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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epidemiological and experimental data suggest that fatty acids may modulate the growth of tumor cells. We have analyzed the effect of different types of fatty acids, bound to serum proteins in physiological conditions, on the lipid composition and growth of human neoplastic B and T-cell lines and compared their effect on normal lymphocyte proliferation. Fatty acids with 0 to 2 unsaturations (stearic, oleic, and linoleic), at concentrations up to 50 or 100 microM did not significantly affect the proliferation of leukemic cells. However, long-chain polyunsaturated fatty acids (PUFA), and mainly docosahexaenoic (22:6, n-3), were cytotoxic at concentrations greater than or equal to 20 microM after 48-72 h in culture. Simultaneous supplementation with vitamin E restored normal cell growth. The amount of end-products of lipid peroxidation in cells correlated with the observed toxicity but the amount of superoxides did not. Fatty acid supplementations increased cell triacylglycerol content but did not affect the degree of unsaturation of phospholipids, cholesterol/phospholipids molar ratio, or membrane fluidity. Glutathione-S-transferase activity was low in Raji and CEM cells, moderate in lymphocytes and high in Ramos cells and did not increase with supplementations. The proliferation of normal lymphocytes, which produced lower amounts of end-products of lipid perodixation, was not inhibited, but in some cases stimulated, by PUFA (with the exception of 30 microM 22:6). The extension of these results to situations in vivo could lead to use of PUFA for delaying leukemia progression or in adjuvant chemotherapy.
Leukemia 1992 Jul
PMID:Increased cytotoxicity of polyunsaturated fatty acids on human tumoral B and T-cell lines compared with normal lymphocytes. 132 Jul 13

A study was made of the content of ubiquinone, vitamins A, E, ascorbic, dehydroascorbic and diketogulonic acids (DKGA), and malonic dialdehyde (MDA) in the liver, of the content of glutathione, the activity of superoxide dismutase (SOD) and glutathione reductase in red blood cells, of the content of vitamins A, E and ubiquinone in the spleen of C57Bl/6jG mice with inoculated leukemia La. It was found that in red blood cells of the animals with leukemia, the content of vitamin E and DKGA reduced, the MDA level increased, and the content of glutathione dropped whereas SOD activity rose. Application of the antioxidant complex of vitamins A, E, C appreciably improved the characteristics of enzymatic and non-enzymatic antioxidant protection of the liver and red blood cells of the leukemic animals without exerting any noticeable effect on the content of vitamin E and ubiquinone in the leukemic spleen tissue.
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PMID:[Use of the antioxidant complex of vitamins A, E and C in murine leukemia]. 258 50

Human T-cell leukemia virus type I was induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and 5-iodo-2'-deoxyuridine (ldUrd) in the MT-1 cell line. Virus expression was monitored by immunofluorescence microscopy with GIN-14, mouse monoclonal antibodies directed toward Mr 19,000 and Mr 28,000 protein-specific virus polypeptides. MNNG (0.1 micrograms/ml) and ldUrd (50 micrograms/ml) both induced virus synthesis in MT-1 cells. MNNG-induced virus expression peaked between 24 and 48 h of incubation, whereas ldUrd induced maximum virus expression between 48 and 72 h of incubation. Superinduction resulted when MNNG was added to cells induced 48 h previously with ldUrd, but not with concomitant treatment. 13-cis-Retinoic acid, retinol, retinol aldehyde, and retinol acetate (10(-6) to 10(-9)M) were concomitantly added with ldUrd to MT-1 cells for 24, 48, and 72 h incubation. All inhibited virus induction to various degrees. The retinoids were ranked as to inhibitory activity: retinol greater than retinoic acid greater than retinol aldehyde greater than retinol acetate. The most sensitive period for inhibiting ldUrd induction by retinoic acid was 24 h postinduction or with concomitant treatment. Vitamin C and vitamin E inhibited ldUrd induction most effectively with 48 h incubation. Retinol and vitamin C also inhibited virus induction by MNNG. None of the retinoids, vitamin C, or vitamin E significantly inhibited virus expression in noninduced cells or were toxic to the cells at the concentrations used in these experiments.
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PMID:Human T-cell leukemia virus I induction by 5-iodo-2'-deoxyuridine and N-methyl-N'-nitro-N-nitrosoguanidine: inhibition by retinoids, L-ascorbic acid, and DL-alpha-tocopherol. 299 Jun 71

