2019
DOI: 10.1039/c8fo01843j
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(+)-Catechin inhibits heart mitochondrial complex I and nitric oxide synthase: functional consequences on membrane potential and hydrogen peroxide production

Abstract: The aim was to study the in vitro effect of nM to low μM concentration of (+)-catechin on the enzymatic activities of mitochondrial complex I and mtNOS, as well as the consequences on the membrane potential and H2O2 production rate.

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Cited by 12 publications
(6 citation statements)
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References 76 publications
(93 reference statements)
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“…Competition between flavonoids and ubiquinone for close binding sites has been suggested. Catechin also inhibits complex I in isolated rat heart mitochondria and decreases H 2 O 2 generation [137]. Nobiletin decreases mitochondrial oxygen consumption and H 2 O 2 production in the presence of glutamate and malate, but a slight increase has been observed with succinate [138].…”
Section: Flavonoids Attenuate Mitochondrial Ros Formationmentioning
confidence: 97%
“…Competition between flavonoids and ubiquinone for close binding sites has been suggested. Catechin also inhibits complex I in isolated rat heart mitochondria and decreases H 2 O 2 generation [137]. Nobiletin decreases mitochondrial oxygen consumption and H 2 O 2 production in the presence of glutamate and malate, but a slight increase has been observed with succinate [138].…”
Section: Flavonoids Attenuate Mitochondrial Ros Formationmentioning
confidence: 97%
“…Recent research showed that catechin also inhibits mitochondrial complex I, resulting in reduced mitochondrial membrane potential and less hydrogen peroxide production in isolated mitochondria (Iglesias et al., 2019). In contrast to the results obtained from quercetin treatment, catechin‐treated N2 exhibited a decrease in TMRE‐staining intensity with minimal reduction in neuronal defects in this study.…”
Section: Resultsmentioning
confidence: 99%
“…In earlier study, flavanol has appear to protect heart mitochondria via various mechanisms. This includes protection effect of flavanol via meddling with ETC complexes activities through deprivation of complex I activity, consequently mitochondrial membrane depolarization which then of ROS production (NO and H 2 O 2 ) [ 116 ]. This has been corroborated by previous study on T2DM model where epigallocatechin-3-gallate (EGCG), a flavanol, attenuated myocardial deterioration and showed beneficial effects on myocardial mitochondrial components.…”
Section: Therapeutic Role Of Flavonoid In Alleviating Mitochondrial Dysfunction-induced Oxidative Stress In Diabetic Cardiomyopathymentioning
confidence: 99%