Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

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.
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PMID:Biochemical studies on mitochondria isolated from Normal and Neoplastic Tissues of the Mouse Mammary Gland. 17 82

Mouse myeloma cells and mitochondria had the same kinds of cytochrome components in the respiratory chain as the normal ones. Their constitution, however, was abnormally different from that found in normal cells and mitochondria. The cytochrome aa3 concentration was especially low in the myeloma as compared with cytochrome c concentration, and the resulting cytochrome aa3/c ratio was 0.25, which was the lowest ever reported in animal mitochondria. Normal lymph node cells, producing the immunoglobulin similar to the myeloma cells, had a ratio of 1.1. Human myeloma mitochondria had the same characteristics as the mouse myeloma. Ascite form myeloma originated from mouse solid from myeloma grew faster, and yet aa3/c of 0.5 in the ascites myeloma was found to be quite similar to that observed in various ascites tumor cells such as hepatomas, Ehrlich and sarcoma 180. A significant part of the cytochromes in the respiratory chain of the mouse myeloma remained in the oxidized form in the cyanide-inhibited or anaerobic states, and was reduced only by the addition of dithionite. The properties of the b cytochromes in mouse myeloma mitochondria are also described and discussed in the context of multiple forms of the b cytochromes in the respiratory chain.
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PMID:An abnormal ratio of cytochromes in the respiratory chain of mouse and human myelomas. 125 59

Iron, apart a for long time well-known function connected with: transportation (hemoglobin), storage (myoglobin), and utilize (cytochromes, cytochrome oxidase) oxygen for respiration, has a critical role in host-pathogen interactions. Iron is essential for microbial growth, but also for immune function. The role of iron in infection, thermoregulation, acute lymphocytic leukemia, neoplasia, rheumatoid arthritis, stimulation of free radical reactions, and studies with iron chelation therapy are discussed.
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PMID:[The role of iron in immunologic processes]. 129 87

Numerous studies on the local rate of energy metabolism of various brain regions during development and following experimental manipulation have been conducted using 2-deoxyglucose uptake and cytochrome oxidase (CO) histochemistry, both considered to be reliable indicators of long-term and short-term alterations in neuronal activity, respectively. Another method which has been related to neuronal activity is neuron-specific enolase (NSE) immunohistochemistry. An isoenzyme of enolase, a key element in the glycolytic pathway, NSE is present in neurons and neural-related cells e.g. neuroendocrine cells, pituicytes, and many tumor cells, but not in glia. The distribution on adjacent tissue sections of immunoreactive NSE and histochemically determined CO were mapped in the rat mesencephalon and adrenal medulla. Both methods showed highly restricted localization of staining which coincided with few exceptions in the most reactive areas, namely the superior colliculus, medial and lateral geniculate nuclei, red nucleus, lateral mammillary nucleus, interpeduncular nucleus and substantia nigra pars lateralis and pars reticulata. Immunoreactivity of varying intensity for NSE was also observed in perikarya and in processes of numerous scattered neurons throughout the mesencephalon, including the substantia nigra pars compacta, and reticular formation. The general correspondence in staining patterns between CO and NSE in the midbrain, supports the utility of NSE as a useful index of metabolic activity in neurons.
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PMID:Neuron-specific enolase reflects metabolic activity in mesencephalic neurons of the rat. 131 69

Cytochrome-c-oxidase (complex IV) was histochemically studied in oncocytic adenoma (n = 10) and carcinoma of the thyroid gland (n = 3), cystadenolymphomas and oncocytic adenomas of the major salivary glands (n = 9), oncocytic neoplasia of the kidney (n = 1) and in 21 parathyroid glands with primary hyperparathyroidism and adenomatous proliferation (n = 17) and secondary hyperparathyroidism with hyperplasia (n = 4). Only in the parathyroids defects of cytochrome-c-oxidase were found being expressed in all 4 glands with hyperplasia (14 defects) and in 5 of the 17 adenomas (11 defects). All defects were confined to foci with oxyphil cell differentiation, the defect areas varying from 0.09 to 21.10 sq mm in hyperplastic glands and from 0.11 to 13.88 sq mm in adenomas, the size of the oxyphil foci varying from 0.12 sq mm-105.38 sq mm. However, not every oxyphil nodule of a gland was devoid of cytochrome-c-oxidase activity. Of 6 predominantly oxyphil adenomas, 4 showed no defects. No defects were observed either in 2 adenomas without oxyphil cells. Further enzymes of the respiratory chain, succinate dehydrogenase (complex II) and ATP synthetase, (complex V) were devoid of defects. In parathyroids with hyperplasia and oxyphil areas, defects of cytochrome-c-oxidase occurred significantly more often and tended to be larger than in adenomas, statistical analysis revealing a significant correlation between the occurrence of defects and the number of oxyphil foci but not with the total oxyphil area.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Random cytochrome-C-oxidase deficiency of oxyphil cell nodules in the parathyroid gland. A mitochondrial cytopathy related to cell ageing? 133 5

