Related Experiment Video

Updated: Aug 8, 2026

Combining Non-reducing SDS-PAGE Analysis and Chemical Crosslinking to Detect Multimeric Complexes Stabilized by Disulfide Linkages in Mammalian Cells in Culture
09:37

Combining Non-reducing SDS-PAGE Analysis and Chemical Crosslinking to Detect Multimeric Complexes Stabilized by Disulfide Linkages in Mammalian Cells in Culture

Published on: May 2, 2019

Thiol modification and cell signalling in chemical toxicity

P Nicotera1, J M Dypbukt, A D Rossi

  • 1Department of Toxicology, Karolinska Institutet Stockholm, Sweden.

Toxicology Letters
|December 1, 1992
PubMed

Insights

Oxidative stress from thiol oxidizing agents can impact cell signaling. Depending on the concentration, oxidants may promote cell growth and proliferation or trigger programmed cell death and necrosis.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Background:

  • Thiol oxidizing agents modify proteins crucial for cell signaling pathways.
  • These modifications can disrupt normal cell metabolism, growth, and responses to stimuli.
  • Aberrant signaling affects phosphoinositide metabolism, protein kinase activation, and intracellular calcium levels.

Purpose of the Study:

  • To investigate the dose-dependent effects of oxidants on cell signaling and cellular fate.
  • To determine how varying oxidant concentrations influence cell proliferation, differentiation, and death.
  • To elucidate the mechanisms by which oxidative stress impacts multiple signaling pathways.

Main Methods:

  • Exposure of cell cultures to varying concentrations of thiol oxidizing agents.
  • Analysis of key signaling pathway components and their modifications.
  • Assessment of cellular responses including proliferation, differentiation, programmed cell death (PCD), and necrosis.

Main Results:

  • Moderate oxidant levels potentiate growth signals, enhancing cell proliferation and differentiation.
  • High oxidant concentrations inhibit growth signals, blocking proliferation and inducing PCD.
  • Significant alterations in signaling pathways and increased catabolic reactions lead to cell death by necrosis.

Conclusions:

  • Oxidant interaction with cell signaling exhibits dose-dependent, opposing effects.
  • Oxidative stress can either mimic growth factor stimulation or inhibit growth signals, activating distinct cellular outcomes.
  • These findings highlight the complex role of oxidative reactions in regulating cell fate, from proliferation to cell death.

More Related Videos

Resin-Assisted Capture Coupled with Isobaric Tandem Mass Tag Labeling for Multiplexed Quantification of Protein Thiol Oxidation07:16

Resin-Assisted Capture Coupled with Isobaric Tandem Mass Tag Labeling for Multiplexed Quantification of Protein Thiol Oxidation

Published on: June 21, 2021

Rapid Quantification of Oxidized and Reduced Forms of Glutathione Using Ortho -phthalaldehyde in Cultured Mammalian Cells In Vitro03:35

Rapid Quantification of Oxidized and Reduced Forms of Glutathione Using Ortho -phthalaldehyde in Cultured Mammalian Cells In Vitro

Published on: June 28, 2024

Related Concept Videos

Covalently Linked Protein Regulators02:04

Covalently Linked Protein Regulators

Proteins can undergo many types of post-translational modifications, often in response to changes in their environment. These modifications play an important role in the function and stability of these proteins. Covalently linked molecules include functional groups, such as methyl, acetyl, and phosphate groups, and also small proteins, such as ubiquitin. There are around 200 different types of covalent regulators that have been identified.
These groups modify specific amino acids in a protein.
Preparation and Reactions of Thiols02:33

Preparation and Reactions of Thiols

Thiols are prepared using the hydrosulfide anion as a nucleophile in a nucleophilic substitution reaction with alkyl halides. For instance, bromobutane reacts with sodium hydrosulfide to give butanethiol.
Phase II Reactions: Glutathione Conjugation and Mercapturic Acid Formation01:22

Phase II Reactions: Glutathione Conjugation and Mercapturic Acid Formation

Glutathione, a tripeptide made up of glutamate, cysteine, and glycine, is a critical player in the detoxification of drugs and xenobiotics via a process known as glutathione conjugation or mercapturic acid formation. This phase II biotransformation reaction involves the covalent binding of glutathione to a drug or its metabolite, enhancing the compound's water solubility and enabling its excretion.
Several distinctive characteristics distinguish glutathione conjugation from other phase II...
Bioactivation and Tissue Toxicity01:25

Bioactivation and Tissue Toxicity

Bioactivation is a metabolic process that transforms less reactive substances into highly reactive metabolites, initiating tissue toxicity. This transformation can lead to various toxic effects, including carcinogenesis and teratogenesis. Reactive metabolites are classified into two main types: electrophiles and free radicals.Electrophiles are electron-deficient species and are produced primarily by the enzyme cytochrome P-450 during the metabolism of compounds containing carbon, nitrogen, or...
Sulfur Assimilation01:20

Sulfur Assimilation

Sulfur is an essential element in biological systems, contributing to synthesizing key biomolecules, including amino acids such as cysteine and methionine, and cofactors such as coenzyme A and biotin. Microorganisms primarily assimilate sulfur as sulfate (SO₄²⁻) from the environment, which must undergo a series of biochemical transformations before it can be incorporated into cellular components. As sulfate is highly oxidized, it must undergo assimilatory sulfate reduction to become...
Cellular Injury I: Introduction01:00

Cellular Injury I: Introduction

Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...