ArticleNeurotoxicity research2019
Guanosine Protects Striatal Slices Against 6-OHDA-Induced Oxidative Damage, Mitochondrial Dysfunction, and ATP Depletion.
Article in Neurotoxicity research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- 2-(Arylamino)thiazol-4(5H)-ones Mitigate Oxidative Stress and Confer Neuroprotection in Cellular andInternational journal of molecular sciences · 2026Article
- Guanosine contributes to rapid purinergic regulation of dopamine during ischemia.Purinergic signalling · 2026Article
- APurinergic signalling · 2026Article
- Lessons from the physiological role of guanosine in neurodegeneration and cancer: Toward a multimodal mechanism of action?Purinergic signalling · 2025Review
- Causality of blood metabolites and metabolic pathways on Graves' disease and Graves' ophthalmopathy: a two-sample Mendelian randomization study.Endocrine · 2024Article
- The protective effect of parthenolide in an in vitro model of Parkinson's disease through its regulation of nuclear factor-kappa B and oxidative stress.Molecular biology reports · 2024Article
- Prevotella copri transplantation promotes neurorehabilitation in a mouse model of traumatic brain injury.Journal of neuroinflammation · 2024Article
- Suppression of Ehrlich ascites tumor cell proliferation via G1 arrest induced by dietary nucleic acid-derived nucleosides.PloS one · 2024Article
- Potential Therapeutic Effects of Policosanol from Insect Wax on Caenorhabditis elegans Models of Parkinson's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023Article
- Influence of Guanine-Based Purines on the Oxidoreductive Reactions Involved in Normal or Altered Brain Functions.Journal of clinical medicine · 2023Review
- Purine nucleoside phosphorylase as a target to treat age-associated lower urinary tract dysfunction.Nature reviews. Urology · 2022Review
- Novel Series of Dual NRF2 Inducers and Selective MAO-B Inhibitors for the Treatment of Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2022Article
- Pinocembrin-7-Methylether Protects SH-SY5Y Cells Against 6-Hydroxydopamine-Induced Neurotoxicity via Modulating Nrf2 Induction Through AKT and ERK Pathways.Neurotoxicity research · 2021Article
- Adenosine APurinergic signalling · 2021Article
- Guanosine Mechanisms of Action: Toward Molecular Targets.Frontiers in pharmacology · 2021Article
- Involvement of adenosine APurinergic signalling · 2020Article
- Novel Targets for Fast Antidepressant Responses: Possible Role of Endogenous Neuromodulators.Chronic stress (Thousand Oaks, Calif.)Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by loss of dopaminergic neurons in substantia nigra pars compacta which induces severe motor symptoms. 6-OHDA is a neurotoxin widely used in PD animal models due to its high affinity by dopamine transporter, its rapid non-enzymatic auto-oxidation which generates reactive oxygen species (ROS), oxidative stress, and for induced mitochondrial dysfunction. We previously reported an in vitro protocol of 6-OHDA-induced toxicity in brain regions slices, as a simple and sensitive assay to screen for protective compounds related to PD. Guanosine (GUO), a guanine-based purine nucleoside, is a neuroprotective molecule that is showing promising effects as an antiparkinsonian agent. To investigate the mechanisms involved on GUO-induced neuroprotection, slices of cortex, striatum, and hippocampus were incubated with GUO in the presence of 6-OHDA (100 μM). 6-OHDA promoted a decrease in cellular viability and increased ROS generation in all brain regions. Disruption of mitochondrial potential, depletion in intracellular ATP levels, and increase in cell membrane permeabilization were evidenced in striatal slices. GUO prevented the increase in ROS generation, disruption in mitochondrial potential, and depletion of intracellular ATP induced by 6-OHDA in striatal slices. In conclusion, GUO was effective to prevent oxidative events before cell damage, such as mitochondrial disruption, intracellular ATP levels depletion, and ROS generation in striatal slices subjected to in vitro 6-OHDA-induced toxicity.
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