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)

Effect of dimethyl sulphoxide (DMSO) on mitochondrial biogenesis in regenerating rat liver and cells of Saccharomyces cerevisiae during aerobiosis has been studied by monitoring the cytochrome oxidase activity. A single dose of DMSO (275 mg/100-125 g body wt) to normal rats stimulated cytochrome oxidase activity in liver mitochondria while the same dose to partial hepatectomized rats inhibited the enzyme activity. Administration of low dose of DMSO (92 mg/100-125 g body wt) to partial hepatectomized rats did not alter the enzyme activity. Anaerobic cells of S. cerevisiae on aerobiosis for 2 hr attained cytochrome oxidase activity level on par with aerobic cells. Inclusion of DMSO (275 mg/100 ml) in the growth medium of S. cerevisiae during respiratory adaptation exerted partial inhibitory effect on the formation of cytochrome oxidase at 2 hr period, while the 10-fold concentration inhibited the enzyme formation completely. However, the inhibitory effect of DMSO on enzyme formation was abolished on prolonged growth (18 hr and above), while these doses had no influence on cytochrome oxidase in aerobic cells of S. cerevisiae. The results imply that DMSO may be exerting its effect on the assembly of subunits into active enzyme complex during mitochondrial biogenesis.
 ...
PMID:Effect of dimethyl sulphoxide on mitochondrial biogenesis in regenerating rat liver and Saccharomyces cerevisiae. 255 Mar 60

A single intraperitoneal injection of dimethyl sulfoxide (275 mg/100 g body wt.) to rats stimulated cytochrome oxidase activity in liver mitochondria 2-5-fold. The enzyme activity remained at this level for as long as 5 days post-injection. There was however only 10.5% increase in the content of cytochromes a and a3 (as determined spectrophotometrically) in the same period in response to DMSO injection. The addition of either DMSO or dimethyl sulfate (a metabolite of DMSO) to isolated liver mitochondria also caused 2-3-fold increase in cytochrome oxidase activity. The results indicate that enhancement in cytochrome oxidase activity in liver mitochondria after administration of DMSO to rats is on account of activation of cytochrome oxidase caused by structural alterations in mitochondrial membranes rather than de novo synthesis of cytochrome oxidase.
 ...
PMID:Dimethyl sulfoxide elicited increase in cytochrome oxidase activity in rat liver mitochondria in vivo and in vitro. 283 86

Rhodamine 123, a fluorescent dye which binds as a result of the transmembrane potential, was used to stain the mitochondria of HL-60 cells, a cell line established from human promelocytic leukemia cells. The DMSO-induced differentiation of promyelocytic cells into mature granulocytes caused a fourfold decrease in fluorescence intensity that paralleled the disappearance of S-phase and G2M cells. This suggests that upon myeloid differentiation whereby the cells enter an irreversible quiescent state, the mitochondrial mass of the cells has decreased. This suggestion is corroborated by electron microscopy, which shows a decrease in the number of mitochondria, and by decreases in total mitochondrial protein and cytochrome oxidase activity. The respiratory rate of isolated mitochondria did not change, suggesting that the transmembrane potential remained the same. Undifferentiated cells in exponential phase of growth exhibit an intracellular heterogeneity of fluorescence intensity. This heterogeneity appears to have a cell age basis, as late S/G2M cells, obtained by centrifugal elutriation, yielded twice the fluorescence intensity of early G1 cells.
 ...
PMID:Differentiation of promyelocytic (HL-60) cells into mature granulocytes: mitochondrial-specific rhodamine 123 fluorescence. 657 92

The significance of metabolic networks in guiding the fate of the stem cell differentiation is only beginning to emerge. Oxidative metabolism has been suggested to play a major role during this process. Therefore, it is critical to understand the underlying mechanisms of metabolic alterations occurring in stem cells to manipulate the ultimate outcome of these pluripotent cells. Here, using P19 murine embryonal carcinoma cells as a model system, the role of mitochondrial biogenesis and the modulation of metabolic networks during dimethyl sulfoxide (DMSO)-induced differentiation are revealed. Blue native polyacrylamide gel electrophoresis (BN-PAGE) technology aided in profiling key enzymes, such as hexokinase (HK) [EC 2.7.1.1], glucose-6-phosphate isomerase (GPI) [EC 5.3.1.9], pyruvate kinase (PK) [EC 2.7.1.40], Complex I [EC 1.6.5.3], and Complex IV [EC 1.9.3.1], that are involved in the energy budget of the differentiated cells. Mitochondrial adenosine triphosphate (ATP) production was shown to be increased in DMSO-treated cells upon exposure to the tricarboxylic acid (TCA) cycle substrates, such as succinate and malate. The increased mitochondrial activity and biogenesis were further confirmed by immunofluorescence microscopy. Collectively, the results indicate that oxidative energy metabolism and mitochondrial biogenesis were sharply upregulated in DMSO-differentiated P19 cells. This functional metabolic and proteomic study provides further evidence that modulation of mitochondrial energy metabolism is a pivotal component of the cellular differentiation process and may dictate the final destiny of stem cells.
 ...
PMID:Mitochondrial biogenesis and energy production in differentiating murine stem cells: a functional metabolic study. 2435 Aug 92