Related Experiment Video

Updated: May 12, 2026

A Neuronal and Astrocyte Co-Culture Assay for High Content Analysis of Neurotoxicity
15:04

A Neuronal and Astrocyte Co-Culture Assay for High Content Analysis of Neurotoxicity

Published on: May 5, 2009

Acrylamide neurotoxicity

Pinar Erkekoglu, Terken Baydar

    Nutritional Neuroscience
    |April 2, 2013
    PubMed

    Keywords:
    AcrylamideNeurodegenerative diseasesNeuropathyNeurotoxicity

    More Related Videos

    Adaptation of Microelectrode Array Technology for the Study of Anesthesia-induced Neurotoxicity in the Intact Piglet Brain08:23

    Adaptation of Microelectrode Array Technology for the Study of Anesthesia-induced Neurotoxicity in the Intact Piglet Brain

    Published on: May 12, 2018

    Examination of Anatomical Features of Retinal Ganglion Cells Under N-methyl-D-aspartic Acid (NMDA)-induced Excitotoxicity07:11

    Examination of Anatomical Features of Retinal Ganglion Cells Under N-methyl-D-aspartic Acid (NMDA)-induced Excitotoxicity

    Published on: September 19, 2025

    Related Concept Videos

    Physical Properties of Amines01:26

    Physical Properties of Amines

    Amines with low molecular weight are usually gaseous at room temperature, while those with high molecular weight are liquid or solids in nature. Usually, low molecular weight amines have a rotten fish-like smell. Diamines typically have a pungent smell. For instance, cadaverine and putrescine, depicted in Figure 1, are two molecules responsible for decaying tissue.
    Amines to Amides: Acylation of Amines01:19

    Amines to Amides: Acylation of Amines

    Various carboxylic acid derivatives (such as acid chlorides, esters, and anhydrides) can be used for the acylation of amines to yield amides. The reaction requires two equivalents of amines. The first amine molecule functions as a nucleophile and attacks the carbonyl carbon to produce a tetrahedral intermediate. This is followed by the loss of the leaving group and restoration of the C=O bond.
    Next, the second equivalent of amine serves as a Brønsted base and deprotonates the quaternary amide...
    Toxic Reactions: Overview01:26

    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,...
    Phase II Reactions: Acetylation Reactions01:24

    Phase II Reactions: Acetylation Reactions

    Acetylation, a phase II biotransformation reaction, introduces an acetyl group to drugs or their metabolites. Acetyltransferase enzymes facilitate this reaction, which resembles α-amino acid conjugation due to the addition of a functional group to the drug molecule.
    The substrates for acetylation are typically drugs or their metabolites with an amino, sulfonamide, or hydrazine functional group. Acetylation can occur at several points in the drug molecule, including primary, secondary, and...
    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...
    Hepatic Encephalopathy01:29

    Hepatic Encephalopathy

    DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...