Mucositis represents one of the most frequent complications during chemotherapy or radiotherapy. Few studies have showed effective prevention against mucositis in this setting. In this randomized study, we tested the efficacy of vitamin E in the treatment of chemotherapy-induced mucositis. Twenty patients with malignant haemopathies were included; 19 patients were evaluable for the prevention of mucositis. Ten patients were treated with induction therapy for acute myelogenous leukaemia and 9 were treated with intensive therapy followed by autologous bone marrow transplantations. The severity of mucositis was evaluated according to World Health Organization classification. Our results showed that vitamin E may be of therapeutical value in the prevention of mucositis especially during induction therapy for acute myelogenous leukaemia.
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PMID:[Treatment of mucositis with vitamin E during administration of neutropenic antineoplastic agents]. 786 1

In the present study we have established that the antitumor activity of alpha-tocopheryl succinate (TS, vitamin E succinate) and cholesteryl succinate (CS) result from the action of the intact TS and CS compounds and not from the release of alpha-tocopherol, cholesterol, or succinate. We report that treatment of murine leukemia cell lines C1498 (myeloid) and L1210 (lymphocytic), with the tris salts of TS or CS, but not alpha-tocopherol and tris succinate or cholesterol and tris succinate, significantly inhibit the growth of these tumor cells and significantly enhance doxorubicin-induced tumor cell kill in a similar fashion. In contrast, the treatments mentioned above did not adversely affect the growth of murine normal bone marrow cells (colony-forming unit-granulocyte-macrophage). In fact, colony-forming unit granulocyte-macrophage cell growth was stimulated by exposure to CS and TS (as well as their ether analogues) at concentrations above 100 microM. Furthermore, pretreatment of colony-forming unit granulocyte-macrophage cells with TS or CS appears to protect these normal cells from the lethal effect of doxorubicin exposure. Selective inhibition of leukemia cell proliferation (identical to that noted for CS and TS) was also observed following the treatment of cells with the nonhydrolyzable ether forms of CS (cholesteryloxybutyric acid) and TS (alpha-tocopheryloxybutyric acid). These findings suggest that TS, alpha-tocopheryloxybutyric acid, CS, and cholesteryloxybutyric acid may prove clinically useful as selective antitumor agents when administered alone or in combination with doxorubicin by a route that ensures tissue accumulation of the intact compound.
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PMID:The selective antiproliferative effects of alpha-tocopheryl hemisuccinate and cholesteryl hemisuccinate on murine leukemia cells result from the action of the intact compounds. 801 47

A murine AIDS model with many similarities to human AIDS, LP-BM5 Murine Leukaemia, suppresses T and B cell numbers and functions in the intestine. This permits chronic colonization by Giardia and Cryptosporidium. Cocaine and the nutrient alcohol, which are immunosuppressive, further reduce resistance to intestinal parasites and intestinal lymphocyte numbers. Protein undernutrition, vitamin E supplementation, and alcohol use further modify immune dysfunction induced by the murine retrovirus infection. This suggests that both undernutrition and nutrient supplementation could affect parasite resistance during AIDS. Thus this murine model of human AIDS has great potential to accelerate studies of the role of nutrients in immune dysfunction and resistance to intestinal parasites.
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PMID:Resistance to intestinal parasites during murine AIDS: role of alcohol and nutrition in immune dysfunction. 811 87

A comparative study has been performed on the relationship between vitamin E and immunofunction in normal and malignant condition in human and murine systems. Further, the effects of supplemental vitamin E on tumor take, host survival and tumor growth have been studied in a transplantable lymphoma in mice. Vitamin E was assayed in serum samples from normal subjects and from patients with leukemia and lymphoma by high performance liquid chromatography (HPLC). The murine group included Dalton's ascitic lymphoma (DL), Schwartz lymphoblastic leukemia (SVL) and Moloney lymphoblastic leukemia (MVL). Serum vitamin E was found to be lower than that of the normal controls in all cases of leukemia and lymphoma both in human and animal system. The levels of immunoglobulins (IgG and IgM) were found to be higher in mice with leukemia and lymphoma. Supplementary vitamin E administered at the initial phase of development of murine lymphomas reduced the rate of tumor growth, improved host survival and elevated serum vitamin E level. Vitamin E supplementation also activated specific mitogen induced blastogenesis of peripheral blood lymphocytes (PBL) and elevated serum IgG level. IgM remained unaltered and macrophage activity did not seem to be affected. The present findings indicated a low status of vitamin E in tumor bearing host and a beneficial effect of supplemental vitamin E on the host which was mediated by the host immune system.
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PMID:Vitamin E--its status and role in leukemia and lymphoma. 827 50

