Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Circulating non-T lymphocytes had higher activities of 5'nucleotidase (plasma membrane), neutral alpha-glucosidase (endoplasmic reticulum) and basal leucine amino-peptidase than did T lymphocytes. Activities of catalase (peroxisomes), malate dehydrogenase (mitochondria), lactate dehydrogenase (cytosol) and N-acetyl-beta-glucosaminidase, beta-glucuronidase and acid phosphatase (lysosomes), were similar in the lymphocyte subfractions. Lymphocyte 5'nucleotidase (plasma membrane) in patients with common variable hypogammaglobulinaemia is much lower than normal. However, the decrease is less marked in X-linked hypogammaglobulinaemia, chronic lymphatic leukaemia or protein loosing enteropathy or in lymphocytes isolated from cord blood. Cells from patients with nephrotic syndrome had normal levels of 5'nucleotidase. Other plasma membrane marker enzymes (gamma-glutamyl transferase, leucine amino-peptidase) were normal in lymphocytes from patients with common variable hypogammaglobulinaemia. There is a selective reduction of mitochondrial (malate dehydrogenase) and cytosolic (lactate dehydrogenase) enzymes, with normal activities of lysosomal, peroxisomal and endoplasmic reticulum enzymes, in patients with common variable hypogammaglobulinaemia. The lymphocyte subcellular organelles in normal subjects and patients with common variable hypogammaglobulinaemia have similar properties on sucrose density gradient centrifugation. It is suggested that lymphocytes from patients with common variable hypogammaglobulinaemia show a specific enzymopathy and that this is not simply a reflection of cellular immaturity.
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PMID:Lymphocyte enzyme activities in immunodeficiency syndromes with particular reference to common variable hypogammaglobulinaemia. 630 45

Neutrophil leukocytes, isolated from normal subjects and subjected to analytical subcellular fractionation by sucrose density gradient centrifugation, showed very similar cytosol distributions of pyridoxal and pyridoxal phosphate and lactate dehydrogenase. The small amounts of pyridoxal and pyridoxal phosphate associated with the dense granule fractions were not associated with the alkaline phosphatase containing granules. The levels of pyridoxal and pyridoxal phosphate were determined in neutrophils from control subjects, women in the third trimester of pregnancy and patients with chronic granulocytic leukaemia. Neutrophil pyridoxal phosphate was increased in women in the third trimester of pregnancy compared to controls, but there was little variation in the level of pyridoxal between the groups. There was no consistent correlation between the pyridoxal phosphate and the neutrophil alkaline phosphatase activity in the patient groups. Although in vitro neutrophil alkaline phosphatase rapidly hydrolyses pyridoxal phosphate, it is suggested that in vivo this is unlikely to be the principal function of the enzyme.
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PMID:Levels and subcellular localisation of pyridoxal and pyridoxal phosphate in human polymorphonuclear leukocytes and their relationship to alkaline phosphatase activity. 657 87

The isoenzymes 1 and 2 (LDH1 and LDH2) of lactic dehydrogenase (LDH) were studied in the serum of 32 patients with malignant haematological diseases. In non-Hodgkin lymphoma (NHL) a diminution in LDH1 and an increase in LDH2 was a sign of evolution towards a more aggressive phase of the disease, or the absence of clinical remission, even when no significant variation of total LDH can be observed in the serum. In acute lymphoblastic leukaemia (ALL), the isoenzymatic variations are not an early indication of relapse. No significant variations in serum LDH or of these isoenzymes was observed in chronic lymphocytic leukaemia (CLL) or Hodgkin's disease (HD). Only in NHL did the variations of LDH1 and LDH2 appear to be a biochemical marker of the tumour process and of cellular differentiation.
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PMID:Lactate dehydrogenase isoenzyme activity in malignant haematological diseases. 659 95

We have observed five patients with smoldering adult T-cell leukemia (ATL) who had skin lesions as premonitory symptoms. The illness developed slowly but flared up after several years. Skin lesions appeared in the form of erythema, papules or nodules. Infiltration of the skin by ATL cells was slight, and the proportion of ATL cells in the peripheral blood was from 0% to 2%. The serum lactic dehydrogenase value was within normal range, and was not associated with hypercalcemia, lymphadenopathy, or hepatosplenomegaly, and bone marrow infiltration was very slight. In most cases, hypergammaglobulinemia was seen, and in one case monoclonal hypergammaglobulinemia was observed. All five patients had lived in an area in which ATL was endemic, and their sera were positive for anti-ATL-associated antigen antibodies. None of them had ever received a blood transfusion. One patient developed typical ATL after more than 13 yr of illness, and died of renal insufficiency. Another patient developed typical ATL after 5 yr of illness, and died or cryptococcus meningitis. These cases were clinically and pathologically different from typical ATL cases already reported, and we feel it necessary to make distinctions from the viewpoints of prognosis and treatment. In discussing these cases, we compared smoldering ATL with typical ATL, and deliberated upon the causes of both.
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PMID:A proposal for smoldering adult T-cell leukemia--diversity in clinical pictures of adult T-cell leukemia--. 660 27

