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The oxidation of an organic compound in the presence of air or oxygen is called autoxidation. For example, cumene reacts with oxygen to form hydroperoxide. Autoxidation involves initiation, propagation, and termination steps. Many organic compounds are susceptible to autoxidation—especially ethers in the presence of oxygen, which form hydroperoxides. Even though this reaction is slow, old ether bottles contain small amounts of peroxide, which leads to laboratory explosions during ether...
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Thiol-Based Redox Molecules: Potential Antidotes for Acrylamide Toxicity.

Valeria Martin1, Michael Trus1, Daphne Atlas1

  • 1Department of Biological Chemistry, Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem 91904, Israel.

Antioxidants (Basel, Switzerland)
|January 8, 2025
PubMed
Summary
This summary is machine-generated.

Acrylamide (ACR) exposure causes oxidative stress and activates mitogen-activated protein kinases (MAPKs). Thiol-based molecules, particularly thioredoxin-mimetic (TXM) peptides with more cysteine residues, effectively suppressed ACR-induced MAPK activation and show promise as antidotes.

Keywords:
AD4/NACAapoptosisoxidative stressthioredoxin reductasetoxicity

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Area of Science:

  • Biochemistry and Molecular Biology
  • Toxicology and Pharmacology
  • Neuroscience

Background:

  • Acrylamide (ACR) is a ubiquitous industrial chemical and food contaminant linked to oxidative stress and neurotoxicity.
  • Oxidative stress induced by ACR involves the activation of mitogen-activated protein kinases (MAPKs), including ERK1/2, p38MAPK, and JNKs.
  • Identifying effective antidotes for ACR toxicity is crucial for mitigating its adverse health effects.

Purpose of the Study:

  • To evaluate the efficacy of thiol-based molecules as potential antidotes against acrylamide (ACR) toxicity.
  • To investigate the ability of these compounds to inhibit ACR-induced activation of extracellular-signal-regulated-kinases (ERK1/2), p38-mitogen-activated-protein-kinases (p38MAPK), and c-Jun-N-terminal-kinases (JNKs).
  • To explore the potential of these molecules in preventing ACR-triggered Parkinson's disease (PD)-like neurotoxic symptoms.

Main Methods:

  • Development of a reproducible assay in PC12 cells to test N-acetylcysteine (NAC), AD4/NACA, and various thioredoxin-mimetic (TXM) peptides.
  • Assessment of the compounds' efficacy in suppressing ACR-induced MAPK activation, both before and after ACR exposure.
  • Dose-response analysis to determine the correlation between compound structure (number of cysteine residues) and inhibitory potency.

Main Results:

  • All tested thiol-based compounds, including NAC, AD4/NACA, and TXM peptides, demonstrated significant efficacy in suppressing ACR-induced MAPK activation.
  • Inhibitory potency was dose-dependent and directly correlated with the number of cysteine (Cys) residues in the molecules.
  • SuperDopa (SD), a TXM peptide containing levodopa and two Cys residues, showed potential in mitigating PD-like symptoms by reducing oxidative stress and replenishing dopamine.

Conclusions:

  • Thiol-based molecules, especially TXM peptides, are effective in counteracting ACR-induced MAPK activation and oxidative stress.
  • The number of cysteine residues is a key factor in the potency of these antidotes.
  • TXM peptides, including SD, hold promise as therapeutic agents for acute/chronic ACR exposure and for preventing ACR-induced Parkinsonism.