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At least 145 records · Page 8Linked to original sources
PubMed1984

Nitrous oxide reduces growth of experimental rat leukemia.

The ability of nitrous oxide to inhibit the in vivo growth of hematological neoplasms was investigated in a rat model for acute myeloid leukemia (BNML). Nitrous oxide, administered in a concentration of 67% with 33% oxygen, resulted in a reduction of spleen and liver weights of approx. 30%, as compared with leukemic rats kept in ambient air. Peripheral white cell counts were also considerably lower in the treated rats. Plasma levels of vitamin B12 were found to be elevated in untreated leukemia, but fell to about normal levels after nitrous oxide exposure. On the contrary, folic acid levels were low in untreated leukemic rats, and significantly higher in animals exposed to nitrous oxide. The observed effects of nitrous oxide appeared to be dose-dependent. The deoxyuridine suppression test performed with leukemic cells became abnormal after nitrous oxide inhalation, in accordance with the effect on normal bone marrow. These results indicate that the interference of nitrous oxide with vitamin B12-related metabolism, which leads to impairment of de novo thymidine synthesis, has the potency to reduce leukemic proliferation in vivo.

Animals↗
PubMed1992

Development of pulmonary leukostasis in experimental myelocytic leukemia in the Brown-Norway rat.

The pathogenesis of pulmonary leukostasis in leukemia was studied in a rat model by investigating the course of its development. Leukemia was induced by inoculating rats with leukemic cells. The earliest stage of leukostasis was found from day 14 onward, when leukemic cells appeared in the peripheral blood, and was characterized by accumulation of leukemic cells at the capillary level. Simultaneous with the increase of leukemic cell concentrations in the peripheral blood, accumulation in capillaries increased gradually over a period of several days. This was accompanied by increasing severity of tachypnea. Shortly before death, aggregates consisting almost solely of leukemic cells were found in medium-sized blood vessels. This stage was rapidly followed by the end-stage, characterized by complete obstruction of the lung vasculature--including the largest arteries and veins--by leukemic cell aggregates, giving rise to extensive hemorrhages and edema. The end-stage was considered to be the cause of death, which occurred 18-26 days after the inoculation. The histological and ultrastructural findings in this study suggest that besides the size and stiffness of individual leukemic cells, interactions not only between leukemic cells, but also between leukemic cells and the endothelium play a role in the pathogenesis of pulmonary leukostasis.

Animals↗
PubMed1986

[Lysosomal enzymes in lymphocytes in experimental lymphatic leukemia in mice].

The activity of lysosomatic enzymes, i.e.: alkaline phosphatase, beta-glucoronidase, lysozyme and non-specific alfa-esterase in the organic lymphocytes and in the lymphocytes of peripheral blood were determined. It was found that the disorders of intracellular distribution of enzymes are the evidence of destabilization of lysozymes membrane with the following translocation of alkaline hydrolases into cytoplasm. There were observed the debilitation of the protective possibilities and the decrease of unspecific immunological resistance of leukaemia lymphocytes.

Animals↗
PubMed1993

Involvement of the complement system in the pathogenesis of pulmonary leukostasis in experimental myelocytic leukemia.

The role of the complement system in the pathogenesis of pulmonary leukostasis in myelocytic leukemia was studied in a rat model. Acute myelocytic leukemia was induced in six Brown-Norway rats, and complement levels were assayed during the course of the disease. Whole complement activity (CH50) and hemolytic activity of C1q, C3, and C4 decreased from day 16 after induction of the leukemia, when the rats developed pulmonary leukostasis. In addition, local complement activation was established in the lung vessels by immunofluorescence microscopy in advanced stages of pulmonary leukostasis. Finally, following systemic activation of the complement system by injection of cobra venom factor (CVF), leukemic rats (n = 6) died of pulmonary leukostasis 4.5 days earlier than did leukemic controls (n = 6). These findings suggest that, in acute myelocytic leukemia in Brown-Norway rats, pulmonary leukostasis is induced by activation of the complement system. This finding could lead to new modes of treatment for a life-threatening complication of leukemia.

Animals↗
PubMed1986

Enhanced therapeutic effect of methotrexate in experimental rat leukemia after inactivation of cobalamin (vitamin B12) by nitrous oxide.

Exposure to nitrous oxide interferes selectively with the coenzyme function of vitamin B12 and causes inactivation of methionine synthetase, with subsequent impairment of folate metabolism and reduction of cellular proliferation. In a rat leukemia model (BNML) we investigated the combined administration of nitrous oxide, inactivating vitamin B12, and methotrexate (MTX), a folate antagonist inhibiting the enzyme dihydrofolate reductase. Through different mechanisms, both agents decrease the availability of tetrahydrofolate, and subsequently of other reduced folates, with increased impairment of folate-dependent synthesis of thymidylate. Effects on leukemic growth and on hematological values in rats demonstrated enhancement of the therapeutic effect of MTX by exposure to nitrous oxide. With several treatment schedules, the results of combined treatment were seen to be better than additive when compared with the effects of single agents. In particular, pretreatment of leukemic rats with nitrous oxide for 3 days before administration of MTX appeared effective. With higher doses of MTX, concomitant exposure to nitrous oxide even resulted in toxic effects. These findings were in accordance with the results of some metabolic studies performed in leukemic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Nitrous oxide selectively reduces the proliferation of the malignant cells in experimental rat leukemia.

A considerable reduction of hepatosplenomegaly and leucocytosis in leukemic rats of the Brown Norway Myeloid Leukemia (BNML) can be achieved by exposure to 50% nitrous oxide/50% oxygen. In this study the differential antiproliferative effect of nitrous oxide, inactivating vitamin B12, on normal and leukemic hemopoiesis was investigated in this rat model. Rats injected with leukemic cells and exposed to nitrous oxide for 10 days showed 30% reduction of hepatosplenomegaly and 50% reduction of leukocytosis. Similarly treated healthy rats showed no signs of impaired hemopoiesis as measured by peripheral blood parameters. Clonogenic assays of erythroid and myeloid progenitors from both healthy and leukemic rats revealed that exposure to nitrous oxide did not suppress normal bone marrow functioning. On the contrary, the reduction of leukemic proliferation by nitrous oxide retarded the leukemic infiltration of the bone marrow compartment.

Animals↗