Disease relevance of Mitochondria, Liver

• Inhibition by propionyl-coenzyme A of N-acetylglutamate synthetase in rat liver mitochondria. A possible explanation for hyperammonemia in propionic and methylmalonic acidemia [1].
• Our aims were to determine if liver mitochondria become resistant to the MPT during cholestasis and, if so, if the resistance is mediated by Bcl-x and/or increased cardiolipin [2].
• APAP toxicity in liver slices (% glutathione-S-transferase alpha released to the medium, GST release) and NAPQI toxicity in isolated liver mitochondria (succinate dehydrogenase inactivation, SDH) from these rats were compared with pair-fed controls [3].
• The K0.5 for activation of glutamate-dependent state 3 respiration by Ca2+ in the presence of ATP at 37 degrees C was determined to be 0.70 +/- 0.05 (S.E.) microM for hepatoma mitochondria and 0.90 +/- 0.03 microM for rat liver mitochondria [4].
• To study the morphologic and biochemical changes occuring in liver mitochondria during recovery from ethanol-induced injury, rats fed a 6-month high-alcohol regimen plus a nutritionally adequate diet which did not induce fatty liver were compared with isocalorically fed controls [5].

Psychiatry related information on Mitochondria, Liver

• Diurnal changes in succinate and D-3-hydroxybutyrate dehydrogenase activities of rat liver mitochondria after chronic alcohol consumption and withdrawal [6].

High impact information on Mitochondria, Liver

• Fumarase activity was virtually absent in both liver mitochondria (53 vs. 2878 +/- 248 nmol per minute per milligram of protein [5 controls]) and skeletal-muscle mitochondria (23 vs. 1997 +/- 717 nmol per minute per milligram [12 controls]) [7].
• A monoclonal antibody was used to prepare immunoaffinity columns that efficiently bind monoamine oxidase B activity but not monoamine oxidase A activity from detergent extracts of human liver mitochondria [8].
• An examination of this hypothesis reveals that the liver mitochondria of ethanol-fed rats show a dissociation between the respiratory functions and the lipid composition and microviscosity of the membranes [9].
• Prolonged consumption of ethanol significantly reduces the capacity of rat liver mitochondria to oxidize acetaldehyde [10].
• In isolated liver mitochondria, state 3 oxidation rates were unchanged or decreased, and activities of the mitochondrial enzymes, citrate synthetase, succinate dehydrogenase, carnitine palmitoyltransferase, and glutamate dehydrogenase (expressed per milligram mitochondrial protein) were unaffected by HCCL treatment [11].

Chemical compound and disease context of Mitochondria, Liver

• [14C]palmitate uptake in isolated rat liver mitochondria: effects of fasting, diabetes mellitus, and inhibitors of carnitine acyltransferase [12].
• BACKGROUND/AIMS: The metabolic capacity of liver mitochondria is impaired in rats with carbon tetrachloride (CCl4)-induced cirrhosis [13].
• Toxicity of amiodarone and amiodarone analogues on isolated rat liver mitochondria [14].
• The results suggest that delayed adenine nucleotide uptake into liver mitochondria may retard initiation of gluconeogenesis in newborns experiencing hypoxia, as in respiratory distress or in newborns of diabetic mothers [15].
• Refsum disease diagnostic marker phytanic acid alters the physical state of membrane proteins of liver mitochondria [16].

Biological context of Mitochondria, Liver

• METHODS: Rat liver mitochondria, cultured rat hepatocytes, or rats were treated with these drugs, and the effects on mitochondrial respiration, beta-oxidation, reactive oxygen species formation, and lipid peroxidation were determined [17].
• The stoichiometry of oxidative phosphorylation at low oxygen tension (less than 3 torr; O2 less than 5 microM) has been measured in rat liver mitochondria [18].
• AA1 exhibited little inhibition of electron transport in isolated rat liver mitochondria; however, it inhibited mitochondrial ATPase with 50% inhibitory concentration of 6 microM [19].
• The ability of methylglyoxal-bis(guanylhydrazone) (MGBG) and 4,4'-diacetyldiphenylurea-bis(guanylhydrazone) to interact with the hypoglycemic agent, phenethylbiguanide (DBI), in affecting the bioenergetic functions of isolated rat liver mitochondria was studied [20].
• We previously demonstrated that mammalian mitochondria from mice efficiently remove 8-oxodG from their genomes and isolated a protein from rat liver mitochondria with 8-oxoguanine (8-oxodG) DNA glycosylase/apurinic DNA lyase activity [21].

