Hussain_1998_Hum.Exp.Toxicol_17_140

Reference

Title : Lack of inhibition of human plasma cholinesterase and red cell acetylcholinesterase by antimony compounds including stibine - Hussain_1998_Hum.Exp.Toxicol_17_140
Author(s) : Hussain SA , Jane DE , Taberner PV
Ref : Hum Exp Toxicol , 17 :140 , 1998
Abstract :

1. The toxic gas hypothesis proposes exposure to stibine (antimony trihydride) generated from microbial contamination of cot mattress materials as a possible cause of unexplained death in infancy (SIDS) as a consequence of cholinesterase inhibition. We have measured the direct effects of antimony compounds including stibine on the activity of plasma cholinesterase, red blood cell acetylcholinesterase (AChE) and mouse neuronal AChE in vitro. 2. Colorimetric assays for the different esterases with potassium antimonyl tartrate or antimony trichloride at concentrations up to 10(-3) M in the presence of substrate concentrations sufficient to produce 80% of the maximum reaction rate produced no inhibition of enzyme activity. Exposure of enzyme preparations to stibine gas at concentrations sufficient to cause denaturation of red cell haemogloblin caused no measurable inhibition of esterase activity. 3. We conclude that stibine gas or soluble antimony compounds are not capable of inhibiting cholinesterase activity at toxicologically relevant concentrations.

PubMedSearch : Hussain_1998_Hum.Exp.Toxicol_17_140
PubMedID: 9587781

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Citations formats

Hussain SA, Jane DE, Taberner PV (1998)
Lack of inhibition of human plasma cholinesterase and red cell acetylcholinesterase by antimony compounds including stibine
Hum Exp Toxicol 17 :140

Hussain SA, Jane DE, Taberner PV (1998)
Hum Exp Toxicol 17 :140