Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Toxic Reactions: Overview

Toxic Reactions: Overview

When toxic substances penetrate the human body, they disseminate to various tissues, undergoing metabolic changes. This process yields reactive metabolites that may covalently bind with specific target molecules, resulting in toxicity.
Toxicity falls into two primary categories: local and systemic.
Local toxicity appears at the exposure site, such as protein denaturation caused by caustic substances.
In contrast, systemic toxicity requires the toxic agent's absorption and distribution,...

Antidotes

Antidotes

Antidotes are medicinal substances used to counteract the harmful effects of toxins or drugs in the body. They function in various ways, each uniquely designed to combat specific toxic compounds.
Specific antidotes operate by inhibiting the enzymes that control biochemical pathways, reducing the production of harmful metabolites.
An example of an antidote is atropine, which counteracts the detrimental effects of cholinesterase inhibitors. It achieves this by deactivating muscarinic receptors,...

Anticholinesterase Agents: Poisoning and Treatment

Anticholinesterase Agents: Poisoning and Treatment

Anticholinesterases, also known as cholinesterase inhibitors, work by blocking the breakdown of acetylcholine, leading to its accumulation in the synaptic cleft. This accumulation indirectly enhances both muscarinic and nicotinic actions. These agents are classified as reversible or irreversible based on their mechanism of action.
Irreversible agents form a strong bond with the cholinesterase enzyme, making it inactive. The breakdown of the phosphorylated enzyme is slower than the...

Drug Toxicity: Dose-Dependent Reactions

Drug Toxicity: Dose-Dependent Reactions

Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...

Toxidromes: Clinical Features

Toxidromes: Clinical Features

Toxidromes are specific patterns of symptoms resulting from toxic substance exposure. They help in the identification and treatment of poisoning. The symptoms of each toxidrome group indicate poisoning by a certain class of chemicals or drugs.1. Sympathomimetic: Stimulates the sympathetic nervous system. Symptoms include agitation, increased heart rate (HR), blood pressure (BP), respiratory rate (RR), temperature, and pupil size. Drugs like cocaine and amphetamines, along with tremors and...

Pharmaceutical Poisoning: Treatment Strategies

Pharmaceutical Poisoning: Treatment Strategies

Treatment strategies for poisoning are a critical aspect of emergency medicine, focusing on preventing the absorption of toxins and enhancing their elimination. When a poisoning incident occurs, the first response is to halt exposure and decontaminate the patient, particularly through gastrointestinal (GI) methods if the poison was ingested.Gastrointestinal Decontamination Techniques:Activated charcoal is the cornerstone of GI decontamination. It works through adsorption, binding the toxin to...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Application of the 2024 and 2017 McDonald criteria at disease onset in a multicenter Korean MS cohort.

Multiple sclerosis (Houndmills, Basingstoke, England)·2026

Same author

Treatment Patterns and Outcomes of Anti-MuSK Antibody-Positive Myasthenia Gravis: A Retrospective Single-Center Study.

Journal of Korean medical science·2026

Same author

Prevalence and Relative Proportions of MS, NMOSD, and MOGAD in the Republic of Korea.

Neurology·2026

Same author

MOG-IgG Positivity Does Not Equal MOGAD: Diagnostic Pitfall and Misapplication of the International MOGAD Panel Proposed Criteria in Real-World Practice.

Journal of clinical neurology (Seoul, Korea)·2026

Same author

Design and evaluation of an automated pediatric acute lymphoblastic leukemia registry from clinical data warehouses.

BMC medical informatics and decision making·2026

Same author

Prevalence and Relative Proportions of Multiple Sclerosis, Neuromyelitis Optica Spectrum Disorder, and Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease in the Republic of Korea.

Neurology·2026

Search research articles

Related Experiment Video

Updated: Jun 28, 2026

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Published on: January 7, 2014

Methidathion Poisoning.

Ki Hoon Kim¹, Se Hun Kim², Charles Her²

¹Department of Surgery, Inje University Haeundae Paik Hospital, Inje University College of Medicine, Busan, Korea.

Korean Journal of Critical Care Medicine

|November 15, 2019

Summary

Methidathion poisoning causes long-lasting acetylcholinesterase inhibition and circulatory collapse. Its high fat solubility and rapid aging limit treatment effectiveness, leading to severe complications like bowel perforation.

Keywords:

acetylcholine aspergillosis ganglia, sympathetic organophosphate poisoning

More Related Videos

Preparation of DMMTAV and DMDTAV Using DMAV for Environmental Applications: Synthesis, Purification, and Confirmation

Preparation of DMMTA^V and DMDTA^V Using DMA^V for Environmental Applications: Synthesis, Purification, and Confirmation

Published on: March 9, 2018

Color Spot Test As a Presumptive Tool for the Rapid Detection of Synthetic Cathinones

Color Spot Test As a Presumptive Tool for the Rapid Detection of Synthetic Cathinones

Published on: February 5, 2018

Related Experiment Videos

Last Updated: Jun 28, 2026

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Published on: January 7, 2014

Preparation of DMMTAV and DMDTAV Using DMAV for Environmental Applications: Synthesis, Purification, and Confirmation

Preparation of DMMTA^V and DMDTA^V Using DMA^V for Environmental Applications: Synthesis, Purification, and Confirmation

Published on: March 9, 2018

Color Spot Test As a Presumptive Tool for the Rapid Detection of Synthetic Cathinones

Color Spot Test As a Presumptive Tool for the Rapid Detection of Synthetic Cathinones

Published on: February 5, 2018

Area of Science:

Toxicology
Pharmacology
Infectious Diseases

Background:

Methidathion, an organophosphate insecticide, exhibits unique toxicity profiles compared to other organophosphates.
Its high lipophilicity leads to extensive body distribution, rendering hemoperfusion ineffective for removal.
Rapid acetylcholinesterase aging in methidathion poisoning prevents effective oxime reactivation, prolonging inhibition.

Observation:

A case report details a 55-year-old male with accidental high-dose methidathion ingestion.
The patient experienced profound circulatory collapse due to sympathetic ganglion blockade.
He developed enteroinvasive aspergillosis with multiple bowel perforations while on mechanical ventilation, leading to a fatal outcome.

Findings:

Methidathion's pharmacokinetic and pharmacodynamic properties contribute to its persistent toxicity.
Sympathetic ganglion blockade may activate the renin-angiotensin axis, reducing splanchnic blood flow and promoting endotoxin translocation.
Excessive acetylcholine acting on non-neuronal receptors might play a role in the development of invasive aspergillosis.

Implications:

Understanding methidathion's unique toxicity is crucial for managing poisoning cases.
The interplay between insecticide toxicity, circulatory compromise, and secondary infections like aspergillosis warrants further investigation.
This case highlights potential mechanisms contributing to severe outcomes in organophosphate poisoning, including gastrointestinal complications.