ArticleFree radical biology & medicine2015
Methylglyoxal, the foe and friend of glyoxalase and Trx/TrxR systems in HT22 nerve cells.
Article in Free radical biology & medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 55 citations in OpenAlex.
- Strain-resolved metabolomic chemotyping identifies tryptophan and γ-glutamyl peptides as MGO-AGEs breaking postbiotic compounds for carbonyl stress mitigation.Gut microbes · 2026Article
- Higher intake of dietary dicarbonyl compounds is associated with lower incidence of type 2 diabetes: European Prospective Investigation into Cancer and Nutrition (EPIC)-InterAct case-cohort study.European journal of nutrition · 2026Article
- Mitigation ofJournal of microbiology and biotechnology · 2025Article
- Does Gut Microbial Methylglyoxal Metabolism Impact Human Physiology?Antioxidants (Basel, Switzerland) · 2025Review
- Redox regulation: mechanisms, biology and therapeutic targets in diseases.Signal transduction and targeted therapy · 2025Review
- Review
- REAP+: A single preparation for rapid isolation of nuclei, cytoplasm, and mitochondria.Analytical biochemistry · 2024Article
- Renoprotective Potency of Sitagliptin versus Pioglitazone in Type 2 Diabetic Patients: Impact on LncMIAT.ACS omega · 2023Article
- Molecular Link between Glo-1 Expression and Markers of Hyperglycemia and Oxidative Stress in Vascular Complications of Type 2 Diabetes Mellitus.Antioxidants (Basel, Switzerland) · 2023Article
- Habitual intake of dietary methylglyoxal is associated with less low-grade inflammation: the Maastricht Study.The American journal of clinical nutrition · 2022Article
- Glyoxalase I activity affects Arabidopsis sensitivity to ammonium nutrition.Plant cell reports · 2022Article
- Metabolic Shades of S-D-Lactoylglutathione.Antioxidants (Basel, Switzerland) · 2022Review
- Glyoxal damages human aortic endothelial cells by perturbing the glutathione, mitochondrial membrane potential, and mitogen-activated protein kinase pathways.BMC cardiovascular disorders · 2021Article
- Patients with Osteoarthritis and Kashin-Beck Disease Display Distinct CpG Methylation Profiles in theCartilage · 2021Article
- Methylglyoxal-Mediated Dopamine Depletion, Working Memory Deficit, and Depression-Like Behavior Are Prevented by a Dopamine/Noradrenaline Reuptake Inhibitor.Molecular neurobiology · 2021Article
- Inhibition of thioredoxin 2 by intracellular methylglyoxal accumulation leads to mitochondrial dysfunction and apoptosis in INS-1 cells.Endocrine · 2020Article
- Repeated Methylglyoxal Treatment Depletes Dopamine in the Prefrontal Cortex, and Causes Memory Impairment and Depressive-Like Behavior in Mice.Neurochemical research · 2020Article
- Hyperosmotic Stress Initiates AMPK-Independent Autophagy and AMPK- and Autophagy-Independent Depletion of Thioredoxin 1 and Glyoxalase 2 in HT22 Nerve Cells.Oxidative medicine and cellular longevity · 2019Article
- Mitochondrial toxicity induced by a thiourea gold(i) complex: mitochondrial permeability transition and respiratory deficit.Toxicology research · 2018Article
- Methylglyoxal-Induced Protection Response and Toxicity: Role of Glutathione Reductase and Thioredoxin Systems.Neurotoxicity research · 2017Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Methylglyoxal (MGO) is a major glycating agent that reacts with basic residues of proteins and promotes the formation of advanced glycation end products (AGEs) which are believed to play key roles in a number of pathologies, such as diabetes, Alzheimer's disease, and inflammation. Here, we examined the effects of MGO on immortalized mouse hippocampal HT22 nerve cells. The endpoints analyzed were MGO and thiol status, the glyoxalase system, comprising glyoxalase 1 and 2 (GLO1/2), and the cytosolic and mitochondrial Trx/TrxR systems, as well as nuclear Nrf2 and its target genes. We found that nuclear Nrf2 is induced by MGO treatment in HT22 cells, as corroborated by induction of the Nrf2-controlled target genes and proteins glutamate cysteine ligase and heme oxygenase 1. Nrf2 knockdown prevented MGO-dependent induction of glutamate cysteine ligase and heme oxygenase 1. The cystine/glutamate antiporter, system xc(-), which is also controlled by Nrf2, was also induced. The increased cystine import (system xc(-)) activity and GCL expression promoted GSH synthesis, leading to increased levels of GSH. The data indicate that MGO can act as both a foe and a friend of the glyoxalase and the Trx/TrxR systems. At low concentrations of MGO (0.3mM), GLO2 is strongly induced, but at high MGO (0.75 mM) concentrations, GLO1 is inhibited and GLO2 is downregulated. The cytosolic Trx/TrxR system is impaired by MGO, where Trx is downregulated yet TrxR is induced, but strong MGO-dependent glycation may explain the loss in TrxR activity. We propose that Nrf2 can be the unifying element to explain the observed upregulation of GSH, GCL, HO1, TrxR1, Trx2, TrxR2, and system xc(-) system activity.
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