ArticleJournal of inherited metabolic disease2005
Promotion of oxidative stress by 3-hydroxyglutaric acid in rat striatum.
Article in Journal of inherited metabolic disease, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 56 citations in OpenAlex.
- 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
- Lipopolysaccharide-Elicited Systemic Inflammation Induces Selective Vulnerability of Cerebral Cortex and Striatum of Developing Glutaryl-CoA Dehydrogenase Deficient (GcdhNeurotoxicity research · 2020Article
- Neurological manifestations of organic acidurias.Nature reviews. Neurology · 2019Review
- Toxic Synergism Between Quinolinic Acid and Glutaric Acid in Neuronal Cells Is Mediated by Oxidative Stress: Insights to a New Toxic Model.Molecular neurobiology · 2018Article
- Oxidative Stress, Disrupted Energy Metabolism, and Altered Signaling Pathways in Glutaryl-CoA Dehydrogenase Knockout Mice: Potential Implications of Quinolinic Acid Toxicity in the Neuropathology of Glutaric Acidemia Type I.Molecular neurobiology · 2016Article
- Article
- Neurotoxic effects of trans-glutaconic acid in rats.Oxidative medicine and cellular longevity · 2013Article
- Article
- Microarray genomic profile of mitochondrial and oxidant response in manganese chloride treated PC12 cells.Neurotoxicology · 2012Article
- Disruption of mitochondrial homeostasis in organic acidurias: insights from human and animal studies.Journal of bioenergetics and biomembranes · 2011Review
- Induction of S100B secretion in C6 astroglial cells by the major metabolites accumulating in glutaric acidemia type I.Metabolic brain disease · 2010Article
- Promotion of lipid and protein oxidative damage in rat brain by ethylmalonic acid.Neurochemical research · 2010Article
- Evidence for oxidative stress in tissues derived from succinate semialdehyde dehydrogenase-deficient mice.Journal of inherited metabolic disease · 2007Article
- Age and brain structural related effects of glutaric and 3-hydroxyglutaric acids on glutamate binding to plasma membranes during rat brain development.Cellular and molecular neurobiology · 2007Article
- Induction of oxidative stress by chronic and acute glutaric acid administration to rats.Cellular and molecular neurobiology · 2007Article
- Energy metabolism is compromised in skeletal muscle of rats chronically-treated with glutaric acid.Metabolic brain disease · 2007Article
- Infant mice with glutaric acidaemia type I have increased vulnerability to 3-nitropropionic acid toxicity.Journal of inherited metabolic disease · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathophysiology of the striatum degeneration characteristic of patients affected by the inherited neurometabolic disorder glutaryl-CoA dehydrogenase deficiency (GDD), also known as glutaric aciduria type I, is still in debate. We have previously reported that 3-hydroxyglutaric acid (3-OH-GA) considered the main neurotoxin in this disorder, induces oxidative stress in rat cerebral cotex. In the present work, we extended these studies by investigating the in vitro effect of 3-OH-GA, at concentrations ranging from 0.01 to 1.0 mmol/L on the brain antioxidant defences by measuring total radical-trapping antioxidant potential (TRAP), total antioxidant reactivity (TAR) and glutathione (GSH) levels, and on the production of hydrogen peroxide (H(2)O(2)), nitric oxide (NO) and malondialdehyde in striatum homogenates from young rats. We observed that TRAP, TAR and GSH levels were markedly reduced (by up to 50%) when striatum homogenates were treated with 3-OH-GA. In contrast, H(2)O(2) (up to 44%), NO (up to 95%) and malondialdehyde levels (up to 28%) were significantly increased by 3-OH-GA. These data indicate that total nonenzymatic antioxidant defences (TRAP) and the tissue capacity to handle an increase of reactive species (TAR) were reduced by 3-OH-GA in the striatum. Furthermore, the results also reflect an increase of lipid peroxidation, probably secondary to 3-OH-GA-induced free radical production. Thus, it may be presumed that oxidative stress is involved in the neuropathology in GDD.
Indexed as
Identifiers
What OpenQuestion holds
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.