scholarly journals Deferasirox reduces oxidative DNA damage in bone marrow cells from myelodysplastic patients and improves their differentiation capacity

2019 ◽  
Vol 187 (1) ◽  
pp. 93-104 ◽  
Author(s):  
Tamara Jiménez‐Solas ◽  
Félix López‐Cadenas ◽  
Irene Aires‐Mejía ◽  
Juan Carlos Caballero‐Berrocal ◽  
Rebeca Ortega ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Bone Marrow Cells ◽  
Differentiation Capacity ◽  
Marrow Cells

Oxidative DNA damage in bone marrow cells of patients with low-risk myelodysplastic syndrome

2009 ◽  
Vol 33 (2) ◽  
pp. 340-343 ◽  
Author(s):  
Bozena Novotna ◽  
Yana Bagryantseva ◽  
Magda Siskova ◽  
Radana Neuwirtova
Keyword(s):  
Bone Marrow ◽  
Dna Damage ◽  
Myelodysplastic Syndrome ◽  
Oxidative Dna Damage ◽  
Bone Marrow Cells ◽  
Low Risk ◽  
Marrow Cells

scholarly journals The effect of quercetin on oxidative DNA damage and myelosuppression induced by etoposide in bone marrow cells of rats.

2014 ◽  
Vol 61 (1) ◽  
Author(s):  
Monika A Papież
Keyword(s):  
Bone Marrow ◽  
Dna Damage ◽  
Cell Line ◽  
Myeloid Leukemia ◽  
Oxidative Dna Damage ◽  
Bone Marrow Cells ◽  
Common Side Effect ◽  
Marrow Cells

There is increasing evidence for the existence of an association between the presence of etoposide phenoxyl radicals and the development of treatment-related acute myeloid leukemia (t-AML), which occurs in a few percent of patients treated with this chemotherapeutic agent. The most common side effect caused by etoposide is myelosuppression, which limits the use of this effective drug. The goal of the study was to investigate the influence of antioxidant querectin on myelosuppression and oxidative DNA damage caused by etoposide. The influence of quercetin and/or etoposide on oxidative DNA damage was investigated in LT-12 cell line and bone marrow cells of rats via comet assay. The effect of quercetin on myelosuppression induced by etoposide was invetsigated by cytological analysis of bone marrow smears stained with May-Grünwald-Giemsa stain. Etoposide caused a significant increase in oxidative DNA damage in bone marrow cells and LT-12 cell line in comparison to the appropriate controls. Quercetin significantly reduced the oxidative DNA damage caused by etoposide both in vitro and in vivo. Quercetin also significantly protected against a decrease in the percentage of myeloid precursors and erythroid nucleated cells caused by etoposide administration in comparison to the group treated with etoposide alone. The results of the study indicate that quercetin could be considered a protectively acting compound in bone marrow cells during etoposide therapy.

scholarly journals The Mitigating Effect ofCitrullus colocynthis(L.) Fruit Extract against Genotoxicity Induced by Cyclophosphamide in Mice Bone Marrow Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Mohammad Shokrzadeh ◽  
Aroona Chabra ◽  
Farshad Naghshvar ◽  
Amirhossein Ahmadi
Keyword(s):  
Bone Marrow ◽  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Bone Marrow Cells ◽  
Micronucleus Assay ◽  
Fruit Extract ◽  
Polychromatic Erythrocytes ◽  
Marked Proliferation ◽  
Different Doses ◽  
Marrow Cells

Possible genoprotective effect ofCitrullus colocynthis(L.) (CCT) fruits extract against cyclophosphamide- (CP-)induced DNA damage in mice bone marrow cells was evaluated using micronucleus assay, as an index of induced chromosomal damage. Mice were preadministered with different doses of CCT via intraperitoneal injection for 7 consecutive days followed by injection with CP (70 mg/kg b.w.) 1 hr after the last injection of CCT. After 24 hr, mice were scarified to evaluate the frequency of micronucleated polychromatic erythrocytes (MnPCEs). In addition, the number of polychromatic erythrocytes (PCEs) among 1000 normochromatic erythrocytes (NCEs) per animal was recorded to evaluate bone marrow. Pretreatment with CCT significantly reduced the number of MnPCEs induced by CP in bone marrow cells (P<0.0001). At 200 mg/kg, CCT had a maximum chemoprotective effect and reduced the number of MnPCEs by 6.37-fold and completely normalized the mitotic activity. CCT also led to marked proliferation and hypercellularity of immature myeloid elements after mice were treated with CP and mitigated the bone marrow suppression. Our study revealed that CCT has an antigenotoxic effect against CP-induced oxidative DNA damage in mice. Therefore, it could be used concomitantly as a supplement to protect people undergoing chemotherapy.

scholarly journals Friend Leukemia Virus Infection Enhances DNA Damage-Induced Apoptosis of Hematopoietic Cells, Causing Lethal Anemia in C3H Hosts

2002 ◽  
Vol 76 (15) ◽  
pp. 7790-7798 ◽  
Author(s):  
Masanobu Kitagawa ◽  
Shuichi Yamaguchi ◽  
Maki Hasegawa ◽  
Kaoru Tanaka ◽  
Toshihiko Sado ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dna Damage ◽  
Knockout Mice ◽  
Bone Marrow Cells ◽  
Leukemia Virus ◽  
Hematopoietic Cells ◽  
Friend Leukemia ◽  
C3h Mice ◽  
Friend Leukemia Virus ◽  
Marrow Cells

