Forensic significance of acetylcholine esterase histochemistry in organophosphate intoxication

Abstract

The reduction of acetylcholine esterase (AChE) activity or the complete blocking of AChE to be observed by histochemical demonstration of AChE in tissue after experimental and spontaneous (human) organophosphate intoxication (especially paraoxone = E600 and parathion = E605) should be interpreted as an indication of an in vivo inhibition of the cholinergic system. In animal experiments, a relationship was demonstrated between AChE activity and the applied dose of organophosphorous compounds. In addition, enzyme inhibition was observed in in vitro systems using AChE-containing mouse tissue sections pretreated with organophosphate solutions or with body fluids containing organophosphates. Examination of the concentration dependency indicated that the inhibiting solution must contain at least 0.15 microgram/ml paraoxone or 5 mg/ml parathion to block AChE in the section. Using the same in vitro system, a half-life of 6-7 min was established for the paraoxone inactivating enzyme in blood. The in vivo and in vitro inhibited AChE was reactivated by consecutive treatment of blocked sections with toxogonin. This possibility of reactivation therefore allows qualitative classifications of the AChE-inhibiting toxin to the alkylphosphates. The postmortem persistence of the AChE inhibitory effect was demonstrable for about a 2-month interval. Since the histochemically demonstrable activity of the enzyme AChE is more or less constant during a postmortem interval of at least 70h, the model of histochemical demonstration is a method which provides a morphological equivalent for acute organophosphate intoxication.

A Study on the Toxicity of a Medicinal Plant, Artemisia Annua L. (Asteracea) Extracts to the Sunn Pest, Eurygaster Integriceps Puton (Hemiptera: Scutelleridae)

“…AChE is a key enzyme that terminates nerve impulses by catalyzing the hydrolysis of neurotransmitter, acetylcholine, in the nervous system in various organisms (Oehmichen and Besserer 1982;Grundy and Still 1985;Wang et al 2004). In this study, A. annua extract inhibited the AChE activity in higher doses which coincided with other reports about effect of botanical insecticides on AChE inhibition.…”

Biocompatible green synthesized silver nanoparticles impact on insecticides resistant developing enzymes of dengue transmitted mosquito vector

“…This acetylcholine is released from pre synaptic neuron into a synaptic cleft bind with the receptor for passing the sodium ions through this channel. Acetylcholinesterase enzyme is released to break the acetylcholine, which is present in the synaptic cleft and send back the choline to the presynaptic terminal to take part in regular cycles for synthesis of acetylcholine along with Acetyl CoA [41]. In our studies, the synthesized AgNPs exposed larvae acetylcholine esterase activity was inhibited revealed by releasing of low quantity of acetylcholine compared to control larva in the experimental result.…”

Biochemical basis of synergism between pathogenic fungus Metarhizium anisopliae and insecticide chlorantraniliprole in Locusta migratoria (Meyen)

“…Increased PO activity can strengthen an insect’s immunity to xenobiotics and promote wound healing343536. Acetylcholinesterase (AChE) is a key enzyme catalysing the hydrolysis of the neurotransmitter acetylcholine in the nervous system of various organisms37. AChE is affected by organophosphate and carbamate insecticides, botanical insecticides and secondary fungal metabolites3839404142.…”