Delayed Neurotoxicity of Organophosphorus Compounds

2013 ◽  
Vol 1 (1) ◽  
pp. 14 ◽  
Author(s):  
Kazim Husain ◽  
1985 ◽  
Vol 10 (2) ◽  
pp. 67-82 ◽  
Author(s):  
Hirotoshi ITOH ◽  
Hidemi KISHIDA ◽  
Eiko TAKEUCHI ◽  
Mamoru TADOKORO ◽  
Toshiyuki UCHIKOSHI ◽  
...  

1985 ◽  
Vol 228 (3) ◽  
pp. 537-544 ◽  
Author(s):  
C D Carrington ◽  
M B Abou-Donia

The experiments described in this paper were designed to isolate [3H]di-isopropyl phosphorofluoridate-binding proteins by sodium dodecyl sulphate/polyacrylamide-gel electrophoresis for the purpose of characterizing and identifying potential initiation sites for organophosphorus-compound-induced delayed neurotoxicity. The major Paraoxon-insensitive Mipafox-sensitive binding protein (Mr 160 000) was found to be identical with one previously identified as neurotoxic esterase, an enzyme that has been proposed to be the target site for organophosphorus-compound-induced delayed neurotoxicity. However, two other binding proteins with suitable binding characteristics were also found in smaller amounts, one of which has not been detected previously. Di-isopropyl phosphorofluoridate was found to phosphorylate all three of these proteins at rates similar to the rate at which neurotoxic esterase is inhibited by di-isopropyl phosphorofluoridate. Varying the concentration of di-isopropyl phosphorofluoridate or the time of incubation produced similar increases in binding to each of the labelled proteins. This suggests that the reaction rates of di-isopropyl phosphorofluoridate with proteins may be described by first-order kinetics, and the concentration of the Michael is complex formed during binding is minimal for all the phosphorylated proteins. The recovery of the binding activity in the 160 000-Mr band was found to be similar to the recovery of neurotoxic esterase activity, lending further support to the contention that this band is identical with neurotoxic esterase.


1981 ◽  
Vol 6 (4) ◽  
pp. 287-300 ◽  
Author(s):  
Hirotoshi ITOH ◽  
Mamoru TADOKORO ◽  
Kiyoshi OIKAWA

2007 ◽  
Vol 41 (10) ◽  
pp. 516-518
Author(s):  
O. A. Khodakovskaya ◽  
N. A. Vodolazskaya ◽  
L. D. Glukhova ◽  
S. I. Timofeeva ◽  
S. I. Dvoretskaya ◽  
...  

1969 ◽  
Vol 160 (1 Biological Ef) ◽  
pp. 314-322 ◽  
Author(s):  
W. N. Aldridge ◽  
J. M. Barnes ◽  
M. K. Johnson

2021 ◽  
Vol 51 (10) ◽  
Author(s):  
Igor Ribeiro dos Santos ◽  
Luan Cleber Henker ◽  
Tainah Pereira Dal Pont ◽  
Welden Panziera ◽  
Saulo Petinatti Pavarini ◽  
...  

ABSTRACT: Forty 1-2-y-old water buffaloes were simultaneously treated with trichlorfon and chlorpyrifos products in the recommended dose for cattle. After a week, 19 animals started presenting clinical signs characterized by apathy, diarrhea, aggressiveness, dehydration, and motor incoordination, followed by flaccid paralysis and permanent lateral recumbency. All affected buffaloes died after a clinical course of 1-4 days. Reduction of serum cholinesterase activity in three cases was indicative of significant exposure to organophosphorus compounds (OPs). Pathological examination of three buffaloes revealed no gross and histological lesions. By thin layer chromatography, chlorpyrifos residues and trace of trichlorfon residues were detected in fresh tissue samples. The epidemiological, clinical, pathological, and toxicological findings were highly compatible with OPs-induced delayed neurotoxicity, a neurological manifestation rarely described in domestic animals.


2018 ◽  
Vol 1 (3) ◽  
pp. e00028
Author(s):  
G.F. Makhaeva ◽  
E.V. Rudakova ◽  
R.J. Richardson

Development of biomarkers of human exposures to organophosphorus compounds OPCs and their quantification is a vital component of a system of prediction and early diagnostics of OPC-induced diseases. Our study was focused on investigation of esterase status as a complex biomarker of exposure to OPCs and an aid in accurate diagnosis. We suggest that this complex biomarker should be more effective and informative than standard assays of plasma butyrylcholinesterase (BChE), erythrocyte acetylcholinesterase (RBC AChE), and lymphocyte neuropathy target esterase (NTE). It will help: 1) to assess an exposure as such and to confirm the nonexposure of individuals suspected to have been exposed; 2) to determine if the exposure was to agents expected to produce acute and/or delayed neurotoxicity; 3) to perform dosimetry of the exposure, which provides valuable information for medical treatment. To confirm this hypothesis, we have examined the changes in activity of blood AChE, NTE, BChE and carboxylesterase (CaE) 1 h after i.p. administration of increasing doses of three OPCs with different esterase profiles: the known neuropathic compound O,O-dipropyl-O-dichlorovinyl phosphate (C3H 7O)2P(O)OCH=CCl2 (diPr-DClVP) as the control compound and two model dialkylphosphates (C2H5O)2P(O)OCH(CF3)2 (diEt-PFP) and (C4H9O)2P(O)OCH(CF3)2 (diBu-PFP). The esterases assay was performed in hemolysed blood by spectrophotometric (AChE, BChE, CaE) and biosensor (NTE) methods. Analysis of the obtained dose-dependences for blood esterases inhibition showed that blood BChE and CaE were the most sensitive biomarkers, allowing detection of low doses. Inhibition of blood NTE and AChE can be used to assess the likelihood that an exposure to OPC would produce cholinergic and/or delayed neuropathic effects.


Sign in / Sign up

Export Citation Format

Share Document