scispace - formally typeset
M

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.

Papers
More filters
Journal ArticleDOI

The Role of Oxidative Stress and Bioenergetic Dysfunction in Sulfite Oxidase Deficiency: Insights from Animal Models.

TL;DR: Findings from in vivo and in vitro findings from animal studies indicating that oxidative stress and mitochondrial dysfunction are involved in the pathophysiology of the brain damage in sulfite oxidase deficiency offer new perspectives for potential therapeutic strategies for this condition.
Journal ArticleDOI

Methylphenidate Decreases ATP Levels and Impairs Glutamate Uptake and Na + ,K + -ATPase Activity in Juvenile Rat Hippocampus

TL;DR: The results suggest that chronic MPH exposure at early age impairs glutamate uptake and Na+,K+-ATPase activity probably by decreasing in ATP levels observed in rat hippocampus.
Journal ArticleDOI

ETHE1 and MOCS1 deficiencies: Disruption of mitochondrial bioenergetics, dynamics, redox homeostasis and endoplasmic reticulum-mitochondria crosstalk in patient fibroblasts

TL;DR: Data demonstrate that previously unrecognized broad disturbances of cellular function are involved in the pathophysiology of ETHE1 and MOCS1 deficiencies, and that reduction of mitochondrial superoxide by JP4-039 is a promising strategy for adjuvant therapy of these disorders.
Journal ArticleDOI

Promotion of Lipid and Protein Oxidative Damage in Rat Brain by Ethylmalonic Acid

TL;DR: In the present work, the in vitro effect of EMA on oxidative stress parameters in rat cerebral cortex is investigated and it is presumed that oxidative stress may represent a pathomechanism involved in the pathophysiology of the neurologic symptoms manifested by patients affected by disorders in which EMA accumulates.