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

---

Query: EC:1.9.3.1 (cytochrome oxidase)
8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using cytochemical methods the authors studied the activity of certain lysosomal enzymes and cytochrome oxidase in peripheral blood leucoytes in 22 patients with Wilson's disease. The control group comprised 50 healthy blood donors. It was found that the activity of acid phosphatase in the lymphocytes of patients was higher than in controls, the mean indices being respectively 90.50 +/- 8.95 and 60.38 +/- 3.95. The activity of beta-glucuronidase was found to be lower in the lymphocytes of patients, the mean value was 25.10 +/- 8.59 in patients and 64.91 +/- 5.78 in controls. The activity of cytochrome oxidase was lower in the granulocytes of patients with Wilson's disease than in controls, the mean values being 54.5 +/- 12.14 and 156 +/- 15.41 respectively. The activity of acid phosphatase in granulocytes as well as that of non-specific esterase in lymphocytes was similar in both groups. Decreased antigen degradation in Wilson's disease may be due not only to liver cirrhosis but also to disturbances in the metabolism of white blood cells, including, among others, decreased activity of cytochrome oxidase. The rise of the activity of acid phosphatase and reduced activity of beta-glucuronidase indicate chronic antigenic stimulation of lymphoid system.
...
PMID:[Cytochemical studies of peripheral white blood cells in Wilson's disease]. 19 62

Thymomodulin and Thymolymphotropin, biologically active thymus derivative peptides exert recovery effects on the functionality of some membrane bound, mitochondrial and lysosomal enzymes (monoamine oxidase, ATPase, phosphatases, cytochrome oxidase, succinate oxidase) affected by gamma-irradiation. These drugs exert antistress effect by re-establishing the function of hypothalamus-pituitary-adrenal axis and that of lymphoid organs.
...
PMID:The effects of thymomodulin and thymolymphotropin on the stress response of neuroendocrine system by gamma-irradiated Wistar rat. 134 4

Chronic copper deficiency in mice impairs both humoral and cell-mediated immunity, but the mechanisms are unknown. Copper deficiency was produced in C58 mice by feeding dams a diet low in copper throughout lactation and weaning the pups to this diet. Control mice were from dams fed the same diet but with copper supplementation the drinking water. Six-week-old mice were sampled for biochemical and morphological studies. Compared to copper-supplemented mice, copper-deficient animals were smaller, anemic and exhibited hypoceruloplasminemia. The copper-deficient mice have small thymus glands, enlarged spleens, and livers equivalent in size to copper-supplemented mice. Thymic atrophy is not caused by elevated serum corticosterone. Liver, spleen, and thymus tissues from copper-deficient mice exhibit low cytochrome oxidase (56, 38, and 45%, respectively) and superoxide dismutase activities (61, 60, and 43%, respectively) compared to tissues from copper-supplemented mice, indicating a functional copper deficiency. Electron micrographs taken of thymus and spleen from copper-deficient mice demonstrate altered morphology characterized by abnormal mitochondria and misshapen nuclei. Chronic copper deficiency alters the size, biochemistry and morphology of primary (thymus) and secondary (spleen) lymphoid tissue.
...
PMID:Chronic dietary copper deficiency alters biochemical and morphological properties of mouse lymphoid tissues. 630 92

The molecular events characterizing lymphoid malignancy have been examined in an animal model system, specifically, the retroviral induction of leukemia and lymphoma in the domestic cat following infection with feline leukemia virus (FeLV). Genes differentially expressed in FeLV-induced lymphomas were isolated using a strategy of differential hybridization. Six genes were identified which demonstrate a higher level of expression in an FeLV-induced feline thymic tumor as compared with normal thymus. The differentially expressed genes encode the feline homologues of ribosomal proteins S3a, S4, S17, and L41, elongation factor-1 alpha, and cytochrome oxidase sub-unit I. Northern-blot analysis and quantification by phosphorimaging demonstrates that these genes are expressed at levels from 1.5- to 3.1-fold higher in J5-1 thymic tumor as compared with normal thymus. Expression of the selected ribosomal protein mRNA was further examined in a series of human and feline tissues, including normal tissues, malignant tumors and cell lines. Our data reveal that elevation of the selected ribosomal protein mRNA is associated with all FeLV-induced thymic lymphomas examined. The differentially expressed ribosomal protein mRNA accumulates in a balanced manner in thymic lymphomas. By contrast, the elevation in ribosomal protein mRNA levels is not associated uniformly with hematopoietic malignancy. T-lymphoid malignancy, solid tumors or actively proliferating cells. Rather, the elevation appears to be a uniform and distinctive feature of T-cell malignancy of this particular type. The elevated expression of these genes may be causally related to the neoplastic process.
...
PMID:Identification of differentially expressed genes in T-lymphoid malignancies in an animal model system. 762 75

