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Biomedical subjects

H J Seidel

Publications and source records attributed to H J Seidel.

At least 37 records · Page 2Linked to original sources
PubMed1990

Haemopoietic stem cells in mice chronically exposed to styrene vapour.

Female C57BL/6X DBA/2 hybrid mice were exposed to two concentrations of styrene in inhalation chambers for 6 h/day, 5 days per week. The concentrations were 220 ppm for a period of up to 8 weeks and 440 ppm for 2 days, followed by 330 ppm for up to 8 weeks due to early deaths after 440 ppm. Parallel groups were also treated with 5% ethanol in the drinking water during the days of styrene exposure. In the peripheral blood only a lymphocytopenia was found. The numbers of pluripotent haemopoietic stem cells, CFU-S, were unaffected, as were granuloid committed stem cells, CFU-C. Early and late erythroid stem cell numbers, BFU-E and CFU-E, showed high variability. At 220 ppm about half of the animals had CFU-E numbers below 80% of controls, at 440/330 ppm about two-thirds of the animals had BFU-E and CFU-E numbers below this level. An additional effect of ethanol was not found.

Air↗
PubMed1990

The influence of ethanol on the stem cell toxicity of benzene in mice.

BDF1 mice were exposed to 100, 300, and 900 ppm benzene vapor, and the numbers of hematopoietic progenitor cells, early and late erythroid progenitors (BFU-E and CFU-E) and granuloid progenitors (CFU-C), were determined with and without additional exposure to ethanol (5, 10, 15 vol%) in the drinking water. The duration of benzene inhalation was up to 4 weeks, 6 hr per day, 5 days per week. It was shown that the number of CFU-E per femur was depressed in a dose-dependent manner by benzene alone and also by ethanol combined with a given benzene concentration. CFU-E showed rapid regeneration after the end of the exposure, but not BFU-E and CFU-C. Prolongation of the ethanol exposure after withdrawal of benzene had only a marginal effect on progenitor cell regeneration.

Administration, Inhalation↗
PubMed1989

The influence of benzene on the erythroid cell system in mice.

Female BDF1 mice were exposed up to 8 weeks to airborne concentrations of 100, 300, and 900 ppm of benzene, 6 h/day, 5 days/week. The erythropoietic cell compartment in the bone marrow and the peripheral blood was studied using the erythroid burst-forming unit (BFU-E) and erythroid colony-forming unit (CFU-E) assays, the incorporation of 59Fe, and standard methods. In the peripheral blood only a slight anemia was observed. In the bone marrow, however, a considerable decrease of CFU-E numbers was seen, the CFU-E being more depressed than the BFU-E numbers. In bone marrow smears a variable content of erythroblasts was found. The 59Fe kinetics showed an enhanced turnover within the erythron, suggesting the decrease in transit time as a compensating mechanism for the low CFU-E numbers. After 4 weeks of exposure to all benzene concentrations, greater than 17 days in benzene-free atmosphere are needed for a complete recovery of BFU-E and CFU-E compartment sizes.

Anemia↗
PubMed1989

The hematopoietic stem cell compartments in mice during and after long-term inhalation of three doses of benzene.

Female BDF1 mice were exposed for 16 weeks to airborne concentrations of 100, 300, and 900 ppm of benzene, 6 h per day, 5 days per week. Bone marrow hemopoietic stem cell compartments and peripheral blood cell counts were studied using clonal assays and standard methods. Dose-dependent depressive effects were observed on all stem cell compartments. Only the erythroid colony-forming units (CFU-E) compartment was depressed during exposures to 100 ppm; CFU-E were more sensitive than the erythroid burst-forming units (BFU-E), spleen CFU (CFU-S), or G-M CFU (CFU-C) during exposure to 300 ppm or 900 ppm. Lymphocytopenia was observed in the peripheral blood. After benzene-free intervals, a regeneration of lymphocyte numbers and slow normalization of stem cell numbers was seen. Complete recovery from the 16 weeks exposure to 300 ppm was seen between 73 and 185 days.

Administration, Inhalation↗
PubMed1988

Murine thymic multicellular complexes during latency period after methylnitrosourea (MNU) injection.

The number of TNC complexes and of stroma cell-thymocyte rosettes was examined during the preleukemic period in mice given MNU to induce leukemia. In parallel, numbers of the complexes were studied following administration of hydrocortisone one day before administering MNU, i.e. after the procedure which clearly inhibited manifestation of induced leukemias. Administration of MNU with or without hydrocortisone is followed by disappearance of TNC complexes and stroma cell-thymocyte rosettes followed by their regeneration between 2 and 6 weeks after MNU. Relative rates of regeneration were different in MNU treated versus MNU + hydrocortisone treated animals.

Animals↗
PubMed1987

Trisomy 15 as a regular finding in chemically induced murine T-cell leukemogenesis.

