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

Mitrochondria isolated from simian virus 40-transformed 3T3 and nontransformed 3T3 cells were compared by various biochemical criteria. Transformed and nontransformed cell mitochondria had identical densities in linear sucrose and discontinuous bovine serum albumin gradients. The activities of several mitochondria-specific enzymes including cytochrome oxidase, adenylate kinase, nicotinamide adenine dinucleotide (NADH)-cytochrome c reductase, and NADH oxidase were similar in both cell types. However, the activity of the mitochondrial outer membrane enzyme, monoamine oxidase. In the virus-transformed cell mitochondria was reduced to 50% of that in nontransformed cell mitochondria.
J Natl Cancer Inst 1975 Jan
PMID:Biochemical properties of simian virus 40-transformed 3T3 cell mitochondria. 16 20

Mitochondria isolated from spontaneous and transplanted mammary adenocarcinomas of two strains of mice were compared, by various biochemical criteria, to mitochondria from mammary glands of midpregnant or hormonally stimulated, cancer-free mice. The specific activities of several mitochondrial enzymes including cytochrome oxidase, alpha-glycerophosphate oxidase, and succinate dehydrogenase were twofold to threefold lower, whereas the activity of monoamine oxidase was two fold higher in tumor mitochondria. Malate dehydrogenase, adenylate kinase, and NADH oxidase showed similar levels of activity in tumor and midpregnant mammary gland mitochondria. In addition, mitochondrial polypeptide composition was analyzed by electrophoresis on sodium dodecyl sulfate-urea polyacrylamide gels. Midpregnant mammary gland and mammary tumor mitochondria were similar in polypeptide composition; however, several differences were observed. A high-molecular-weight polypeptide, present in mid-pregnant mammary gland mitochondria was absent from tumor mitochondria. Also, tumor mitochondria contained an additional high-molecular-weight polypeptide not found in the midpregnant mammary gland. There were numerous differences in the relative proportions of many polypeptides common to both tumor and midpregnant mammary gland mitochondria.
J Natl Cancer Inst 1976 Jan
PMID:Biochemical studies on mitochondria isolated from Normal and Neoplastic Tissues of the Mouse Mammary Gland. 17 82

Experimental data suggest that contrary to the findings obtained for normal and regenerating liver of mouse, the greater part of hexokinase (HK) in transplantable hepatomas is firmly bound to mitochondrial membranes. It is shown that the ratio of the bound HK activity (HKbound) to that of total HK activity (HKtotal) diminishes with a hepatoma growth. Malignization of hepatocytes also leads to a sharp decrease in the cytochrome oxidase (CO) octivity. Though the data obtained are well-correlated with the Warburg hypothesis, there is no direct correlation between the malignancy of hepatomas evaluated by their growth rates, and the biochemical parameters of the tumours studied. On the basis of fundamental principles of Warburg's, it is proposed to evaluate energy metabolism of hepatomas by the activity and subcellular distribution patterns of HK as well as be the activity of CO, according to the expression: [(HKtotal)2//HKbound-CO+HKbound-CO]. It is demonstrated that there exists a certain linear dependence between the integral characteristics of hepatoma energetics and their growth rates.
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PMID:[Biochemical characteristics determining the rates of tumour growth in the organism]. 19 Nov 4

Electron microscopic observations of THP-1/E (an etoposide-resistant human monocytic leukaemia cell line) showed a remarkable change of mitochondrial structure. Mitochondria were swollen and cristae were relatively intact. There was no difference in the activity of cytochrome oxidase, an enzyme which contains three subunits coded by mitochondrial DNA (mtDNA) between THP-1/E and THP-1 (the parent cell of THP-1/E). No measurable quantitative change of mitochondrial RNA was observed, but the level of mtDNA in THP-1/E was increased by a factor of about 4 compared with that of mtDNA in THP-1. These results suggest that, on acquisition of resistance to etoposide, some factors affect mitochondria, change its morphology and amplify its DNA.
Eur J Cancer 1991
PMID:Increased levels of mitochondrial DNA in an etoposide-resistant human monocytic leukaemia cell line (THP-1/E). 183 60

Isolated vegetative tumour cells from mice bearing the Lewis lung carcinoma showed low rates of basal respiration with both low oxygen uptake rates and cytochrome-c oxidase activity. The cells were affected by a marked Crabtree effect and a high rate of lactate production in the presence of 10 mM glucose. The glycolytic capacity of the tumour was also assessed through the measurement of the maximum activities for hexokinase, phosphofructokinase, pyruvate kinase and lactate dehydrogenase. These activities were similar to the ones found in other fast-growing, undifferentiated tumours. The concentration of fructose-2,6-bisphosphate in the tumour was 2,3 nmoles/g fresh tissue wt., a value which is of the same order of magnitude as that found in other types of highly glycolytic cells. It is concluded that the Lewis lung carcinoma follows the same pattern as other undifferentiated tumours with a high capacity for both glucose and amino acid utilization.
Cancer Lett 1990 Apr 30
PMID:The impairment of respiration by glycolysis in the Lewis lung carcinoma. 215 46

