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Showing papers by "Mateus Grings published in 2010"

Journal Article•DOI•
Long-chain 3-hydroxy fatty acids accumulating in LCHAD and MTP deficiencies induce oxidative stress in rat brain.

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Anelise Miotti Tonin1, Mateus Grings1, Estela Natacha Brandt Busanello1, Alana Pimentel Moura1, Gustavo da Costa Ferreira1, Carolina Maso Viegas1, Carolina Gonçalves Fernandes1, Patrícia Fernanda Schuck1, Patrícia Fernanda Schuck2, Moacir Wajner1 •
Universidade Federal do Rio Grande do Sul1, Universidade do Extremo Sul Catarinense2
01 Jul 2010-Neurochemistry International
TL;DR: The present data showing that 3HDA, 3HTA and 3HPA elicit oxidative stress in rat brain indicate that oxidative damage may represent an important pathomechanism involved in the neurologic symptoms manifested by patients affected by LCHAD and MTP deficiencies.

34 citations

Journal Article•DOI•
Disturbance of mitochondrial energy homeostasis caused by the metabolites accumulating in LCHAD and MTP deficiencies in rat brain.

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Anelise Miotti Tonin1, Gustavo da Costa Ferreira1, Mateus Grings1, Carolina Maso Viegas1, Estela Natacha Brandt Busanello1, Alexandre Umpierrez Amaral1, Ângela Zanatta1, Patrícia Fernanda Schuck1, Patrícia Fernanda Schuck2, Moacir Wajner1 •
Universidade Federal do Rio Grande do Sul1, Universidade do Extremo Sul Catarinense2
22 May 2010-Life Sciences
TL;DR: The data indicate that the long-chain 3-hydroxy fatty acids that accumulate in LCHAD/MTP deficiencies act as uncouplers of oxidative phosphorylation, while 3HTA also behaves as a metabolic inhibitor.

29 citations

Journal Article•DOI•
In vitro evidence that phytanic acid compromises Na+,K+-ATPase activity and the electron flow through the respiratory chain in brain cortex from young rats

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Estela Natacha Brandt Busanello1, Carolina Maso Viegas1, Alana Pimentel Moura1, Anelise Miotti Tonin1, Mateus Grings1, Carmen Regla Vargas1, Moacir Wajner1 •
Universidade Federal do Rio Grande do Sul1
17 Sep 2010-Brain Research
TL;DR: The data indicate that Phyt impairs brain bioenergetics at the level of energy formation, as well as neurotransmission, in brain cortex of young rats.

24 citations

Journal Article•DOI•
Promotion of Lipid and Protein Oxidative Damage in Rat Brain by Ethylmalonic Acid

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Patrícia Fernanda Schuck1, Patrícia Fernanda Schuck2, Estela Natacha Brandt Busanello1, Alana Pimentel Moura1, Anelise Miotti Tonin1, Mateus Grings1, Luciana Ritter1, Carmen Regla Vargas, Gustavo da Costa Ferreira1, Moacir Wajner1 •
Universidade Federal do Rio Grande do Sul1, Universidade do Extremo Sul Catarinense2
01 Feb 2010-Neurochemical Research
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.
Abstract: High concentrations of ethylmalonic acid are found in tissues and biological fluids of patients affected by ethylmalonic encephalopathy, deficiency of short-chain acyl-CoA dehydrogenase activity and other illnesses characterized by developmental delay and neuromuscular symptoms. The pathophysiological mechanisms responsible for the brain damage in these patients are virtually unknown. Therefore, in the present work we investigated the in vitro effect of EMA on oxidative stress parameters in rat cerebral cortex. EMA significantly increased chemiluminescence and thiobarbituric acid-reactive species levels (lipoperoxidation), as well as carbonyl content and oxidation of sulfhydryl groups (protein oxidative damage) and DCFH. EMA also significantly decreased the levels of reduced glutathione (non-enzymatic antioxidant defenses). In contrast, nitrate and nitrite levels were not affected by this short organic acid. It is therefore 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.

19 citations