Cells from a rapidly growing rat Zajdela hepatoma were shown to contain (on a protein basis) five-times less mitochondria than hepatocytes from resting or regenerating rat liver. Transcripts of four nuclear genes for representative mitochondrial membrane proteins (beta-F1 subunit and N,N'-dicyclohexyl-carbodiimide-binding protein of ATP synthase, subunit IV of cytochrome oxidase and ADP/ATP translocase) were present in 2-4 times higher amounts in the poly(A)-rich RNA of the hepatoma than in the corresponding RNA fraction from resting or regenerating rat liver. The liver and hepatoma transcripts for the beta-F1 subunit were translated in an in-vitro system with equal efficiency. Pulse-chase labeling of isolated Zajdela hepatoma cells and hepatocytes from resting and regenerating liver revealed a relative excess of the newly synthesized beta-F1 subunit in the tumor cells. The half-life of the beta-F1 subunit was significantly shorter in the hepatoma cells than in hepatocytes from resting and regenerating liver. The contents of transcripts of three mitochondrial genes examined (cytochrome oxidase subunits I and II and NADH-ubiquinone reductase subunit 2) in Zajdela hepatoma mitochondria were about five-times higher than in the mitochondria of the resting cells and 3-4 times higher than in the organelles of the regenerating organ. The results indicate that events other than transcription (most likely post-translational) may be responsible for the reduced content of mitochondria in tumor cells.
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PMID:Increased steady-state levels of several mitochondrial and nuclear gene transcripts in rat hepatoma with a low content of mitochondria. 137 34

We have used a polyclonal antibody probe to isolate cDNA clones for mouse cytochrome oxidase subunit Vb from a bone marrow tumor cell mRNA library in lambda gt11 expression vector. The mouse cDNA contains an open reading frame of 128 amino acids, which shows 81% positional identity with the predicted amino acid sequences of the human subunit. Northern blot analysis and sequencing of cDNA from a mouse kidney library show no tissue specific variations in subunit Vb.
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PMID:Nucleotide sequence of cDNA for nuclear encoded subunit Vb of mouse cytochrome-c oxidase. 216 17

1. Basal levels and allyl-isopropylacetamide (AIA) or veronal induced levels of delta-aminolevulinate synthetase (ALA-S), cytochrome P-450 (cyt P-450) and cytochrome oxidase were determined in tumor (T) and liver of both normal mice (NM) and T bearing mice (TBM). 2. Basal levels of ALA-S were nearly the same in either source. The amount of cyt P-450 was lower in TBM liver than in NM liver, and no detectable in T. While the basal activity of cytochrome oxidase in TBM liver and T were higher than those of NM liver. 3. In AIA intoxicated animals there was a lower induction of ALA-S in liver of TBM than in NM liver. There was no induction in T ALA-S. The loss of cyt P-450 was less in TBM liver when compared with NM liver. 4. The induction level of cyt P-450 after veronal administration was nearly the same in liver of both TBM and NM. 5. We conclude that lower induction of liver ALA-S activity in TBM liver is due to correspondingly lower drug metabolism ability of TBM liver. Otherwise our results suggest that the control mechanism operating in T and probably in its original tissue are different from those described for normal liver.
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PMID:Heme regulation in mouse mammary carcinoma and liver of tumor bearing mice--I. Effect of allyl-isopropylacetamide and veronal on delta-aminolevulinate synthetase, cytochrome P-450 and cytochrome oxidase. 217 97

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.
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PMID:The respiratory behavior of Lewis carcinoma cells--existence of a cyanide-resistant respiration. 277 18

The effect of t-butyl-4-hydroxyanisole (BHA), a widely used food antioxidant additive, on the culture growth, oxygen consumption, and redox state of some electron carriers of intact TA3 and 786A ascites tumor cells has been studied. BHA inhibited culture growth and respiration of these two tumor cell lines, by inhibiting the electron flow through the respiratory chain. Experiments to determine its site of action showed that BHA did not inhibit noticeably the electron flow through cytochrome oxidase, due to the ability of N,N,N',N'-tetramethyl-p-phenylenediamine to bypass the BHA inhibition of the respiration. Electron flow through the ubiquinone-cytochrome b-c1 complex also was unaffected by BHA; in fact, BHA failed to inhibit the oxidation of duroquinol. Spectrophotometric experiments are in accordance with studies carried out using synthetic electron donors. The redox state of NAD(P)+, determined in steady-state conditions, changed to a more reduced level, and the redox states of ubiquinone, cytochrome b, cytochromes c + c1 and cytochromes a + a3 changed to a more oxidized level. These observations suggest that the electron transport in the tumor mitochondria was inhibited by BHA at the NADH-dehydrogenase-ubiquinone level (energy-conserving site 1). These findings could explain, in part, the cytotoxic effect of BHA.
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PMID:t-butyl-4-hydroxyanisole as an inhibitor of tumor cell respiration. 281 35


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