Ditercalinium (a 7H-pyridocarbazole dimer) has been designed to bisintercalate into double-stranded DNA with high affinity. In this paper we provide evidence for inhibitory interactions of ditercalinium with electron transport in isolated rat liver mitochondria. It is shown that ditercalinium probably inhibits the electron transfer between membrane cytochrome c and oxygen (cytochrome c oxidase activity) and the electron transfer between the matrix side of inner membrane (Complexes II and III) and membrane cytochrome c. The level of inhibition of the last oxidation step of the respiratory chain appears to be highly dependent on the drug/membrane diphosphatidylglycerol ratio. It is suggested that the mechanism of cytochrome c oxidase inhibition by ditercalinium could be due to the complexation with the diphosphatidylglycerol environment essential for its activity rather than to a drug-enzyme direct interaction. This hypothesis is strengthened by experiments with pure cytochrome oxidase. Therefore, the interaction of ditercalinium with diphosphatidylglycerol may be envisaged as one factor, among others, responsible for its hepatotoxicity.
Cancer Res 1990 Dec 15
PMID:Ditercalinium, a nucleic acid binder, inhibits the respiratory chain of isolated mammalian mitochondria. 217 39

The respiratory O2 consumption of vegetative, non-necrotic, Lewis lung carcinoma cells was found to be very low compared with that of non-tumor tissues and was highly resistant to cyanide. However, the resistant rate was inhibited by salicylhydroxamic acid (SHAM) in either isolated cells or tissue fragments. In addition, this compound did not affect their cytochrome-c oxidase activity. The results support the existence of an alternative oxidase system that significantly contributes to oxygen uptake in Lewis carcinoma cells. To our knowledge, this is the first report showing significant SHAM-sensitivity of tumor respiration and perhaps of higher animal cell respiration.
Cancer Biochem Biophys 1989 May
PMID:The respiratory behavior of Lewis carcinoma cells--existence of a cyanide-resistant respiration. 277 18

The mechanistic vectorial H+/O translocation ratios characteristic of energy-conserving sites 2 + 3 and site 3 of the respiratory chain of two tumor cell lines were determined using succinate and ferrocytochrome c, respectively, as electron donors. The measurements were carried out on mitoplasts in order to allow ferrocytochrome c free access to its binding site on the inner mitochondrial membrane. The tumor cell lines used were Ehrlich ascites tumor and the AS30-D ascites tumor. K+ was used as charge-compensating cation in the presence of valinomycin. The O2 uptake rate measurements were made with a fast-responding membrane-less electrode whose response time was closely matched with that of a pH electrode. The rates of O2 uptake and H+ ejection during the apparent zero-order rate phase of respiration, analyzed by computer, were extrapolated to zero time. The observed H+/O ratios for succinate oxidation in both tumors exceeded 7 and approached 8 and the H+/O ratios for the cytochrome oxidase reaction closely approached 4.0, in agreement with data or normal mitochondria. However, the rates of H+ back decay in the tumor mitochondria are relatively high and may influence the net efficiency of oxidative phosphorylation under intracellular conditions.
Cancer Res 1988 Feb 01
PMID:Proton stoichiometry of electron transport in rodent tumor mitoplasts. 282 79

The enzyme activity of cancerous tissue and the adjacent normal epithelium of 40 patients with breast cancer was determined. This enzymatic activity was correlated with the responsiveness of those tumors to the chemotherapy. It was found that the presence of cytochrome oxidase and alkaline phosphatase and the absence of leucine aminopeptidase, beta-glucuronidase and dehydrogenases in cancerous tissues was related to good response. On the contrary, the absence of alkaline phosphatase and cytochrome oxidase and the presence of leucine aminopeptidase, beta-glucuronidase and dehydrogenases in the cancerous tissues was related to poor response and therefore to poor survival.
Cancer Lett 1988 Nov
PMID:Correlation of histoenzymological studies with the response to chemotherapy and survival in breast cancer patients. 284 63

Morphologic and enzymatic changes due to exposure to the radiosensitizing chemical, misonidazole, have been identified in V79 cells grown in a system in which oxygen tensions and culture density have been controlled. Misonidazole prevented the increase in mitochondrial size normally seen during exposure of these cells to conditions of moderate hypoxia (2 X 10(3) ppm O2). Mitochondrial size was also significantly decreased in cells from exponential cultures exposed to 1 mmol/l misonidazole. Morphologic changes to the mitochondria that varied from data reported elsewhere were also noted. Misonidazole caused a significant initial decrease in cytochrome oxidase activity after 4 hours of exposure of aerobic and moderately hypoxic cultures that did not return to normal in chronically hypoxic cells during continued exposure to the drug.
Cancer 1985 Feb 15
PMID:Changes in ultrastructure and function of hypoxic V79 fibroblast cells after treatment with misonidazole. 298 2


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