induction of oxidative stress and acetylcholinesterase inhibition in organophosphorous pesticide manufacturing workers. Hum Exp Toxicol 2002; 21: 179 – 182 .[Abstract/Free Full Text]
- 7 Akhgari MAbdollahi MKebryaeezadeh AHosseini RSabzevari O. Biochemical evidence for free radical-induced lipid peroxidation as a mechanism for subchronic toxicity of malathion in blood and liver of rats. Hum Exp Toxicol 2003; 22: 205 – 211 .[Abstract/Free Full Text]
- 8 Chan JYChan SHChang AY. Differential contributions of NOS isoforms in the rostral ventrolateral medulla to cardiovascular responses associated with mevinphos intoxication in the rat. Neuropharmacology 2004; 46: 1184 – 1194 .[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- 9 Casares FMMantione K. Pesticides may be alterating constitutive nitric oxide release, thereby compromising health. Med Sci Monit 2006; 12: RA235 – RA240 .[Web of Science][Medline]
[Order article via Infotrieve]
- 10 Satoh T. Release of liver microsomal beta-glucuronidase from hepatocytes in vitro and in vivo by organophosphates and hepatotoxic agents. J Toxicol Sci 1991; Suppl. 1: 133 – 142 .
- 11 Satoh TSuzuki SKawai NNakamura THosokawa M. Toxicological significance in the cleavage of esterase–beta-glucuronidase complex in liver microsomes by organophosphorus compounds. Chem Biol Interact 1999; 119–120: 471 – 478 .
- 12 Inayat-Hussain SHLubis SHSakian NIGhazali ARAli NSEl Sersi M. Is plasma beta-glucuronidase a novel human biomarker for monitoring anticholinesterase pesticides exposure? A Malaysian experience. Toxicol Appl Pharmacol 2007; 219: 210 – 216 .[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- 13 Fujikawa YSatoh TSuganuma ASuzuki SNiikura YYui S. Extremely sensitive biomarker of acute organophosphorus insecticide exposure. Hum Exp Toxicol 2005; 24: 333 – 336 .[Abstract/Free Full Text]
- 14 George PMAbernety MH. Improved Ellman procedure for erythrocyte cholinesterase. Clin Chem 1983; 29: 365 – 368 .[Abstract/Free Full Text]
- 15 Goldstein G. Serum beta-glucuronidase assay by the phenolphthalein mono-beta-glucuronide method. Clin Chem 1961; 7: 136 – 142 .[Abstract]
- 16 Griess Reagent System. Instruction for product G2930. USA : Promega; 2005.
- 17 Hu MLDillaerd CJ. Plasma SH and GSH measurment. Method Enzymol 1994; 233: 35 – 37 .
- 18 Abdollahi MMostafalou SPournormohammadi SShadnia S. Oxidative stress and cholinesterase inhibition in saliva and plasma of rats following subchronic exposure to malathion. Comp Biochem Physiol C Toxicol Pharmacol 2004; 137: 29 – 34 .[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- 19 Teimouri FAmirkabirian NEsmaily HMohammadirad AAliahmadi AAbdollahi M. Alteration of hepatic cells glucose metabolism as a non-cholinergic detoxification mechanism in counteracting diazinon-induced oxidative stress. Hum Exp Toxicol 2006; 25: 697 – 703 .[Abstract/Free Full Text]
- 20 Poovala VSKanji VKTachikawa HSalahudeen AK. Role of oxidant stress and antioxidant protection in acephate-induced renal tubular cytotoxicity. Toxicol Sci 1998; 46: 403 – 409 .[Abstract/Free Full Text]
- 21 Kikuchi HSuzuki YHashimoto Y. Increase of beta-glucuronidase activity in the serum of rats administered organophosphate and carbamate insecticides. J Toxicol Sci 1981; 6: 27 – 35 .[Medline]
[Order article via Infotrieve]
- 22 Nishimura YKato KHimeno M. Biochemical characterization of liver microsomal, Golgi, lysosomal, and serum beta-glucuronidase in dibutyl phosphate-treated rats. J Biochem 1995; 118: 56 – 66 .[Abstract/Free Full Text]
Human & Experimental Toxicology, Vol. 26, No. 12,
963-966 (2007)
DOI: 10.1177/0960327107085349
 CiteULike  Complore  Connotea  Del.icio.us  Digg  Reddit  Technorati  Twitter What's this?
|
|
