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Biomedical subjects

F Fey

Publications and source records attributed to F Fey.

At least 19 recordsLinked to original sources
PubMed1992

Copper(II)-substituted horse liver alcohol dehydrogenase: structure of the minor species.

Oxygen treatment of horse liver alcohol dehydrogenase EE isozyme substituted with Cu(II) at the catalytic site leads to bleaching with concomitant reduction to Cu(I) of approximately 90% of total Cu(II). The Cu(II) of the remaining 'minor species' cannot be reduced nor does it interact with exogenous ligands, e.g. 2-mercaptoethanol, imidazole, pyrazole, or azide ions. The EPR spectrum is axial with a super-hyperfine splitting of 15.6 G indicating binding of one nitrogen atom to Cu(II). These data as well as the energies and intensities of the absorption and CD spectra suggest the Cu(II) ion of the minor species to be located in the catalytic site of HLADH in a position and geometry different from that of the major species.

Alcohol Dehydrogenase↗
PubMed1987

Further characterization of the leukemogenic activity of haloperidol in mice.

Haloperidol, a butyrophenon, is widely used for the treatment of psychotic disorders in man. Recently we reported that this drug causes, with high incidence, the development of monocytic-myeloid leukemias in male NMRI mice upon 5 X 5 mg/kg i.p. administration. Here we present evidence for the leukemogenic effect of haloperidol in two other strains of mice (XVII AKF1 hybrids, and the low leukemic BALB/c/BOM). The strain-dependent incidence of leukemias ranged both in males and females between 34% (AKR) and 69% (XVII AKF1) with average latencies between approximately 200 (AKR) and 600 (BALB/c) days. On the basis of cytological and cytochemical criteria the predominating type of leukemias was classified as monocytic-myeloid. These leukemic were serially transplantable. Cell-free extracts of leukemic tissues did not induce the disease indicating that no virus was activated by haloperidol. However, when the drug was administered to AKR mice after a suboptimal dose of nitrosomethylurea (NMU), a higher incidence of mixed-type leukemias was observed as with haloperidol alone. NMU alone induced lymphatic leukemias with proven viral involvement. The tumor promoter 12-0-tetradecanoylphorbol-13-acetate did not influence haloperidol-induced leukemogenesis.

Animals↗
PubMed1983

[Detection of cellular sensitization in mice after treatment with chemical carcinogens].

Mice were treated epicutaneously (DMBA, benzene) and subcutaneously (BP, MNH) with chemical carcinogens. As detected by the MEM-test a cellular sensitization developed against fetal antigens, which are present in 3M KCl-extracts of mouse fetal tissue. The sensitization was detected before formation of tumors occurred. The conclusion was drawn that sensitization to fetal antigens is not a characteristic feature of tumor-bearing animals.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1982

Characterization of an RNA-directed DNA polymerase from mouse spleen infected with leukaemia virus activated during N-methyl-N-nitroso urea-induced leukaemogenesis.

An RNA-directed DNA polymerase was purified from mouse spleen infected with leukaemia virus activated during N-methyl-N-nitroso urea- (MNU-) induced leukaemogenesis. The enzyme was isolated from the microsomal fraction and purified by successive chromatography of Sephadex G-200 and phosphocellulose. Estimation of molecular weight from the sedimentation rate of the purified enzyme in a sucrose gradient gave a value of 70,000. The enzyme had a pH optimum of 7.4, a KC1 optimum of 50 mmol/l, an Mn2+ optimum of 0.2 mmol/l, and a temperature optimum of 25 degrees C, when (rA)n . (dT) 10 was used as the template-primer. It preferred (rA)n . (dT)10 as the template-primer and transcribed (rC)n . (dG) 12 and (OMeC)n . (dG)12. A comparison of the properties of this DNA polymerase with the enzyme purified from murine type C retroviruses showed that the MNU-activated virus enzyme was both biochemically and biophysically indistinguishable from murine leukaemia virus DNA polymerases.

Animals↗
PubMed1981

Demonstration of a syncarcinogenic effect of endogenous MuLV, rescued from MNU-induced leukemias, and suboptimal MNU doses in mice.

