Mitochondria exposed

R. J. Sokol, B. M. Winklhofer-Roob, M. W. Devereaux and J. M. McKim, Jr., Generation of hydroperoxides in isolated rat hepatocytes and hepatic mitochondria exposed to hydrophobic bile acids, Gastroenterology, 1995, 109(4), 1249. 

Iron damages hepatocellular organelles. Mitochondria exposed to excessive iron show increased fragility, increased volume, increased pH, decreased fluidity, and increased lipid peroxidation (Britton, 1996). Lysosomes exposed to iron overload show increased fragility and... 

No effects in isolated mitochondrial preparations on state 4 respiration, ADP-stimulated or 2,4-dinitrophenol-stimulated respiration, the respiratory control ratio, the adenosine diphosphate/oxygen ratio, the rate of calcium-induced mitochondrial swelling at 50 pM. Loss of MMP was seen rally at the highest concentration of ximelagatrtm tested, 300 pM, in mitochondria exposed for 24 h. No effects on P-oxidation of fatty acids up to 300 pM... 

Intramitochondrial hydrolysis of pyridine nucleotides and release of nicotinamide from mitochondria exposed to hydroperoxide [9] suggested the existence of an intramitochondrial NAD" glycohydrolase. Subsequent studies [12] located the enzyme on the inner side of the inner mitochondrial membrane. Activity was also present in the matrix fraction of mitochondria, but release from the iiuier membrane into the matrix fraction during isolation of the membrane was not ruled out. The activity in iimer mitochondrial membranes (submitochondrial particles, SMP) is inhibitable by ATP [11]. In addition, ATP-sensitive covalent modification of SMP concomitant with enzymatic hydrolysis of NAD was indicated. 

As discussed previously, the mitochondrial theory of ageing rests on the observation that mitochondrial DNA is exposed to high levels of reactive oxygen species when the mitochondrion is performing its redox chemistry. These reactive oxygen species cause mutation. These mutations accumulate, gradually damaging the mitochondrion s ability to function. This happens in... 

During acidosis, the cells of the renal tubule can respond by inserting two proteins into the apical region of the plasma membrane. (The apical part is that region that is exposed to the developing urine.) The two proteins are H,K-ATPase and H+-ATPase. H,K-ATPase, and the enzymes that act in concert with it, is better known as a component of the parietal cell where it creates stomach acid. The other proton pump of the renal tubule, which is H" -ATPase, is closely related to FoFiH" -ATPase of the mitochondrial membrane. Hence, anyone who imderstands how protons are pumped out of the mitochondrion and how stomach acid is made will clearly understand how the renal tubule can shuttle protons to the lumen of the renal tubule and into the developing urine. 

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