Trisomy 15 is described as a common finding in all T-cell leukemias induced by a single dose of methylnitrosourea (MNU) in BDF1 mice and in the leukemias induced by 7 doses of benzo(a)pyrene. Additional trisomies were found in about half of the leukemias. The organ distribution suggests that the leukemic cells with trisomy 15 originate in the thymus. Trisomy 15 was detected in the thymus as early as 6 weeks after the application of MNU, i.e. during the latency period.

Animals↗
PubMed1987

Effects of radiation and other influences on chemical lymphomagenesis.

Methylnitrosourea (MNU) or butylnitrosourea (BNU) was used to induce T cell lymphomas (thymomas) in BDF1 mice. In addition to the chemical, X-rays in various dose schedules were applied. An effect of the irradiation (shortening of the latency period) was seen with 12 X 0.25 Gy in protocols with a prolonged median induction time in the controls as a result of a dose reduction of the chemical (median induction time 27-36 weeks instead of 16-18 weeks under 'optimal' conditions using 50 mg kg-1 of MNU). Preirradiation 2-5 weeks before 40 mg kg-1 of MNU resulted in enhanced leukaemogenesis. Also, mice with regenerating lympho-haemopoiesis after lethal irradiation and bone marrow transplantation were more sensitive to the effect of both chemicals than were the controls. Treatment with anti-thy 1.2 and with corynebacterium parvum during the latency period had no influence.

Animals↗
PubMed1986

Natural killer cells in leukemogenesis.

In order to relate a reduced natural killer (NK) cell function to leukemogenesis, NK cells in the spleen and peritoneal exudate cells, with and without stimulation by Corynebacterium parvum, were tested in mice of various strains after split dose irradiation and after leukemogenic treatment with butyl- and methylnitrosourea. The investigations included also mice submitted to non-leukemogenic irradiation (1 X 1.5 and 1 X 4.5 Gy) and mice submitted to an additional treatment with hydrocortisone, which delays leukemia development after methylnitrosourea. There was, indeed, a NK-cell depression, but no major differences were seen between mice prone to leukemia development and those after cytotoxic, but nonleukemogenic, treatment.

Animals↗
PubMed1986

T-cell markers in the thymus during methylnitrosourea-induced leukemogenesis.

T-cell leukemias were induced in adult BDF1 mice by a single i.v. injection of 50 mg/kg of methylnitrosourea (MNU). During the latency period and in leukemic mice the expression of peanut agglutinin (PNA) receptors, terminal deoxynucleotidyl transferase (TdT) and thymus leukemia antigen (TLm4) in the thymus was studied. First, TLm4-positive thymocytes were found 6 wk after MNU. Further, there was a continuous reduction of the percentage of PNA-positive thymocytes. The expression of TdT remained unaltered late in the latency period and in leukemic mice. Four phenotype patterns could be defined for the expression of TdT and PNA in thymocytes: PNA+ TdT+, PNA+ TdT-, PNA- TdT+ and PNA- TdT-. Thymuses negative for TdT were rare, the majority was PNA+ TdT+. However, thymuses late after MNU treatment and leukemic thymus were PNA- TdT+. The discrepancy in the expression of PNA and TdT as cellular markers in leukemic mice as compared to normal cell populations is discussed.

Animals↗
PubMed1986

T-cell subsets in the murine thymus during chemically induced leukemogenesis.

T cell leukemias were induced in BDF 1 mice by methylnitrosourea (MNU). The phenotype of the leukemic cells is Thy1.2 +, PNA-, TdT+, TL+ and heterogeneous with respect to Lyt-1 and Lyt-2. About 70% of the leukemias have elevated amounts of gp70. During latency period of at least 9 + 12 weeks an early reduction in the various thymic cells and the CFU-S is observed, with almost complete recovery. Later PNA+ cells are reduced. Hydrocortisone treatment delays or enhances leukemogenesis, dependent on the time interval between hydrocortisone and MNU. Some mice show elevated amounts of gp70 in their bone marrow 2--3 weeks after MNU. The problem of target cells in the bone marrow and the thymus is discussed.

Animals↗
PubMed1985

RNA virus expression during and after methylnitrosourea-induced T-cell leukemogenesis in mice.

The expression of RNA tumor virus was studied in BDF 1 mice after leukemogenic treatment with a single dose of methylnitrosourea (MNU) and in leukemic thymuses by a cell ELISA using antibodies against the viral glycoprotein gp 70 and by co-culture for the detection of eco- and xenotropic virus. The majority of the thymomas were positive for gp 70; ecotropic, but not xenotropic infectious virus could be detected in some of them. Early after MNU application the thymus and the bone marrow were positive for gp 70 in some animals. Later, after a phase with positive results with spleen cells, the bone marrow and the spleen were negative again. Only the thymus of some mice were positive during the last weeks before the first leukemias appeared.

Animals↗
PubMed1985

T-cell phenotypes in chemically induced leukemia in mice.

