ArticleFree radical biology & medicine2006
Up-regulation of gamma-glutamyl transpeptidase activity following glutathione depletion has a compensatory rather than an inhibitory effect on mitochondrial complex I activity: implications for Parkinson's disease.
Article in Free radical biology & medicine, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 43 citations in OpenAlex.
- Natural variation in age-related dopamine neuron degeneration is glutathione dependent and linked to life span.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- S-Glutathionylation and S-Nitrosylation in Mitochondria: Focus on Homeostasis and Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- Gamma-glutamyltransferase, arterial remodeling and prehypertension in a healthy population at low cardiometabolic risk.Journal of human hypertension · 2021Article
- Non-linear relationship between gamma-glutamyl transferase and type 2 diabetes mellitus risk: secondary analysis of a prospective cohort study.The Journal of international medical research · 2020Article
- Prevention of progression in Parkinson's disease.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2018Review
- Neurodegeneration in Parkinson's disease: interactions of oxidative stress, tryptophan catabolites and depression with mitochondria and sirtuins.Molecular neurobiology · 2014Review
- Protective effects of zonisamide against rotenone-induced neurotoxicity.Neurochemical research · 2013Article
- Glutathione metabolism and Parkinson's disease.Free radical biology & medicine · 2013Review
- Evaluation of markers of oxidative stress, antioxidant function and astrocytic proliferation in the striatum and frontal cortex of Parkinson's disease brains.Neurochemical research · 2011Article
- S-glutathionylation: from molecular mechanisms to health outcomes.Antioxidants & redox signaling · 2011Review
- Quantitative mapping of reversible mitochondrial Complex I cysteine oxidation in a Parkinson disease mouse model.The Journal of biological chemistry · 2011Article
- Iron mediates neuritic tree collapse in mesencephalic neurons treated with 1-methyl-4-phenylpyridinium (MPP+).Journal of neural transmission (Vienna, Austria : 1996) · 2011Article
- Protective Effects of Emodin and Chrysophanol Isolated from Marine Fungus Aspergillus sp. on Ethanol-Induced Toxicity in HepG2/CYP2E1 Cells.Evidence-based complementary and alternative medicine : eCAM · 2011Article
- Mouse cerebellar astrocytes protect cerebellar granule neurons against toxicity of the polybrominated diphenyl ether (PBDE) mixture DE-71.Neurotoxicology · 2009Article
- Glutathione and apoptosis.Free radical research · 2008Review
- Oxidative and nitrative protein modifications in Parkinson's disease.Free radical biology & medicine · 2008Review
- Coupling endoplasmic reticulum stress to the cell death program in dopaminergic cells: effect of paraquat.Neuromolecular medicine · 2008Article
- 1-methyl-4-phenylpyridinium-induced alterations of glutathione status in immortalized rat dopaminergic neurons.Toxicology and applied pharmacology · 2007Article
- GSTpi expression mediates dopaminergic neuron sensitivity in experimental parkinsonism.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Up-regulation of activity of gamma-glutamyl transpeptidase (GGT) has been reported to occur in the Parkinsonian substantia nigra, the area of the brain affected by the disease. Increased GGT activity has been hypothesized to play a role in subsequent mitochondrial complex I (CI) inhibition by increasing cysteine as substrate for cellular uptake. Intracellular cysteine has been proposed to form toxic adducts with dopamine which can be metabolized to compounds which inhibit CI activity. We have demonstrated that in addition to CI inhibition, GGT activity is up-regulated in dopaminergic cells as a consequence of glutathione depletion. Inhibition of GGT rather than resulting in increased CI inhibition results in exacerbation of this inhibitory effect. This suggests that increased GGT activity is likely an adaptive response to the loss of glutathione to conserve intracellular glutathione content and results in a compensatory effect on CI activity rather than in its inhibition as has been previously widely hypothesized.
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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.