It was demonstrated that the combined action of activated endogenous MuLV isolated from MNU-induced leukemias and suboptimal doses of MNU yields a significantly high incidence of leukemias and tumors. Treatment with one agent alone shows low effects only. The findings were discussed in view of the mechanisms in which viruses and chemical carcinogens interact in a syncarcinogenic processes.

Animals↗
PubMed1981

Effectivity of living and non-living BCG vaccine on experimental metastatic spread in mice and the stimulation of the reticulohistiocytic system (RHS).

Heat-killed or formalin-killed BCG vaccine caused statistically significant increases in weight of lungs, spleen and liver, which were in the same range as after administration of equal doses of viable BCG vaccine. Similarly, there was no quantitative or temporal difference in the phosphatase-positive proliferations of the RHS in liver spleen and lungs when using identical doses of viable or heat- or formalin-killed BCG vaccines. The metastasis-prophylactic effect demonstrated for viable BCG was present also after administration of the killed vaccines to a statistically significant degree. The increases in organ weight, extent of phosphatase-positive proliferation foci in liver, spleen and lungs as well as the metastasis-prophylactic effect were entirely identical; they seem to be in a close relationship with each other.

Acid Phosphatase↗
PubMed1980

Induction of extra-thymic lymphatic leukemias in nude mice by means of administration of N-methyl-N-nitrosourea (MNU).

Experiments concerning the chemical leukemogenesis in nude mice were performed. Following administration of N-methyl-N-nitrosourea (MNU) 4 out of 11 nude mice developed extra-thymic lymphatic leukemias. The findings are demonstrated by means of histological and histochemical methods. The successful cellular transplantation of an induced lymphatic leukemia is reported.

Animals↗
PubMed1980

Demonstration of C-type viruses in N-methyl-N-nitroso urea (MNU)-induced leukemia of mice by reverse transcriptase activity and XC assay.

A significantly higher MuLV expression was demonstrated in cells of MNU-induced leukemia of mice compared to corresponding cells of untreated control animals by reverse transcriptase activity and XC cell assay. These positive findings were verified by determination of indirect immunofluorescence test to look for intracytoplasmic MuLV p30. The problem is discussed whether these viruses play a role in chemical leukemogenesis.

Animals↗
PubMed1980

Antiviral effect of haloperidol on Rauscher murine leukemia virus.

The neuroleptic drug haloperidol (Hal) shows, when administered in multiple intraperitoneal or intravenous injections beginning at 5 hrs post inoculation of Rauscher leukemia virus to male NMRI mice, a marked activity in inhibiting virus-induced splenomegaly and prolonging mean survival time. Evidence is presented that a direct action of the drug on the virus is involved in its inhibitory effect.

Animals↗
PubMed1979

[Studies of the target cell problem in N-nitroso-N-methylurea induced leukemogenesis].

After i.p. application of 14C-nitrosomethylurea (NMU), mice were killed at different periods and the 14C-activity in various organs was determined by scintillation counting and by autoradiography. Contrary to expectations, bone marrow showed a significantly higher activity than the thymus, which is the supposed target-organ for the lymphatic leukemogenesis. The specificity was secured by examinations of the proliferation kinetics. The radioautographic results of bone marrow favorize the lymphatic cells as the target for NMU. The target-cell problem is discussed in respect to thymectomy examinations and recent results on nude mice. With high probability the thymus is not essential for lymphatic leukemogenesis.

Animals↗
PubMed1978

[Thrombocytic reactions in experimentally induced neoplasms (author's transl)].

Strain XVII mice with Graffi virus induced leukemia of various hematological types showed a pronounced thrombocytopenia which was severe in erythroblastic leukemia and weaker in lymphatic ones. The thrombocytic reactions shortly following Friend and Rauscher virus applications and occurred 3 weeks after birth in AKR mice are not found in Graffi virus system. A significant preleukemic thrombocytopenia did appear only 8 weeks after Graffi virus infection. The origin of both the preleukemic and the secondary thrombocytic reactions are discussed. (XVII X AKR) F1 hybrids, neonatally treated with N-nitroso-N-methylurea (NMU), resulted also in a decline in the number of thrombocytes after manifestation of leukemia. In contrast to the expection following NMU treatment a preleukemic thrombocytopenia appeared as in viral leukemogenesis too. The possibility of a co-operation of oncogenic viruses in chemical carcinogenesis is considered.

Animals↗