C. Cecatto

发表

α-Ketoadipic Acid and α-Aminoadipic Acid Cause Disturbance of Glutamatergic Neurotransmission and Induction of Oxidative Stress In Vitro in Brain of Adolescent Rats

G. Leipnitz, C. Vargas, M. Wajner, 2017, Neurotoxicity Research.

S-Adenosylmethionine Promotes Oxidative Stress and Decreases Na+, K+-ATPase Activity in Cerebral Cortex Supernatants of Adolescent Rats: Implications for the Pathogenesis of S-Adenosylhomocysteine Hydrolase Deficiency

G. Leipnitz, M. Wajner, A. Wyse, 2018, Molecular Neurobiology.

Ethylmalonic Acid Induces Permeability Transition in Isolated Brain Mitochondria

G. Leipnitz, M. Wajner, A. U. Amaral, 2014, Neurotoxicity Research.

Mevalonolactone disrupts mitochondrial functions and induces permeability transition pore opening in rat brain mitochondria: Implications for the pathogenesis of mevalonic aciduria

C. Vargas, M. Wajner, A. U. Amaral, 2017, Neurochemistry International.

Experimental evidence that maleic acid markedly compromises glutamate oxidation through inhibition of glutamate dehydrogenase and α-ketoglutarate dehydrogenase activities in kidney of developing rats

M. Wajner, A. U. Amaral, S. Wajner, 2019, Molecular and Cellular Biochemistry.

Disturbance of bioenergetics and calcium homeostasis provoked by metabolites accumulating in propionic acidemia in heart mitochondria of developing rats.

M. Wajner, A. U. Amaral, S. Wajner, 2020, Biochimica et biophysica acta. Molecular basis of disease.

Impairment of mitochondrial bioenergetics and permeability transition induction caused by major long-chain fatty acids accumulating in VLCAD deficiency in skeletal muscle as potential pathomechanisms of myopathy.

M. Wajner, A. U. Amaral, R. F. Castilho, 2020, Toxicology in vitro : an international journal published in association with BIBRA.

2‐Methylcitric acid impairs glutamate metabolism and induces permeability transition in brain mitochondria

M. Wajner, A. U. Amaral, R. F. Castilho, 2016, Journal of neurochemistry.

Disturbance of mitochondrial functions associated with permeability transition pore opening induced by cis-5-tetradecenoic and myristic acids in liver of adolescent rats.

M. Wajner, A. U. Amaral, S. Wajner, 2019, Mitochondrion.

Metabolite accumulation in VLCAD deficiency markedly disrupts mitochondrial bioenergetics and Ca2+ homeostasis in the heart

M. Wajner, A. U. Amaral, S. Wajner, 2018, The FEBS journal.

Disturbance of mitochondrial functions provoked by the major long-chain 3-hydroxylated fatty acids accumulating in MTP and LCHAD deficiencies in skeletal muscle.

M. Wajner, A. U. Amaral, Janaina da Silva, 2016, Toxicology in vitro : an international journal published in association with BIBRA.

mitochondrial permeability transition pore opening in rat brain and liver : possible implications for the pathogenesis of MCAD deficiency

M. Wajner, A. U. Amaral, R. Ribeiro, 2016 .

Reduction of Na+, K+-ATPase activity and expression in cerebral cortex of glutaryl-CoA dehydrogenase deficient mice: a possible mechanism for brain injury in glutaric aciduria type I.

M. Wajner, C. Fernandes, B. Seminotti, 2012, Molecular genetics and metabolism.

Marked reduction of Na(+), K(+)-ATPase and creatine kinase activities induced by acute lysine administration in glutaryl-CoA dehydrogenase deficient mice.

M. Wajner, C. Fernandes, B. Seminotti, 2012, Molecular genetics and metabolism.

Deregulation of mitochondrial functions provoked by long‐chain fatty acid accumulating in long‐chain 3‐hydroxyacyl‐CoA dehydrogenase and mitochondrial permeability transition deficiencies in rat heart – mitochondrial permeability transition pore opening as a potential contributing pathomechanism of

M. Wajner, A. U. Amaral, C. Cecatto, 2015, The FEBS journal.

Mechanistic Bases of Neurotoxicity Provoked by Fatty Acids Accumulating in MCAD and LCHAD Deficiencies

M. Wajner, A. U. Amaral, C. Cecatto, 2017 .

Ethylmalonic acid impairs brain mitochondrial succinate and malate transport.

G. Leipnitz, M. Wajner, A. U. Amaral, 2012, Molecular genetics and metabolism.

Experimental evidence that bioenergetics disruption is not mainly involved in the brain injury of glutaryl-CoA dehydrogenase deficient mice submitted to lysine overload

M. Wajner, B. Seminotti, A. U. Amaral, 2015, Brain Research.

High vulnerability of the heart and liver to 3‐hydroxypalmitic acid–induced disruption of mitochondrial functions in intact cell systems

C. Vargas, M. Wajner, A. U. Amaral, 2018, Journal of cellular biochemistry.

Ethylmalonic acid impairs bioenergetics by disturbing succinate and glutamate oxidation and induces mitochondrial permeability transition pore opening in rat cerebellum

F. Guma, G. Leipnitz, M. Wajner, 2021, Journal of neurochemistry.

Evidence that thiol group modification and reactive oxygen species are involved in hydrogen sulfide-induced mitochondrial permeability transition pore opening in rat cerebellum.

G. Leipnitz, M. Wajner, A. U. Amaral, 2019, Mitochondrion.

Uncoupling, metabolic inhibition and induction of mitochondrial permeability transition in rat liver mitochondria caused by the major long-chain hydroxyl monocarboxylic fatty acids accumulating in LCHAD deficiency.

M. Wajner, A. U. Amaral, R. F. Castilho, 2015, Biochimica et biophysica acta.

G. Leipnitz, M. Wajner, A. Wyse, 2018, Molecular Neurobiology.

M. Wajner, A. U. Amaral, S. Wajner, 2019, Molecular and Cellular Biochemistry.

Ethylmalonic Acid Induces Permeability Transition in Isolated Brain Mitochondria

G. Leipnitz, M. Wajner, A. U. Amaral, 2014, Neurotoxicity Research.

Glycine disrupts myelin, glutamatergic neurotransmission, and redox homeostasis in a neonatal model for non ketotic hyperglycinemia.

G. Leipnitz, M. Wajner, B. Seminotti, 2023, Biochimie.

cis-4-Decenoic and decanoic acids impair mitochondrial energy, redox and Ca(2+) homeostasis and induce mitochondrial permeability transition pore opening in rat brain and liver: Possible implications for the pathogenesis of MCAD deficiency.

M. Wajner, A. U. Amaral, R. Ribeiro, 2016, Biochimica et biophysica acta.