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Mateus Grings

Researcher at Universidade Federal do Rio Grande do Sul

Publications -  60
Citations -  883

Mateus Grings is an academic researcher from Universidade Federal do Rio Grande do Sul. The author has contributed to research in topics: Glutathione & Oxidative stress. The author has an hindex of 15, co-authored 54 publications receiving 663 citations. Previous affiliations of Mateus Grings include University of Pittsburgh.

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Evaluation of mitochondrial bioenergetics, dynamics, endoplasmic reticulum-mitochondria crosstalk, and reactive oxygen species in fibroblasts from patients with complex I deficiency.

TL;DR: Treatment of ACAD9 deficient cells with JP4-039, a novel mitochondria-targeted reactive oxygen species, electron and radical scavenger, decreased superoxide level and increased basal and maximal respiratory rate is identified, identifying a potential therapeutic intervention opportunity in CI deficiency.
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Antioxidant properties of mesenchymal stem cells against oxidative stress in a murine model of colitis

TL;DR: The oxidative stress is a pathomechanism underlying the pathophysiology of colitis and MSC play an important role in preventing the impairment of antioxidants defenses in inflamed colon.
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Bezafibrate prevents mitochondrial dysfunction, antioxidant system disturbance, glial reactivity and neuronal damage induced by sulfite administration in striatum of rats: Implications for a possible therapeutic strategy for sulfite oxidase deficiency.

TL;DR: Findings provide strong evidence that sulfite induces neurotoxicity that leads to glial reactivity and neuronal damage and bezafibrate exerts neuroprotective effects against sulfite toxicity, which may be an attractive agent for the development of novel therapeutic strategies for SO-deficient patients.
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Physical Exercise During Pregnancy Prevents Cognitive Impairment Induced by Amyloid-β in Adult Offspring Rats

TL;DR: A potential protective effect of exercise during pregnancy against amyloid-β neurotoxicity in the adult offspring brain is demonstrated, by mitigating the neurodegenerative process triggered by Alzheimer-associated AβOs through programming the brain metabolism.
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Long-chain 3-hydroxy fatty acids accumulating in long-chain 3-hydroxyacyl-CoA dehydrogenase and mitochondrial trifunctional protein deficiencies uncouple oxidative phosphorylation in heart mitochondria.

TL;DR: The present data indicate that major 3-hydroxylated fatty acids accumulating in MTP and LCHAD deficiencies behave as strong uncouplers of oxidative phosphorylation potentially impairing heart energy homeostasis.