Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.9.3.1 (cytochrome oxidase)
 8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Avers, Charlotte J. (Rutgers, The State University, New Brunswick, N. J.), Cynthia R. Pfeffer, and Martha W. Rancourt. Acriflavine induction of different kinds of "petite" mitochondrial populations in Saccharomyces cerevisiae. J. Bacteriol. 90:481-494. 1965.-Mutant frequencies induced by 1 or 2 hr in 16 and 64 mug/ml of acriflavine were significantly higher during acceleration and log-phase exposures than during lag or stationary phases. From these induced petites, 59 colonies were selected at random and established in pure culture. All strains were analyzed histochemically for mitochondrial cytochrome oxidase and succinic dehydrogenase (SDH) reactions. On the basis of counts of stained mitochondria per cell obtained by light microscopy, four different cell phenotypes were recognized among the mutant strains: (i) reduced cytochrome oxidase, wild-type SDH; (ii) reduced cytochrome oxidase, high SDH; (iii) absent cytochrome oxidase, high SDH; and (iv) absent cytochrome oxidase, wild-type SDH. The last group was the most common, characterizing 43 of the 59 strains. Electron microscopy showed differences in mitochondrial ultrastructure for the various cell phenotype classes. Electron histochemical localizations showed cytochrome oxidase reaction product only on mitochondrial membranes of respiration-competent cells. Both reactive and unreactive mitochondria occurred in the same cell in mutants with partial respiratory competence. Different mitochondrial subpopulation mixtures characterized the mutant strains, many of which had at least two kinds of respiratory-competent types per chondriome. The diverse chondriomes comprised a stable feature of the mutants, since they have been maintained unchanged during serial transfer for more than 1 year in culture. Together with earlier reports of at least two kinds of mitochondria in wild-type cells, the evidence indicated that mitochondria were capable of regulating some portion of their phenotype. The recognition of mitochondrial phenotypes was proposed as an initial step in a formal analysis of organelle heredity.
 ...
PMID:ACRIFLAVINE INDUCTION OF DIFFERENT KINDS OF "PETITE" MITOCHONDRIAL POPULATIONS IN SACCHAROMYCES CEREVISIAE. 1432 64

Methylene blue (MB) has been used clinically for about a century to treat numerous ailments. We show that MB and other diaminophenothiazines extend the life span of human IMR90 fibroblasts in tissue culture by >20 population doubling (PDLs). MB delays senescence at nM levels in IMR90 by enhancing mitochondrial function. MB increases mitochondrial complex IV by 30%, enhances cellular oxygen consumption by 37-70%, increases heme synthesis, and reverses premature senescence caused by H2O2 or cadmium. MB also induces phase-2 antioxidant enzymes in hepG2 cells. Flavin-dependent enzymes are known to use NAD(P)H to reduce MB to leucomethylene blue (MBH2), whereas cytochrome c reoxidizes MBH2 to MB. Experiments on lysates from rat liver mitochondria suggest the ratio MB/cytochrome c is important for the protective actions of MB. We propose that the cellular senescence delay caused by MB is due to cycling between MB and MBH2 in mitochondria, which may partly explain the increase in specific mitochondrial activities. Cycling of MB between oxidized and reduced forms may block oxidant production by mitochondria. Mitochondrial dysfunction and oxidative stress are thought to be key aberrations that lead to cellular senescence and aging. MB may be useful to delay mitochondrial dysfunction with aging and the decrease in complex IV in Alzheimer disease.
 ...
PMID:Methylene blue delays cellular senescence and enhances key mitochondrial biochemical pathways. 1792 58

Recently we demonstrated the utility of optical fluorometry to detect a change in the redox status of mitochondrial autofluorescent coenzymes NADH (Nicotinamide Adenine Dinucleotide) and FAD (oxidized form of Flavin Adenine Dinucleotide (FADH2,)) as a measure of mitochondrial function in isolated perfused rat lungs (IPL). The objective of this study was to utilize optical fluorometry to evaluate the effect of rat exposure to hyperoxia (>95% O2 for 48 hours) on lung tissue mitochondrial redox status of NADH and FAD in a nondestructive manner in IPL. Surface NADH and FAD signals were measured before and after lung perfusion with perfusate containing rotenone (ROT, complex I inhibitor), potassium cyanide (KCN, complex IV inhibitor), and/or pentachlorophenol (PCP, uncoupler). ROT- or KCN-induced increase in NADH signal is considered a measure of complex I activity, and KCN-induced decrease in FAD signal is considered a measure of complex II activity. The results show that hyperoxia decreased complex I and II activities by 63% and 55%, respectively, as compared to lungs of rats exposed to room air (normoxic rats). Mitochondrial complex I and II activities in lung homogenates were also lower (77% and 63%, respectively) for hyperoxic than for normoxic lungs. These results suggest that the mitochondrial matrix is more reduced in hyperoxic lungs than in normoxic lungs, and demonstrate the ability of optical fluorometry to detect a change in mitochondrial redox state of hyperoxic lungs prior to histological changes characteristic of hyperoxia.
 ...
PMID:Novel Flurometric Tool to Assess Mitochondrial Redox State of Isolated Perfused Rat Lungs after Exposure to Hyperoxia. 2537 60