T-cell leukemias were induced in adult BDF mice by a single i.v. injection of 50 mg kg-1 of methylnitrosourea (MNU). Leukemic cells from the thymus and other organ sites showed the theta antigen and were peanut-negative, but were heterogeneous with respect to Lyt-1 and Lyt-2. The acute cytotoxic effect of the MNU showed no preferential toxicity to a special T-cell subset in the thymus. During the latency period of leukemogenesis a continuous fall in peanut-positive cells in the thymus was found.

Animals↗
PubMed1985

The sensitivity to methylnitrosourea-induced T-cell leukemogenesis in mice is modified by the injection of hydrocortisone.

T-cell leukemias were induced in adult BDF1 mice by a single i.v. injection of methylnitrosourea (MNU). Leukemogenesis was delayed by a single or repeated injections of hydrocortisone (HC) after MNU and also when HC was given one day before MNU. Enhancement of leukemogenesis was seen in experiments with 10 and 14 days' intervals between HC and MNU. The T-cell subset composition of the thymus after HC treatment was studied at these time intervals, but a specific target cell for the action of MNU, reduced one day after HC and increased in number during the thymic regeneration at 10 and 14 days could not be defined. HC did not prohibit the toxic action of MNU as measured by hemopoietic stem cell numbers in the femur.

Animals↗
PubMed1985

On the role of the spleen in Friend virus (F-MuLV-P) erythroleukemia.

About 30% of Friend virus (F-MuLV-P)-infected C57BL/6 mice became leukemic more than ten weeks after virus infection. This late leukemia development could not be essentially influenced by drug treatment, such as injection of hydroxyurea (2 X 500 mg/kg), actinomycin D (3 X 120 micrograms/kg), phenylhydrazine (3 X 60 mg/kg), or 30 micrograms endotoxin or by bone marrow transplantation following lethal irradiation. Endotoxin (30 micrograms) given prior to virus caused the loss of resistance to F-MuLV-P, but it had only a slight effect if applied one or three months after virus infection. Leukemia development has never been observed in C57BL/6 mice after splenectomy. In DBA/2 mice, highly susceptible to F-MuLV-P, leukemia development was markedly impaired if the mice were splenectomized. These results clearly indicate that the spleen plays a crucial role in the mechanism of susceptibility or resistance to the Friend virus.

Animals↗
PubMed1985

Leukemogenesis by methylnitrosourea in BDF1 mice. The origin of transplantable cells and the activity of the natural killer cells during the preleukemic period.

BDF1 mice injected with methylnitrosourea (MNU, 50 mg/kg) developed T cell leukemias within 9-35 weeks (median induction time 18 weeks). Leukemic cells, determined by transplantation, were found 2-5 weeks before the death of the animals. Natural killer (NK) cell activity in the spleen and peritoneal exudate cells was studied using YAC-1 cells as targets. MNU-treated mice showed reduced lytic activity with or without stimulation by Corynebacterium parvum. NK activity was essentially the same in mice with and without transplantable leukemic cells. No correlation could be demonstrated between the degree of NK cell depression, as studied in the spleen after splenectomy, and the survival time of individual mice.

Animals↗
PubMed1984

Leukemia induction by methylnitrosourea (MNU) in selected mouse strains. Effects of MNU on hemopoietic stem cells, the immune system and natural killer cells.

T cell leukemias were induced by a single dose of methylnitrosourea (MNU) in DBA/2, C57/Bl/6, NMRI, BDF1, and CBA mice. The latency period in the CBA strain was much longer than in the others. Studies on the pluripotent stem cells in the bone marrow and T cell reactions of thymus and spleen cells showed a toxicity of MNU for these parameters but no significant differences between the strains. The activity of the natural killer (NK) cells in the spleen and peritoneal exudate cells, studied also after additional stimulation by injection of Corynebacterium parvum, was influenced by MNU, but again no relation to leukemogenesis could be established. The first leukemic (transplantable) cells were found in the thymus. The presence of leukemic cells could be responsible for low NK cell activities found in BDF1 and DBA/2 mice late after MNU.

Animals↗
PubMed1984

Studies on natural killer cell activity and the influence of Corynebacterium parvum on murine T-cell leukemogenesis induced by butylnitrosourea.

Butylnitrosourea (BNU) was used to induce thymic lymphomas in BDF1 mice. During and after the 12-week BNU exposure the spontaneous NK cell activity against YAC-1 cells and that arising 4 days after stimulation with Corynebacterium parvum (CP) were measured, as were the mitogen responses of splenic T and B cells. In addition to BNU, groups of mice received multiple injections of the interferon inducer CP during or after the BNU exposure period. The results show a slight impairment of the NK cell activity by BNU and also after the injections of CP depending heavily on the treatment protocol. After the multiple injections of CP, either into BNU-treated mice or into controls, no further stimulation by CP was possible. The mitogen responses, reduced after BNU, were further reduced after the additional treatment. Both effects can be explained by the known induction of suppressor cells by CP. Although these treatments had pronounced effects on the parameters tested in vitro there was no significant influence on the development of thymic lymphomas in vivo.

Animals↗