2010
DOI: 10.1016/j.neuint.2009.11.011
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Sustained deficiency of mitochondrial complex I activity during long periods of survival after seizures induced in immature rats by homocysteic acid

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Cited by 69 publications
(61 citation statements)
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“…In particular, carbonylation of complex I subunits in the range of 20 to 75 kDa was detected, and the extent of inhibition of complex I activity seemed to be directly correlated with the extent of protein carbonylation (Taylor et al, 2003;Keeney et al, 2006;Choksi et al, 2008;Folbergrová et al, 2010). Carbonylation of several subunits of complex I, such as NDUFS1, NDUFS2, NDUFV1, NDUFA9, ND4, and NDUFS4, has been reported previously (Wen and Garg, 2004;Keeney et al, 2006;Choksi et al, 2008).…”
Section: Discussionsupporting
confidence: 60%
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“…In particular, carbonylation of complex I subunits in the range of 20 to 75 kDa was detected, and the extent of inhibition of complex I activity seemed to be directly correlated with the extent of protein carbonylation (Taylor et al, 2003;Keeney et al, 2006;Choksi et al, 2008;Folbergrová et al, 2010). Carbonylation of several subunits of complex I, such as NDUFS1, NDUFS2, NDUFV1, NDUFA9, ND4, and NDUFS4, has been reported previously (Wen and Garg, 2004;Keeney et al, 2006;Choksi et al, 2008).…”
Section: Discussionsupporting
confidence: 60%
“…In human breast cancer cells, RA reduces the activities of antioxidant enzymes such as catalase and glutathione peroxidase (Hong and Lee-Kim, 2009). Complex I is particularly sensitive to oxidative insults, resulting in nitrosylation and/or carbonylation of its subunits (Folbergrová et al, 2010). In HeLa cells combination of retinoic acids and interferon induces overproduction of reactive oxygen species (ROS), with loss of mitochondrial function and cell death (Huang et al, 2007).…”
Section: Introductionmentioning
confidence: 99%
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“…A maintained oxidative energy production by the respiratory chain during complex II inhibition can, at least in part, be explained by electron entry via complex I of the mitochondrial respiratory chain. In support of this, a study by Folbergrová and colleagues has demonstrated that complex I inhibition was not accompanied by impaired ATP production, which is apparently attributable to excess capacity of complex I as documented by energy thresholds (Folbergrová et al 2009). Thus, elevated ROS production seems to be the major reason for NPA-mediated cell death in striatal astrocytes.…”
Section: Discussionmentioning
confidence: 87%
“…Usually, the succinate dehydrogenase (SDH) activity staining clearly shows the subsarcolemmal accumulation of mitochondria (SDH-positive) and the activity assay of COX is particularly useful in the evaluation of mitochondrial myopathies (COX-negative fibers) because Complex IV contains subunits encoded by both the mtDNA and nuclear DNA (Taylor et al, 2004). Recently, Folbergrová et al (2010) reported that the persistent inhibition of Complex I led to the overproduction of ROS, which could contribute to the neuronal injury in a rat model of seizures and in the patients with epileptogene s i s . I n a p r e v i o u s s t u d y , w e o b s e r v e d a significant decrease in the copy number of mtDNA in the leukocytes of patients with mitochondrial encephalomyopathies including MERRF and MELAS syndromes, respectively (Liu et al, 2006).…”
Section: Biochemical Hallmarks In Mitochondrial Encephalomyopathiesmentioning
confidence: 99%