ArticleOxidative medicine and cellular longevity2012
Reversible oxidation of myometrial voltage-gated potassium channels with hydrogen peroxide.
Article in Oxidative medicine and cellular longevity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Compact on-chip fluorescence microscope for dynamic imaging of cellular processes and biomimetic systems.JPhys photonics · 2026Article
- Redox Regulation of Microvascular Physiology and Pathophysiology: Insights into Therapeutic Strategies and Limitations.Antioxidants & redox signaling · 2025Review
- Ibogaine-Mediated ROS/Antioxidant Elevation in Isolated Rat Uterus Is β-Adrenergic Receptors and KAntioxidants (Basel, Switzerland) · 2021Article
- The Effects of Ibogaine on Uterine Smooth Muscle Contractions: Relation to the Activity of Antioxidant Enzymes.Oxidative medicine and cellular longevity · 2018Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The uteri, spontaneously active or Ca(2+) (6 mM) induced, were allowed to equilibrate, and to inhibit voltage-gated potassium (K(V)) channels 1 mM 4-amino pyridine (4-AP) was applied for 15 min before adding H(2)O(2). H(2)O(2) was added cumulatively: 2 μM, 20 μM, 200 μM, 400 μM, and 3 mM. Average time for H(2)O(2) concentrations (2, 20, 200, and 400) μM to reach its full effect was 15 min. H(2)O(2) 3 mM had a prolonged effect and therefore was left to act for 30 min. Two-way ANOVA showed significant differences in time dependency between spontaneous and Ca(2+)-induced rat uteri after applying 3 mM H(2)O(2) (type of contraction, P = 0.0280), but not 400 μM H(2)O(2) (P = 0.9271). Our results indicate that H(2)O(2) oxidises channel intracellular thiol groups and activates the channel, inducing relaxation. Cell antioxidative defence system quickly activates glutathione peroxidase (GSHPx) defence mechanism but not catalase (CAT) defence mechanism. Intracellular redox mechanisms repair the oxidised sites and again establish deactivation of K(V) channels, recuperating contractility. In conclusion, our results demonstrate that K(V) channels can be altered in a time-dependent manner by reversible redox-dependent intracellular alterations.
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