ABSTRACT Exposure of hematopoietic progenitors to gamma irradiation induces p53-dependent apoptosis. However, host responses to DNA damage are not uniform and can be modified by various factors. Here, we report that a split low-dose total-body irradiation (TBI) (1.5 Gy twice) to the host causes prominent apoptosis in bone marrow cells of Friend leukemia virus (FLV)-infected C3H mice but not in those of FLV-infected DBA mice. In C3H mice, the apoptosis occurs rapidly and progressively in erythroid cells, leading to lethal host anemia, although treatment with FLV alone or TBI alone induced minimal apoptosis in bone marrow cells. A marked accumulation of P53 protein was demonstrated in bone marrow cells from FLV-infected C3H mice 12 h after treatment with TBI. Although a similar accumulation of P53 was also observed in bone marrow cells from FLV-infected DBA mice treated with TBI, the amount appeared to be parallel to that of mice treated with TBI alone and was much lower than that of FLV- plus TBI-treated C3H mice. To determine the association of p53 with the prominent enhancement of apoptosis in FLV- plus TBI-treated C3H mice, p53 knockout mice of the C3H background (C3H p53−/− ) were infected with FLV and treated with TBI. As expected, p53 knockout mice exhibited a very low frequency of apoptosis in the bone marrow after treatment with FLV plus TBI. Further, C3H p53−/− → C3H p53+/+ bone marrow chimeric mice treated with FLV plus TBI survived even longer than the chimeras treated with FLV alone. These findings indicate that infection with FLV strongly enhances radiation-induced apoptotic cell death of hematopoietic cells in host animals and that the apoptosis occurs through a p53-associated signaling pathway, although the response was not uniform in different host strains.

An oxovanadium(IV) complex protects murine bone marrow cells against cisplatin-induced myelotoxicity and DNA damage

2016 ◽  
Vol 40 (3) ◽  
pp. 359-367 ◽  
Author(s):  
Abhishek Basu ◽  
Arin Bhattacharjee ◽  
Amalesh Samanta ◽  
Sudin Bhattacharya
Keyword(s):  
Bone Marrow ◽  
Dna Damage ◽  
Bone Marrow Cells ◽  
Murine Bone Marrow ◽  
Marrow Cells

Novel Markers for the Isolation of Primary Bone Marrow Derived MSC with Multi-Lineage Differentiation Capacity.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 2573-2573 ◽  
Author(s):  
Hans-Jorg Buhring ◽  
Venkata L. Battula ◽  
Sabrina Treml ◽  
Lothar Kanz ◽  
Wichard Vogel
Keyword(s):  
Bone Marrow ◽  
Stem Cell ◽  
Bone Marrow Cells ◽  
Embryonic Stem ◽  
Stem Cell Marker ◽  
Color Flow ◽  
Differentiation Capacity ◽  
Lineage Differentiation ◽  
Isolation And Characterization ◽  
Marrow Cells

Abstract We have previously described a novel culture protocol to grow MSC from bone marrow (BM) and non-amniotic placenta (PL) with an immature phenotype and multi-lineage differentiation capacity (1). Using the low affinity nerve growth factor receptor (CD271) (2) as a key marker for isolation of MSC derived from femur shaft bone marrow cells (BM-MSC) of patients undergoing a total hip replacement, we could identify two CD271+ distinct populations: CD271dull and CD271bright cells. Two-color flow cytometer analysis revealed that only the CD271bright population coexpressed the mesenchymal markers CD10, CD13, CD73, and CD105, but was negative for CD45. CD271dull cells were positive for CD45 and HLA-DR but negative for the other markers. To analyze the mesenchymal stem cell potential, colony-forming-unit fibroblast (CFU-F) assays were performed. Not surprisingly, the CFU-F were exclusively detected in the CD271bright but not in the CD271dull fraction. By screening a battery of antibodies against known and unknown antigens, we identified several reagents that selectively detected the CD271brightCD45- population but no other bone marrow cells. These markers included the PDGF-RB (CD140b), the embryonic stem cell marker TRA-1-49, the clustered markers HER-2/erbB2 (CD340), the recently described W8B2 antigen (3), as well as the cell surface antigens defined by the antibodies W1C3, W3D5, W4A5, W5C4, W5C5, W7C6, 9A3, 58B1, F9-3C2F1, and HEK-3D6. In conclusion we identified several novel markers for the prospective isolation and characterization of BM-MSC.

Prolonged Quercetin Administration Diminishes the Etoposide-Induced DNA Damage in Bone Marrow Cells of Rats

2007 ◽  
Vol 30 (1) ◽  
pp. 67-81 ◽  
Author(s):  
Maria Kapiszewska ◽  
Agnieszka Cierniak ◽  
Monika A. Papiez ◽  
Agata Pietrzycka ◽  
Marek Stepniewski ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dna Damage ◽  
Bone Marrow Cells ◽  
Marrow Cells

Pendimethalin induces oxidative stress, DNA damage, and mitochondrial dysfunction to trigger apoptosis in human lymphocytes and rat bone-marrow cells

2017 ◽  
Vol 149 (2) ◽  
pp. 127-141 ◽  
Author(s):  
Sabiha M. Ansari ◽  
Quaiser Saquib ◽  
Sabry M. Attia ◽  
Eslam M. Abdel-Salam ◽  
Hend A. Alwathnani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bone Marrow ◽  
Dna Damage ◽  
Mitochondrial Dysfunction ◽  
Bone Marrow Cells ◽  
Human Lymphocytes ◽  
Rat Bone ◽  
Marrow Cells
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