Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Anticholinesterase Agents: Poisoning and Treatment01:26

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...
Prevention of Further Absorption of Poison01:14

Prevention of Further Absorption of Poison

In cases of acute poisoning, the primary objective is to prevent further absorption of the toxic substance into the body. Immediate interventions using various decontamination techniques targeting the gastrointestinal (GI) tract can achieve this. Decontamination is crucial to prevent poison from entering the systemic circulation, which involves washing affected areas with water and mild soap and removing contaminated clothing. Once external decontamination is done, attention must be turned to...
Pharmaceutical Poisoning: Treatment Strategies01:26

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...
Enhanced Elimination of Poison01:26

Enhanced Elimination of Poison

Poison can be effectively removed from the gastrointestinal (GI) tract through various decontamination procedures.
Antidotes serve a crucial role in counteracting the effects of poison by inhibiting enzymes responsible for producing harmful drug metabolites. In some cases, these toxic metabolites can be neutralized by endogenous cosubstrates, which are maintained at specific concentrations to prevent interaction with cellular macromolecules and subsequent cell death.
Renal excretion is the...
Antiasthma Drugs: Muscarinic Receptor Antagonists01:20

Antiasthma Drugs: Muscarinic Receptor Antagonists

Muscarinic receptor antagonists, also known as antimuscarinic agents, are a class of bronchodilators used to treat asthma, although they are more commonly used to treat COPD. They work by inhibiting the action of acetylcholine (ACh), a neurotransmitter, on muscarinic receptors found in the airways.
Antimuscarinic agents compete with ACh for the same binding site on the muscarinic receptors. By binding to these receptors, they inhibit the downstream effects of ACh and block the parasympathetic...
Indirect-Acting Cholinergic Agonists: Pharmacological Actions01:30

Indirect-Acting Cholinergic Agonists: Pharmacological Actions

Indirect-acting cholinergic agonists, also known as anticholinesterases, exert their pharmacological effects by enhancing cholinergic transmission in various body parts, including the neuromuscular junction, autonomic cholinergic synapses, and the brain.
At the neuromuscular junction, these agents work by inhibiting the breakdown of acetylcholine, allowing it to remain bound to the receptor and bind to nearby receptors. This process leads to repetitive firing of the endplate, causing muscle...

You might also read

Related Articles

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

Sort by
Same author

The effect of the cryoprotectant dimethyl sulfoxide on water upon supercooling: A molecular dynamics study.

The Journal of chemical physics·2025
Same author

Inventory of landslides triggered by an extreme rainfall event in Marche-Umbria, Italy, on 15 September 2022.

Scientific data·2023
Same author

Amniotic fluid stem cell-derived vesicles protect from VEGF-induced endothelial damage.

Scientific reports·2017
Same author

The bridge between transplantation and regenerative medicine: Beginning a new Banff classification of tissue engineering pathology.

American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons·2017
Same author

Pharmacokinetics of Benznidazole in Healthy Volunteers and Implications in Future Clinical Trials.

Antimicrobial agents and chemotherapy·2017
Same author

Inherited alpha1-antitrypsin deficiency: is the level the key message?

Revue des maladies respiratoires·2014

Related Experiment Video

Updated: May 24, 2026

Exploring the Two Herb Combination Strategy to Treat Injured PC12 Cells
10:33

Exploring the Two Herb Combination Strategy to Treat Injured PC12 Cells

Published on: November 18, 2022

Protection against acute paraquat toxicity by ambroxol.

L Perin1, M Donnini, L Diomede

  • 1Laboratorio di Enzimologia, Istituto di Ricerche Farmacologiche "Mario Negri", Via Eritrea62, 20157, Milan, Italy.

Cytotechnology
|February 24, 2012
PubMed
Summary

The herbicide paraquat (PQ) damages lung cells, but the drug ambroxol may protect them by boosting surfactant production. Ambroxol pretreatment increased cell resistance to paraquat toxicity both in vitro and in vivo.

Related Experiment Videos

Last Updated: May 24, 2026

Exploring the Two Herb Combination Strategy to Treat Injured PC12 Cells
10:33

Exploring the Two Herb Combination Strategy to Treat Injured PC12 Cells

Published on: November 18, 2022

Area of Science:

  • Biochemistry
  • Cell Biology
  • Toxicology

Background:

  • Paraquat (PQ) herbicide exposure causes early damage to type II pneumocytes, leading to surfactant depletion.
  • Ambroxol is a drug known to stimulate surfactant synthesis in alveolar type II cells.

Purpose of the Study:

  • To investigate the protective effect of ambroxol against paraquat-induced lung cell damage.
  • To explore the role of surfactant synthesis in counteracting paraquat toxicity.

Main Methods:

  • In vitro exposure of A-549 cell line to varying concentrations of paraquat (PQ).
  • Pretreatment of cells with ambroxol (10 mg/ml) before paraquat exposure.
  • Measurement of cell viability and membrane microviscosity.
  • In vivo studies to assess partial protection from PQ-induced mortality.

Main Results:

  • Paraquat exposure caused a dose-dependent decrease in A-549 cell viability.
  • Ambroxol pretreatment enhanced cell resistance to paraquat, with viability decreasing at higher PQ concentrations.
  • Paraquat reduced membrane microviscosity, an effect counteracted by ambroxol.
  • Cell viability and membrane microviscosity changes correlated, suggesting surfactant stimulation is key.

Conclusions:

  • Ambroxol demonstrates a protective effect against paraquat-induced lung cell damage.
  • Stimulation of surfactant synthesis by ambroxol appears crucial for counteracting early paraquat toxicity.
  • The findings suggest a potential therapeutic strategy for paraquat poisoning.