Cu has long been known to influence immune responses. An in vitro model system was established in which human myeloid (HL-60), B-lymphoid (Raji) and T-lymphoid (Molt-3) cell lines could be grown in culture media of varying Cu levels. Initially Cu was removed from the medium by dialysis of fetal calf serum against a metal-ion chelator, minor depletion of other trace metals being obviated by repletion with appropriate metal salts. The growth rate of HL-60 was significantly (P < 0.05) inhibited by 72 h Cu depletion. Molt-3 cells required a longer period, up to 144 h, in Cu-depleted medium before growth was impaired. Raji-cell growth was not affected. These results confirmed clinical observations that T-cell functions were more sensitive to Cu deprivation than B cells. Analysis of intracellular metal levels in Molt-3 cells showed that Cu levels had been significantly lowered (P < 0.05) although Ca2+ levels were raised. Intracellular activity of the antioxidant enzyme superoxide dismutase (EC 1.15.1.1) was significantly impaired (P < 0.05) in Molt-3 cells grown in Cu-depleted medium. Activity of the mitochondrial enzyme cytochrome c oxidase (EC 1.9.3.1) was also significantly impaired (P < 0.05) by Cu depletion. Each of these findings indicates an increase in the potential for cellular damage by reduced antioxidant activity, impairment of normal mitochondrial activity and excessive Ca2+ influx. A major consequence of the type of damage occurring under these circumstances is membrane disruption. This was confirmed by scanning electron microscopy of Molt-3 cells grown under varying Cu levels.
...
PMID:The effects of copper deficiency on human lymphoid and myeloid cells: an in vitro model. 878 94

Hepatic leukemia factor (HLF) is a bZIP transcription factor related to the CES-2 protein, which controls apoptosis of the NSM serotoninergic neurons in Caenorhabditis elegans. Ectopic expression of HLF as an E2A-HLF fusion protein in t(17;19)-positive human pro-B cell acute lymphoblastic leukemias is believed to promote malignancy by interfering with apoptosis. While HLF has been linked to malignancies of the lymphoid system, it is not normally expressed in these cells. Rather, HLF transcripts are detected in the liver, kidney, lung and adult nervous system by Northern blotting. Despite the links to cell death, little is known of the distribution or function of HLF in the adult and developing mammalian nervous system. Therefore, we cloned mouse Hlf and studied its expression by in situ hybridization. During embryonic brain development, Hlf expression was restricted to the anterior pituitary and meninges. By early postnatal life, Hlf was highly expressed in somatosensory cortex, thalamic nuclei, and structures arising from ectodermal placodes. Subsequently, Hlf expression increased in the central nervous system and was found throughout the brain by adulthood. In the developing pituitary gland, Hlf was highly expressed in the rostral tip of the anterior lobe. This pattern is similar to that of Tef, an Hlf-related bZIP protein. However, while Tef is expressed in the anterior pituitary of the adult mouse, Hlf was detected in both the anterior and posterior pituitary. Hlf expression was not associated with cells undergoing programmed cell death in the nervous system. Hlf expression increased markedly with synaptogenesis and was coincident with barrel formation revealed by cytochrome oxidase staining. Together, these data suggest that Hlf plays a role in the function of differentiated neurons in the adult nervous system rather than programmed cell death.
...
PMID:Expression patterns of the hepatic leukemia factor gene in the nervous system of developing and adult mice. 1002 25