Anatomical context of Mitochondria, Liver

• Membrane binding of ethanol, anesthetics, and hydrophobic molecules in brain synaptosomes and liver mitochondria from rats is conspicuously reduced after long-term consumption of ethanol [22].
• We previously demonstrated an alternate pathway for the biosynthesis of 5-aminolevulinic acid (ALA) in bovine liver mitochondria and of tetrapyrroles in suspensions of rat hepatocytes (1980. J. Biol. Chem. 255: 3742; 1981. Proc. Natl. Acad. Sci. USA. 78: 5335) [23].
• Rat liver mitochondria have a multicomponent system that underlies the remarkable ability of mitochondria to take up and retain glutathione [24].
• Metallothionein (MT) localizes in the intermembrane space of liver mitochondria as well as in the cytosol and nucleus [25].
• The precursor of rat liver ornithine transcarbamylase (ornithine carbamoyltransferase; carbamoylphosphate:L-ornithine carbamoyltransferase, EC 2.1.3.3) (pre-ornithine transcarbamylase), which was synthesized in a reticulocyte lysate cell-free system, was converted to an apparently mature form of the enzyme by isolated rat liver mitochondria [26].

Associations of Mitochondria, Liver with chemical compounds

• The occurrence of an efficient sterol nucleus hydroxylase activity in liver mitochondria appears to be unique for fetal liver [27].
• The resistance to Ca(2+)-induced MPT was enhanced in liver mitochondria of genipin-treated mice [28].
• METHODS: The effects of tacrine on mitochondrial function were determined in isolated rat liver mitochondria, cultured rat hepatocytes, and isolated human lymphocytes [29].
• Oxidation of glutamine by avian liver mitochondria was substantially less than that of glutamate [30].
• With rat liver mitochondria, the order for inhibition of NAD(+)-linked O2 consumption (6-min preincubations) was as follows: MPP+ = 2-methylharmine greater than 2-methylharmol = 2-methylharmaline much greater than 2-methylharmalol greater than 2-methylnorharman greater than 6-OH-2-methylharmalan much greater than 2-methylharman [31].

Gene context of Mitochondria, Liver

• Using Western analysis and immunogold labeling, A-RAF was selectively localized in highly purified rat liver mitochondria [32].
• MAO A-3C9 appears to have a lower affinity for purified MAO A than the other three antibodies and does not immunoprecipitate either MAO A or MAO B from human platelets or from Triton X-100 extracts of human placental and liver mitochondria [33].
• Given published evidence that NF kappaB is antiapoptotic and that UCP-2 may decrease mitochondrial oxidant production in some cells, these results suggest that TNF-dependent increases in oxidant production by liver mitochondria promote the induction of antioxidant defenses in the regenerating liver [34].
• However, the level of total glutathione was 30% less in liver mitochondria of the Sod2(-/+) mice [35].
• Moreover, the liver mitochondria were found to release markedly increased hydrogen peroxide, a Gpx1 substrate, and have decreased mitochondrial respiratory control ratio and power output index [36].

Analytical, diagnostic and therapeutic context of Mitochondria, Liver

• The folate-binding protein of rat liver mitochondria [Zamierowski, M. & Wagner, C. (1977) J. Biol. Chem. 252, 933-938] has been purified to homogeneity by a combination of gel filtration, DEAE-cellulose, and affinity chromatography [37].
• To solve this problem, we fractionated five short-chain acyl-CoA dehydrogenases (isovaleryl-CoA, n-butyryl-CoA, isobutyryl-CoA, n-octanoyl-CoA, and glutaryl-CoA dehydrogenases) from rat liver mitochondria by isoelectric focusing and DEAE-cellulose column chromatography [38].
• Rat liver mitochondria were purified by differential and Percoll gradient centrifugation, and mtODE was extracted from Triton X-100-solubilized mitochondria [39].
• In the present work, unlabeled chargerin II was purified from intact rat liver mitochondria by high performance liquid chromatography [40].
• Adenosine triphosphatase from rat liver mitochondria. Crystallization and x-ray diffraction studies of the F1-component of the enzyme [41].

References