scholarly journals Toxic effects of various zinc dosages on poultry hemopoiesis

2020 ◽  
Vol 164 ◽  
pp. 06011
Author(s):  
Aleksandr Vishnyakov

The aim of the study was to determine the main patterns of the manifestation of the toxic effect of zinc chloride on the cells of the red bone marrow in the first three days after exposure. Our experiment involved broiler chickens of the “Smena-7” cross. The work presents new data on the effects of zinc salts in doses of 40 mg/kg and 60 mg/kg on the hemopoietic cells of the red bone marrow of birds at the ultrastructural level. Thus, the results of the study showed zinc poisoning of chickens even within 1-3 days led to damage to bone marrow cells. The cytoplasm of blood-forming and stromal cells of the bone marrow detects mostly signs of destructive processes, which are amplified as the duration and the dose of exposure increase. At the same time, the structure of cell nuclei often gets changed in the bone marrow. Emerging morphological signs indicate a decrease in the transcription of ribosomal RNA genes of bone marrow cells. In the bone marrow, the number of basophil erythrokaryocytes increases and the number of hemoglobinized forms of red blood cells decreases. Zinc mainly causes disorders of morpho-functional structures in erythroblasts and mature cells of other bone marrow cell lines.

Blood ◽  
1996 ◽  
Vol 87 (10) ◽  
pp. 4136-4142 ◽  
Author(s):  
I Kawashima ◽  
ED Zanjani ◽  
G Almaida-Porada ◽  
AW Flake ◽  
H Zeng ◽  
...  

Using in utero transplantation into fetal sheep, we examined the capability of human bone marrow CD34+ cells fractionated based on Kit protein expression to provide long-term in vivo engraftment. Twelve hundred to 5,000 CD34+ Kit-, CD34+ Kit(low), and CD34+ Kit(high) cells were injected into a total of 14 preimmune fetal sheep recipients using the amniotic bubble technique. Six fetuses were killed in utero 1.5 months after bone marrow cell transplantation. Two fetuses receiving CD34+ Kit(low) cells showed signs of engraftment according to analysis of CD45+ cells in their bone marrow cells and karyotype studies of the colonies grown in methylcellulose culture. In contrast, two fetuses receiving CD34+ Kit(high) cells and two fetuses receiving CD34+ Kit- cells failed to show evidence of significant engraftment. Two fetuses were absorbed. A total of six fetuses receiving different cell populations were allowed to proceed to term, and the newborn sheep were serially examined for the presence of chimerism. Again, only the two sheep receiving CD34+ Kit(low) cells exhibited signs of engraftment upon serial examination. Earlier in studies of murine hematopoiesis, we have shown stage-specific changes in Kit expression by the progenitors. The studies of human cells reported here are in agreement with observations in mice, and indicate that human hematopoietic stem cells are enriched in the Kit(low) population.


2006 ◽  
Vol 291 (5) ◽  
pp. C1049-C1055 ◽  
Author(s):  
Takashi Kawasaki ◽  
Mashkoor A. Choudhry ◽  
Martin G. Schwacha ◽  
Kirby I. Bland ◽  
Irshad H. Chaudry

Traumatic and/or surgical injury as well as hemorrhage induces profound suppression of cellular immunity. Although local anesthetics have been shown to impair immune responses, it remains unclear whether lidocaine affects lymphocyte functions following trauma-hemorrhage (T-H). We hypothesized that lidocaine will potentiate the suppression of lymphocyte functions after T-H. To test this, we randomly assigned male C3H/HeN (6–8 wk) mice to sham operation or T-H. T-H was induced by midline laparotomy and ∼90 min of hemorrhagic shock (blood pressure 35 mmHg), followed by fluid resuscitation (4× shed blood volume in the form of Ringer lactate). Two hours later, the mice were killed and splenocytes and bone marrow cells were isolated. The effects of lidocaine on concanavalin A-stimulated splenocyte proliferation and cytokine production in both sham-operated and T-H mice were assessed. The effects of lidocaine on LPS-stimulated bone marrow cell proliferation and cytokine production were also assessed. The results indicate that T-H suppresses cell proliferation, Th1 cytokine production, and MAPK activation in splenocytes. In contrast, cell proliferation, cytokine production, and MAPK activation in bone marrow cells were significantly higher 2 h after T-H compared with shams. Lidocaine depressed immune responses in splenocytes; however, it had no effect in bone marrow cells in either sham or T-H mice. The enhanced immunosuppressive effects of lidocaine could contribute to the host's enhanced susceptibility to infection following T-H.


