EditorialMitochondrial hepatopathies
Section snippets
Acknowledgements
PFC is a Wellcome Trust Senior Fellow in Clinical Science. SDM is supported by NIH grants NS11766, and HD32062, a grant from the Muscular Dystrophy Association, and by the Marriott Mitochondrial Disorder Clinical Research Fund (MMDCRF).
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Mitochondrial dysfunction and oxidative stress in liver of male albino rats after exposing to sub-chronic intoxication of chlorpyrifos, cypermethrin, and imidacloprid
2021, Pesticide Biochemistry and PhysiologyCitation Excerpt :The liver is the main detoxifying organ and the primary involved in xenobiotic metabolism in the mammalian body. It is one of the richest organs in terms of the number and density of mitochondria (Chinnery and DiMauro, 2005). In physiological conditions, mitochondria have significant roles in the metabolism and energy regulation as a source of reactive oxygen species (ROS) that generating approximately 85% of the total cellular superoxide radical (O2•-) (Samarghandian et al., 2016).
Novel large-range mitochondrial DNA deletions and fatal multisystemic disorder with prominent hepatopathy
2011, Biochemical and Biophysical Research CommunicationsCitation Excerpt :In some infants, liver dysfunction may spontaneously reverse or remain stable, but in some there is rapid progression to cholestasis, coagulopathy, and ascites. Biochemical studies reveal single or multiple respiratory chain enzymes defects, which may be restricted to the liver and remain undetectable in skeletal muscle or skin fibroblasts [6]. Prominent liver involvement is rarely related to primary pathogenic point mutations [32], or single deletions of mtDNA [33], but is most often associated with conditions characterized by reduced amounts of mtDNA in affected tissues and grouped as MDS [34–36].
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