Methods have been developed for the quantitative assay of cytochrome oxidase, esterase, and 11 acid hydrolases in rat-spleen homogenates. These methods seem to be applicable also to other lymphoid tissues. Preliminary studies, extended to nine of the acid hydrolases, indicate that these enzymes occur in partly latent and sedimentable form and that they can be unmasked and rendered soluble by some of the treatments that liberate the enzymes from rat-liver lysosomes. The spleen particles appear to be very sensitive to mechanical injury, a property which necessitates special precautions in homogenizing the tissue. Agglutination of spleen particles takes place to a larger extent in 0.25 M sucrose than in 0.15 M KCl.
...
PMID:Lysosomes in lymphoid tissue. I. The measurement of hydrolytic activities in whole homogenates. 1097 25

Cell respiration is controlled by nitric oxide (NO) reacting with respiratory chain complexes, particularly with Complex I and IV. The functional implication of these reactions is different owing to involvement of different mechanisms. Inhibition of complex IV is rapid (milliseconds) and reversible, and occurs at nanomolar NO concentrations, whereas inhibition of complex I occurs after a prolonged exposure to higher NO concentrations. The inhibition of Complex I involves the reversible S-nitrosation of a key cysteine residue on the ND3 subunit. The reaction of NO with cytochrome c oxidase (CcOX) directly involves the active site of the enzyme: two mechanisms have been described leading to formation of either a relatively stable nitrosyl-derivative (CcOX-NO) or a more labile nitrite-derivative (CcOX-NO (2) (-) ). Both adducts are inhibited, though with different K(I); one mechanism prevails on the other depending on the turnover conditions and availability of substrates, cytochrome c and O(2). SH-SY5Y neuroblastoma cells or lymphoid cells, cultured under standard O(2) tension, proved to follow the mechanism leading to degradation of NO to nitrite. Formation of CcOX-NO occurred upon rising the electron flux level at this site, artificially or in the presence of higher amounts of endogenous reduced cytochrome c. Taken together, the observations suggest that the expression level of mitochondrial cytochrome c may be crucial to determine the respiratory chain NO inhibition pathway prevailing in vivo under nitrosative stress conditions. The putative patho-physiological relevance of the interaction between NO and the respiratory complexes is addressed.
...
PMID:Mitochondria and nitric oxide: chemistry and pathophysiology. 2239 19

To characterize mitochondrial/apoptotic parameters in chronically human immunodeficiency virus (HIV-1)-infected promonocytic and lymphoid cells which could be further used as therapeutic targets to test pro-mitochondrial or anti-apoptotic strategies as in vitro cell platforms to deal with HIV-infection. Mitochondrial/apoptotic parameters of U1 promonocytic and ACH2 lymphoid cell lines were compared to those of their uninfected U937 and CEM counterparts. Mitochondrial DNA (mtDNA) was quantified by rt-PCR while mitochondrial complex IV (CIV) function was measured by spectrophotometry. Mitochondrial-nuclear encoded subunits II-IV of cytochrome-c-oxidase (COXII-COXIV), respectively, as well as mitochondrial apoptotic events [voltage-dependent-anion-channel-1(VDAC-1)-content and caspase-9 levels] were quantified by western blot, with mitochondrial mass being assessed by spectrophotometry (citrate synthase) and flow cytometry (mitotracker green assay). Mitochondrial membrane potential (JC1-assay) and advanced apoptotic/necrotic events (AnexinV/propidium iodide) were measured by flow cytometry. Significant mtDNA depletion spanning 57.67% (P < 0.01) was found in the U1 promonocytic cells further reflected by a significant 77.43% decrease of mitochondrial CIV activity (P < 0.01). These changes were not significant for the ACH2 lymphoid cell line. COXII and COXIV subunits as well as VDAC-1 and caspase-9 content were sharply decreased in both chronic HIV-1-infected promonocytic and lymphoid cell lines (<0.005 in most cases). In addition, U1 and ACH2 cells showed a trend (moderate in case of ACH2), albeit not significant, to lower levels of depolarized mitochondrial membranes. The present in vitro lymphoid and especially promonocytic HIV model show marked mitochondrial lesion but apoptotic resistance phenotype that has been only partially demonstrated in patients. This model may provide a platform for the characterization of HIV-chronicity, to test novel therapeutic options or to study HIV reservoirs.
...
PMID:HIV-1 promonocytic and lymphoid cell lines: an in vitro model of in vivo mitochondrial and apoptotic lesion. 2775 70

---