2000 ◽  
Vol 68 (6) ◽  
pp. 3455-3462 ◽  
Author(s):  
Nicola J. Rogers ◽  
Belinda S. Hall ◽  
Jacktone Obiero ◽  
Geoffrey A. T. Targett ◽  
Colin J. Sutherland

ABSTRACT With the aim of developing an appropriate in vitro model of the sequestration of developing Plasmodium falciparumsexual-stage parasites, we have investigated the cytoadherence of gametocytes to human bone marrow cells of stromal and endothelial origin. Developing stage III and IV gametocytes, but not mature stage V gametocytes, adhere to bone marrow cells in significantly higher densities than do asexual-stage parasites, although these adhesion densities are severalfold lower than those encountered in classical CD36-dependent assays of P. falciparum cytoadherence. This implies that developing gametocytes undergo a transition from high-avidity, CD36-mediated adhesion during stages I and II to a lower-avidity adhesion during stages III and IV. We show that this adhesion is CD36 independent, fixation sensitive, stimulated by tumor necrosis factor alpha, and dependent on divalent cations and serum components. These data suggest that gametocytes and asexual parasites utilize distinct sets of receptors for adhesion during development in their respective sequestered niches. To identify receptors for gametocyte-specific adhesion of infected erythrocytes to bone marrow cells, we tested a large panel of antibodies for the ability to inhibit cytoadherence. Our results implicate ICAM-1, CD49c, CD166, and CD164 as candidate bone marrow cell receptors for gametocyte adhesion.


Blood ◽  
1984 ◽  
Vol 63 (4) ◽  
pp. 784-788 ◽  
Author(s):  
VF LaRussa ◽  
F Sieber ◽  
LL Sensenbrenner ◽  
SJ Sharkis

Abstract In this article, we present evidence that sialic acid-containing surface components play a role in the regulation of erythropoiesis. A 1- hr exposure of mouse bone marrow cells to high concentrations of neuraminidase reduced erythroid colony formation. Coculture of 10(6) untreated thymocytes with neuraminidase-treated bone marrow cells restored erythroid colony growth. Neuraminidase-treated thymocytes retained their ability to suppress erythroid colony formation by untreated marrow cells, but lost their ability to enhance erythroid colony formation. Continuous exposure to low concentrations of neuraminidase enhanced erythroid bone marrow cell colony growth in response to a suboptimal dose of erythropoietin.


2019 ◽  
Vol 64 (No. 7) ◽  
pp. 317-322
Author(s):  
N Mandro ◽  
YA Kopeikin ◽  
ZA Litvinova

The use of bone marrow-derived immunostimulants is a promising direction in poultry production. The objective of this research was to study the effect of introducing a bone marrow cell protein formulation on the immunity of chickens vaccinated against salmonellosis. According to the principle of analogues, a control and two experimental groups of chickens were formed with 20 heads each (in total 60 individuals). To Group 1 birds, a protein preparation from bovine bone marrow cells was administered with feed by irrigation with 10% suspension in physiological saline at a rate of 0.2 ml per head once per day from the first day of life for three days. In Group 2, the drug was administered once, on day 1, at a rate of 0.2 ml per head. Control chickens were injected with saline in the same volumes. All chickens were vaccinated against salmonellosis. Blood for analysis of cellular, biochemical and humoral indicators was taken on days 7 and 14 of bird life. The use of the bone marrow cell-derived protein preparation resulted in higher values in the blood of chickens of Groups 1 and 2, respectively, by day 14 of age in comparison with controls as follows: erythrocytes (15.51% and 22.28%) and leukocytes (3.93% and 3.70%), T- and B- lymphocytes (67.5% and 69.16%; 23.24% and 23.75%), neutrophil phagocytic activity (10.14% and 25.36%) and phagocytic index (17.25% and 18.74%), bactericidal (13.32% and 20.25%) and lysozyme activity (23.88% and 24.41%), total protein (13.23% and 14.21%), immunoglobulins (19.59% and 20.76%), specific antibody titre (47.50% and 51.25%). Our study confirms the suitability of using bone marrow-derived protein preparations in poultry production. In practical terms, our study has particular importance for the development and implementation of preparations based on proteins of bone marrow cells.


