ArticleAntioxidants & redox signaling2009
H2S protects against methionine-induced oxidative stress in brain endothelial cells.
Article in Antioxidants & redox signaling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
84 citing papers in PubMed, 167 citations in OpenAlex.
- Unlocking the gasotransmitter: hydrogen sulfide as a multitarget regulator in ischemia-reperfusion injury.Medical gas research · 2026Review
- Transport Across the Blood-Brain Barrier.Advances in experimental medicine and biology · 2026Review
- Role and Relationship Between Homocysteine and HMolecular neurobiology · 2025Review
- Influence of homocysteine on regulating immunothrombosis: mechanisms and therapeutic potential in management of infections.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Modeling the Interactions Between Chemicals and Proteins to Predict the Health Consequences of Air Pollution.International journal of environmental research and public health · 2025Article
- Ferroptosis: a double-edged sword that enhances radiation sensitivity and facilitates radiation-induced injury in tumors.Frontiers in immunology · 2025Review
- Epigenetics of Homocystinuria, Hydrogen Sulfide, and Circadian Clock Ablation in Cardiovascular-Renal Disease.Current issues in molecular biology · 2024Review
- Methionine deficiency inhibited pyroptosis in primary hepatocytes of grass carp (Ctenopharyngodon idella): possibly via activating the ROS-AMPK-autophagy axis.Journal of animal science and biotechnology · 2024Article
- Supplementation of sperm cryopreservation media with HScientific reports · 2024Article
- Neurodegenerative Etiology of Aromatic L-Amino Acid Decarboxylase Deficiency: a Novel Concept for Expanding Treatment Strategies.Molecular neurobiology · 2024Review
- Homocysteine and mitochondrial quality control in diabetic retinopathy.Eye and vision (London, England) · 2024Article
- Targeting Homocysteine and Hydrogen Sulfide Balance as Future Therapeutics in Cancer Treatment.Antioxidants (Basel, Switzerland) · 2023Review
- The Role of Hydrogen Sulfide in Regulation of Cell Death following Neurotrauma and Related Neurodegenerative and Psychiatric Diseases.International journal of molecular sciences · 2023Review
- Comparative Study of Different HAntioxidants (Basel, Switzerland) · 2023Article
- Effect of Supplementation of Diets with L-Carnitine and Methionin on Broiler Chicken Productive Performance.Archives of Razi Institute · 2023Article
- Oxidative stress impairs cognitive function by affecting hippocampal fimbria volume in drug-naïve, first-episode schizophrenia.Frontiers in neuroscience · 2023Article
- Protective Effect of Hydrogen Sulfide on Cerebral Ischemia-Reperfusion Injury.Cellular and molecular neurobiology · 2023Review
- Quantification of In Vitro Blood-Brain Barrier Permeability.Methods in molecular biology (Clifton, N.J.) · 2022Article
- HAntioxidants (Basel, Switzerland) · 2021Article
- One-pot synthesis of AuAgPd trimetallic nanoparticles with peroxidase-like activity for colorimetric assays.Analytical and bioanalytical chemistry · 2021Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Homocysteine (Hcy) causes cerebrovascular dysfunction by inducing oxidative stress. However, to date, there are no strategies to prevent Hcy-induced oxidative damage. Hcy is an H2S precursor formed from methionine (Met) metabolism. We aimed to investigate whether H2S ameliorated Met-induced oxidative stress in mouse brain endothelial cells (bEnd3). The bEnd3 cells were exposed to Met treatment in the presence or absence of NaHS (donor of H2S). Met-induced cell toxicity increased the levels of free radicals in a concentration-dependent manner. Met increased NADPH-oxidase-4 (NOX-4) expression and mitigated thioredxion-1(Trx-1) expression. Pretreatment of bEnd3 with NaHS (0.05 mM) attenuated the production of free radicals in the presence of Met and protected the cells from oxidative damage. Furthermore, NaHS enhanced inhibitory effects of apocynin, N-acetyl-l-cysteine (NAC), reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), Nomega-nitro-l-arginine methyl ester (L-NAME) on ROS production and redox enzymes levels induced by Met. In conclusion, the administration of H2S protected the cells from oxidative stress induced by hyperhomocysteinemia (HHcy), which suggested that NaHS/H2S may have therapeutic potential against Met-induced oxidative stress.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.