ArticleMolecular neurobiology2019
Disruption of Brain Redox Homeostasis, Microglia Activation and Neuronal Damage Induced by Intracerebroventricular Administration of S-Adenosylmethionine to Developing Rats.
Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Nitrosative Stress Mediates Disruption of Redox Homeostasis and Oxidative Phosphorylation Caused by 3-Hydroxyisobutyric Acid in Cerebral Cortex of Developing Rats.Molecular neurobiology · 2025Article
- A novel role of exostosin glycosyltransferase 2 (EXT2) in glioblastoma cell metabolism, radiosensitivity and ferroptosis.Cell death and differentiation · 2025Article
- SAM Alleviates Neuroinflammation by Regulating M1/M2 Polarization of Microglia Through α7nAChR/Nrf2/HO-1 Signaling Pathway.Neurochemical research · 2025Article
- Altered serum glutathione disulfide levels in acute relapsed schizophrenia are associated with clinical symptoms and response to electroconvulsive therapy.BMC psychiatry · 2025Article
- In Vivo Intracerebral Administration of α-Ketoisocaproic Acid to Neonate Rats Disrupts Brain Redox Homeostasis and Promotes Neuronal Death, Glial Reactivity, and Myelination Injury.Molecular neurobiology · 2024Article
- Combination of epigallocatechin 3 gallate and curcumin improves D-galactose and normal-aging associated memory impairment in mice.Scientific reports · 2023Article
- L-2-Hydroxyglutaric Acid Administration to Neonatal Rats Elicits Marked Neurochemical Alterations and Long-Term Neurobehavioral Disabilities Mediated by Oxidative Stress.Neurotoxicity research · 2023Article
- Disturbance of Mitochondrial Dynamics, Endoplasmic Reticulum-Mitochondria Crosstalk, Redox Homeostasis, and Inflammatory Response in the Brain of Glutaryl-CoA Dehydrogenase-Deficient Mice: Neuroprotective Effects of Bezafibrate.Molecular neurobiology · 2022Article
- Curcumin improves D-galactose and normal-aging associated memory impairment in mice: In vivo and in silico-based studies.PloS one · 2022Article
- S-adenosylmethionine induces mitochondrial dysfunction, permeability transition pore opening and redox imbalance in subcellular preparations of rat liver.Journal of bioenergetics and biomembranes · 2021Article
- Melatonin and Microglia.International journal of molecular sciences · 2021Review
- Methionine Diet Evoked Hyperhomocysteinemia Causes Hippocampal Alterations, Metabolomics Plasma Changes and Behavioral Pattern in Wild Type Rats.International journal of molecular sciences · 2021Article
- Free Radical Scavengers Prevent Argininosuccinic Acid-Induced Oxidative Stress in the Brain of Developing Rats: a New Adjuvant Therapy for Argininosuccinate Lyase Deficiency?Molecular neurobiology · 2020Article
- 3-Hydroxy-3-Methylglutaric Acid Impairs Redox and Energy Homeostasis, Mitochondrial Dynamics, and Endoplasmic Reticulum-Mitochondria Crosstalk in Rat Brain.Neurotoxicity research · 2020Article
- Phagocytosis of full-length Tau oligomers by Actin-remodeling of activated microglia.Journal of neuroinflammation · 2020Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
S-Adenosylmethionine (AdoMet) concentrations are highly elevated in tissues and biological fluids of patients affected by S-adenosylhomocysteine hydrolase deficiency. This disorder is clinically characterized by severe neurological symptoms, whose pathophysiology is not yet established. Therefore, we investigated the effects of intracerebroventricular administration of AdoMet on redox homeostasis, microglia activation, synaptophysin levels, and TAU phosphorylation in cerebral cortex and striatum of young rats. AdoMet provoked significant lipid and protein oxidation, decreased glutathione concentrations, and altered the activity of important antioxidant enzymes in cerebral cortex and striatum. AdoMet also increased reactive oxygen (2',7'-dichlorofluorescein oxidation increase) and nitrogen (nitrate and nitrite levels increase) species generation in cerebral cortex. Furthermore, the antioxidants N-acetylcysteine and melatonin prevented most of AdoMet-induced pro-oxidant effects in both cerebral structures. Finally, we verified that AdoMet produced microglia activation by increasing Iba1 staining and TAU phosphorylation, as well as reduced synaptophysin levels in cerebral cortex. Taken together, it is presumed that impairment of redox homeostasis possibly associated with microglia activation and neuronal dysfunction caused by AdoMet may represent deleterious pathomechanisms involved in the pathophysiology of brain damage in S-adenosylhomocysteine hydrolase deficiency.
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