Blood ◽  
1982 ◽  
Vol 59 (2) ◽  
pp. 408-420 ◽  
Author(s):  
G Pigoli ◽  
A Waheed ◽  
RK Shadduck

Abstract Radioiodinated L-cell-derived colony-stimulating factor (CSF) was used to characterize the binding reaction to murine bone marrow cells. The major increment in cell-associated radioactivity occurred over 24 hr incubation at 37 degrees C, but virtually no binding was observed at 4 degrees C. The reaction was saturable with approximately 1 ng/ml of purified CSF. Unlabeled CSF prevented the binding, whereas a number of other hormones and proteins did not compete for CSF uptake. Further specificity studies showed virtually no binding to human bone marrow, which is unresponsive to this form of murine CSF. Minimal CSF uptake was noted with murine peritoneal macrophages, but virtually no binding was detected with thymic, lymph node, liver, or kidney cells. The marrow cell interaction with tracer appeared to require a new protein synthesis, as the binding was prevented by cycloheximide or puromycin. Preincubation of marrow cells in medium devoid of CSF increased the degree of binding after 1 hr exposure to the tracer. This suggests that CSF binding sites may be occupied or perhaps decreased in response to ambient levels of CSF in vivo. Approximately 70% of the bound radioactivity was detected in the cytoplasm at 24 hr. This material was partially degraded as judged by a decrease in molecular weight from approximately 62,000 to 2 peaks of approximately 32,000 and approximately 49,000, but 72% of the binding activity was retained. After plateau binding was achieved, greater than 80% of the radioactivity released into the medium was degraded into biologically inactive peptides with molecular weights less than 10,000. These findings suggest that the interaction of CSF with marrow cells is characterized by binding with subsequent internalization and metabolic degradation into portions of the molecule that are devoid of biologic activity.


Blood ◽  
1990 ◽  
Vol 76 (8) ◽  
pp. 1586-1592 ◽  
Author(s):  
Y Shibata ◽  
PG McCaffrey ◽  
H Sato ◽  
Y Oghiso

Abstract Eicosanoid release during multilineage hematopoiesis was assessed using freshly isolated mouse bone marrow cells cultured in the presence of interleukin-3 (IL-3) (10% WEHI-3 culture-conditioned medium). Cells that could release prostaglandin E2 (PGE2) when stimulated with calcium ionophore A23187, but not with phorbol ester (PMA), appeared within 4 days. The cells harvested on day 10 released 42 ng of PGE2/10(6) cells/mL after A23187 stimulation. Leukotriene B4 (LTB4) (4 ng/mL) was also detected after A23187 stimulation, but there was no detectable LTC4 (less than 0.5 ng/mL). Nonadherent bone marrow cells were isolated from 28-day cultures and cloned. All clones were strongly IL-3- dependent. Although other growth factors such as granulocyte colony- stimulating factor (G-CSF), granulocyte-macrophage CSF (GM-CSF), and CSF-1 failed to promote survival or support proliferation of the cells, three clones (11–1-A6, 3–2-D5, and 11–1-A1) showed significant increases in 3H-thymidine incorporation, respectively, after PMA treatment for 24 hours. Surviving cells displayed dominantly myeloid type morphology and phenotypic characteristics. The data suggest that IL-3 is important in the formation of PGE2-producing cells. In contrast to many macrophages (MO), neither the IL-3-dependent cell lines nor the IL-3-cultured bone marrow cells released significant amounts of PGE2 when stimulated with PMA or IL-3, although PMA and IL-3 both induced translocation of protein kinase C (PKC) to the membrane fraction. The lack of production of PGE2 and other eicosanoids by the PMA- and IL-3- stimulated cell lines was confirmed by measuring the release of 3H- arachidonic acid. The data suggest that in IL-3-dependent bone marrow cell lines the activation of eicosanoid metabolism requires elevated cellular Ca2+; PKC activation alone does not appear to be a sufficient stimulus.