The cytostatic unsaturated ketonucleosides, 1, 2, 3 and 4 are highly reactive sulfhydryl blocking agents. Kinetics of their reactions with reduced glutathione (GSH) were measured and their reactivity was compared to that of N-ethylmaleimide (NEM), acrylonitrile and chloroacetamide. Their reaction products with N-acetyl-L-cysteine (AcCys) were prepared and characterized by chemical analysis and nuclear magnetic resonance (NMR) spectroscopy. Compounds 1, 2 and 3 gave Michael type 1:1 addition products. Compound 4 reacted with AcCys by a three step mechanism; the primary addition product 8 underwent an unusual elimination reaction giving the unsaturated compound 9, which yielded the addition product 10 with AcCys. In the reaction with GSH, compound 4 behaved like a bifunctional SH alkylating agent. Compounds 1, 2, 3 and 4 also reacted with protein thiols as shown by their ability to inhibit lactate dehydrogenase (LDH). Unsaturated ketonucleosides had diversified effect on L1210 leukemia cells. While the most potent cytostatics, compounds 1 and 3, reduced considerably the membrane surface SH level, they were without effect on soluble intracellular protein thiols. In contrast, nucleosides 2 and 4, less active than the former, only slightly affected the membrane surface sulfhydryls and considerably depleted the intracellular soluble protein thiols. Only slight differences were found between the reactions of the four nucleosides with non-protein SH (NPSH). The correlation found between in vivo biological activity and cell membrane impairment suggests that selective alkylation of certain key membrane thiols by unsaturated ketonucleosides might be an important event in their biological effect.
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PMID:Interactions of cytostatic unsaturated ketonucleosides with sulfhydryl containing cell constituents. 661 5

Serum biochemical analyses were done on F344 rats in the early and late stages of mononuclear cell leukemia. There were marked increases in serum bilirubin, alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase and alkaline phosphatase. Increases in these parameters generally were more severe in the late stages of leukemia. Both direct and indirect-reacting bilirubin were increased with the unconjugated form predominating early and the conjugated form predominating late in the course of the disease. Lactate dehydrogenase isoenzyme determination correlated with histological examination indicated that liver damage was responsible for the observed changes. Urinalysis revealed marked hemoglobinuria, bilirubinuria and increased urine urobilinogen. Serum protein electrophoresis revealed marked reductions in the alpha globulin fractions.
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PMID:Pathology of the mononuclear cell leukemia of Fischer rats. III. Clinical chemistry. 664 40

A cytotoxic activity, highly selective for neoplastic cells, is expressed by 1-alkyl-2-methoxy-sn-glycero-3-phosphocholine and by other derivatives closely related to the chemical structure of platelet activating factor. The antineoplastic potencies of a new series of analogs tested in HL-60 human leukemia cells and human polymorphonuclear neutrophils are reported. The degree of cytotoxicity was documented according to the ability of each analog to 1) destroy leukemic or normal cells or 2) to release lactic acid dehydrogenase from these cells. An index of selectivity of the analogs for their cytotoxicity toward leukemia cells is presented. Substitution by the twenty carbon branched-chain phytanyl moiety in place of the straight chain alkyl ether-linked group at the sn-1 position of various phospholipid analogs resulted in a 3- to 10-fold reduction in their cytotoxic potency in HL-60 leukemia cells. The enantiomeric isomers (D-forms) of several of the analogs possessed slightly greater phospholipid analogs possessing the sn-2-acetyl (platelet activating factor) or sn-2- propionoyl substituents, both biologically active in their ability to aggregate platelets and to induce hypotension, were relatively innocuous in terms of the measured cytotoxic responses in both HL-60 cells and neutrophils.
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PMID:Cytotoxicity of ether-linked phytanyl phospholipid analogs and related derivatives in human HL-60 leukemia cells and polymorphonuclear neutrophils. 673 56