Serum antioxidant vitamins A (retinol) and E (alpha-tocopherol), beta-carotene, zinc and selenium for 418 children with newly diagnosed malignancy were compared with those of 632 cancer-free controls. Incident cancer cases and controls were 1-16 years old and recruited in 1986-1989. Age- and sex-adjusted serum concentrations of retinol, beta-carotene and alpha-tocopherol were significantly inversely associated with cancer. In similar models, the odds ratio (OR) comparing the highest with the lowest quintile was 2.06 (95% confidence interval [CI] 1.40-3.02) for retinol, 3.87 (95% CI: 2.54-5.90) for beta-carotene, 2.15 (95% CI: 1.48-3.10) for alpha-tocopherol, 1.29 (95% CI: 0.75-2.23) for selenium, and 1.94 (95% CI: 1.17-2.23) for zinc. The cancer sites that were associated with serum beta-carotene were, in general, leukaemia, lymphoma, central nervous system, bone and renal tumours. Moreover, leukaemia was associated with low mean serum levels of retinol, selenium and zinc. Subjects with lymphoma, bone and renal tumours also had lower mean retinol and alpha-tocopherol levels than controls. Brain tumour patients had low vitamin E levels. Low serum values of antioxidant vitamins were associated with childhood neoplasm occurrence. Some site-specific effect was reported. Low peripheral nutrient levels are not considered as cancer promoters but rather as an impairment of the body's defence mechanism occurring during the cancer-related metabolic and nutritional disturbances and inflammation processes.
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PMID:Serum beta-carotene and antioxidant micronutrients in children with cancer. The 'Cancer in Children and Antioxidant Micronutrients' French Study Group. 828 53

Currently there is little evidence that vitamins of any type are able to greatly modify the progression of established malignancy with the exception of promyelocytic leukaemia. In contrast, there is considerable laboratory evidence from chemical, cell culture and animal studies that antioxidant vitamins and related micronutrients are able to slow, or possibly prevent the carcinogenic process. There is a good theoretical basis for these findings. Current theories for the mechanism of tumourigenesis suggest that reactive species and prooxidants promote and encourage the process whilst antioxidants are inhibitory and protective. Retinoids and folate with limited or no antioxidant activity may protect DNA in other ways. In man there is support for this role from the extraordinarily high concentrations of ascorbate and possibly alpha-tocopherol at sites where oxidant stress is likely to be most intense, with loss of such antioxidant protection in some conditions which predispose to malignancy. There is also impressive epidemiological agreement, particularly from observational studies, where the lowest fruit and vegetable intake has been consistently associated with increased risk of cancer, especially of the lung and gastrointestinal tract, but much less evidence that such low intakes can encourage the development of cancers which are under hormonal control. Where individual micronutrients have been considered, beta-carotene appears to have the strongest protective effect followed by vitamin C and vitamin E. Whilst the experimental studies have suggested a role for retinoids, this has not been confirmed by the observational studies. Unfortunately, with the exception of oral leukoplakia, studies investigating reversal of premalignant conditions have been disappointing, and two intervention studies aimed at prevention in large populations have produced conflicting results. All this begs the question as to what dietary advice or intervention, if any, should be provided prior to the publication of the many randomized intervention studies that are presently investigating the role of micronutrients in cancer prevention. Gey [73] has produced recommendations for minimum blood concentrations and intakes of antioxidant micronutrients. (ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Micronutrients, antioxidants and risk of cancer. 877 55

Much of what is known about the antioxidant mechanism of vitamin E has been learned from studies of lipid dispersions, solutions, or subcellular organelles. We have investigated the effect of vitamin E supplementation on intact live eucaryotic cells. L1210 murine leukemia cells were exposed to an oxidative stress induced by 20 microM Fe2+ and 100 microM ascorbic acid introduced immediately before oxidative measurements were begun, and the kinetics of the generation of lipid-derived free radicals, as measured by EPR spin trapping (a product) and O2 consumption (a reactant) were measured. Cells grown for 24 h with supplemental (5-100 microM) vitamin E in their media had a slower rate of lipid radical generation compared to cells grown without vitamin E supplementation; this inhibition in the rate of oxidation was generally dependent upon the amount of vitamin E supplementation. In complementary studies measuring O2 consumption, 5-100 microM vitamin E slowed the rate of oxidation (10-fold with 100 microM supplemental vitamin E) consistent with the EPR studies. The membrane active drug edelfosine accentuated the vitamin E effects; vitamin E introduced a discernible lag phase (time delay) in both lipid radical generation and O2 consumption that was not seen in the absence of edelfosine. Vitamin E supplementation of cells also altered the kinetics of ascorbate free radical formation. We conclude that vitamin E inhibits lipid peroxidation in cells by slowing the rate of lipid peroxidation; but with iron/ascorbate as the initiating system, vitamin E does not delay the onset of peroxidation. Of special interest is that these free radical peroxidation events parallel cell membrane damage as detected using trypan blue exclusion. These observations are consistent with the free radical events preceding and causing the observed membrane damage.
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PMID:Vitamin E slows the rate of free radical-mediated lipid peroxidation in cells. 890 Apr


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