1976 ◽  
Vol 144 (2) ◽  
pp. 543-548 ◽  
Author(s):  
AE Silverstone ◽  
H Cantor ◽  
G Goldstein ◽  
D Baltimore

Terminal deoxynucleotidyl transferase is an enzyme which has the unique property of polymerizing polydeoxynucleotides onto a primer in the absence of a template (1,2). This enzyme is found both in the thymus and the bone marrow of birds, rodents, and humans (3-7). Whether the marrow cells that contain terminal transferase are related to thymocytes, or are on a separate pathway of differentiation, is not yet known (7,8). To determine the lineage of the murine bone marrow cells that have terminal transferase, we have investigated whether these cells have the antigen Thy-1 induced on the cells by treatment with thymopoietin (9). Thymopoietin is known to induce a set of characteristic T-cell markers including the Thy-1 alloantigen on the surface of a subpopulation of bone marrow cells committed to T-cell differentiation (prothymocytes) (10). Destruction of Thy- 1-positive cells after exposure to thymopoietin allows elimination of a substantial fraction of those bone marrow cells that can repopulate an irradiated thymus (11). We find that such an elimination after induction with the thymic polypeptide removes a substantial amount of terminal transferase from the bone marrow cell population, suggesting that at least one-half of the marrow cells bearing this enzyme are related to those found in the thymus.


2021 ◽  
Author(s):  
SHULAN SHI ◽  
HENG ZHAO ◽  
MINGBIAO MA ◽  
XIAOJUAN LI ◽  
JI XU ◽  
...  

Abstract Background: Visceral leishmaniasis related-hemophagocytic lymphohistiocytosis (VL-HLH) is a hemophagocytic syndrome caused by Leishmania infection. VL-HLH is rare, especially in nonendemic areas where the disease is severe, and mortality rates are high. The key to diagnosing VL-HLH is to find the pathogen; therefore, the Leishmania must be accurately identified for timely clinical treatment.Case presentationWe retrospectively analyzed the clinical data, laboratory examination results and bone marrow cell morphology of two children with VL-HLH diagnosed via bone marrow cell morphology between July 2017 and January 2021 at Kunming Children’s Hospital of Yunnan, China.Two cases suspected of having malignant tumors at other hospitals and who had undergone ineffective long-term treatment were transferred to Kunming Children’s Hospital. They had repeated fevers, pancytopenia, hepatosplenomegaly, hypertriglyceridemia, and hypofibrinogenemia over a long period and met the HLH-2004 standard. Their HLH genetic test results were negative, and primary HLH was excluded. Both children underwent chemotherapy as per the HLH-2004 chemotherapy regimen , but it was ineffective and accompanied by serious infections. We found Leishmania amastigotes in their bone marrow via morphological examination of their bone marrow cells, which showed hemophagocytic cells; thus, the children were diagnosed with VL-HLH. After being transferred to a specialty hospital for treatment, the condition was well-controlled. Conclusion: Morphological examination of the bone marrow cells played an important role in diagnosing VL-HLH. When clinically diagnosing secondary HLH, VL-HLH should be considered in addition to common pathogens, especially in patients for whom HLH-2004 chemotherapy regimens are ineffective. For infants and young children, bone marrow cytology examinations should be performed several times and as early as possible to find the pathogens to reduce potential misdiagnoses.


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