Since it is known that the metabolism of acetaminophen is involved in its hepatotoxicity and that drug metabolizing enzyme activity is decreased in tumor bearing animals, it was of interest to study the influence of L-1210 leukaemia on acetaminophen hepatotoxicity in BDF-1 male mice. A single oral dose of acetaminophen, 125 mg/kg, was given at the fifth day of the mice survival period (7.7 days) and the animals killed twenty-four hours later. As revealed by serum glutamic-pyruvic transaminase, serum glutamic-oxaloacetic transaminase and lactic dehydrogenase, acetaminophen was less hepatotoxic in leukaemic mice than in control mice by comparison with their own saline group; on the other hand the difference between control and leukaemic mice treated with acetaminophen was significant only for glutamic-pyruvic transaminase. Moreover, we found higher unchanged acetaminophen concentrations in plasma, liver, kidneys, brain and fat of the leukaemic mice as compared to controls, less conjugated metabolites in plasma and liver, decreased in vitro aniline hydroxylation and ethylmorphine N-demethylation. Finally, following acetaminophen administration, reduced hepatic glutathione was depleted to a much lesser extent in the tumor bearing animals than in controls. In conclusion, the L-1210 leukaemia seems to modify the acetaminophen hepatotoxicity and this effect might be explained by decreased acetaminophen biotransformation into toxic metabolites or intermediates.
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PMID:Influence of leukaemia on acetaminophen-induced hepatotoxicity in mice. 689 Feb 27

Serum total lactic dehydrogenase (LDH) levels were examined in 42 patients with acute leukemia, 9 patients with chronic myeloid leukemia, 6 of them in blastic crisis, and 53 patients with lymphoma and other lymphoproliferative disorders. The mean range of serum LDH leveles in Hodgkin's and non-Hodgkin's lymphoma was 402 +/- 210 IU/liter and 313 +/- 113 IU/liter, while that of patients with nonmalignant disorders was 308 +/- 74 IU/liter. In acute nonlymphoblastic leukemia (ANLL), the range was 126-684 IU/liter (mean value 413 +/- 146 IU/liter). In 6 of the patients (11.3%) with lymphoma and in 6 cases (26.8%) with ANLL, the LDH levels were above 500 IU/liter. None of these patients had levels over 900 IU/liter. Patients with acute lymphoblastic leukemia (ALL) had a range of 402-3582 IU/liter (mean value of 1669 + 1038 IU/liter). In 15 of the 19 patients (78.9%) with ALL, serum LDH values were above 900 IU/liter. In addition, 3 patients with chronic myeloid leukemia (CLM) in blastic crisis had levels of 970-1940 IU/liter. One of these 3 patients had lymphoblastic crisis, while the second case responded clinically to vincristine and prednisone, but was not regarded as ALL. The differences in serum LDH levels between ALL and ANLL are statisticaly significant (p < 0.001). It appears that markedly elevated serum LDH levels in acute leukemia are suggestive of ALL, and that in individual patients, the LDH levels were correlated with the number of blasts during remission and relapse.
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PMID:Serum lactic dehydrogenase (LDH) levels in acute leukemia: marked elevations in lymphoblastic leukemia. 693 18

Intracellular activities of total lactic dehydrogenase (LDH) and phosphohexose isomerase (PHI) were investigated in the leukaemic cells of 14 patients with acute myeloid leukaemia (AML), five with chronic myeloid leukaemia (CML), seven with acute lymphoblastic leukaemia (ALL), 19 with chronic lymphocytic leukaemia (CLL), 16 with leukaemic non-Hodgkin's lymphoma (NHL) and in the lymphocytes of 14 normal persons. Intracellular total LDH-activity of the blasts of AML and ALL was in the same range as the normal lymphocytes. Patients with CLL and NHL had significantly lower levels (P less than 0.01) of total intracellular LDH than the controls. Intracellular PHI activity was consistently lower in the lymphoid malignancies (ALL, CLL, NHL) than in normal lymphocytes (P less than 0.05), or in leukaemic myeloblasts (P less than 0.01). The intracellular LDH/PHI index of the leukaemic lymphoblasts was significantly elevated as compared to lymphocytes from normal subjects (P less than 0.0001) or to leukaemic cells from patients with AML (P less than 0.001), with CLL (P less than 0.0001) or with NHL (P less than 0.001). The patients with CLL and NHL, on the other hand, had significantly lower levels of LDH/PHI ratio than the normal subjects (P less than 0.0001 and P less than 0.025 respectively).
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PMID:Intracellular lactic dehydrogenase and phosphohexose isomerase activity in leukaemia and malignant lymphoma. 706 11


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