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.

Glucosamine Protects Rat Bone Marrow Cells Against Cisplatin-induced Genotoxicity and Cytotoxicity

2019 ◽  
Vol 19 (14) ◽  
pp. 1695-1702 ◽  
Author(s):  
Mohsen Cheki ◽  
Salman Jafari ◽  
Masoud Najafi ◽  
Aziz Mahmoudzadeh
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Micronucleus Assay ◽  
Ros Generation ◽  
Polychromatic Erythrocytes ◽  
Hematological Analysis ◽  
Antagonistic Potential ◽  
Harmful Effects ◽  
Rat Bone ◽  
Marrow Cells

Background and Objective: Glucosamine is a widely prescribed dietary supplement used in the treatment of osteoarthritis. In the present study, the chemoprotectant ability of glucosamine was evaluated against cisplatin-induced genotoxicity and cytotoxicity in rat bone marrow cells. Methods: Glucosamine was orally administrated to rats at doses of 75 and 150 mg/kg body weight for seven consecutive days. On the seventh day, the rats were treated with a single injection of cisplatin (5 mg/kg, i.p.) at 1h after the last oral administration. The cisplatin antagonistic potential of glucosamine was assessed by micronucleus assay, Reactive Oxygen Species (ROS) level analysis, hematological analysis, and flow cytometry. Results: Glucosamine administration to cisplatin-treated rats significantly decreased the frequencies of Micronucleated Polychromatic Erythrocytes (MnPCEs) and Micronucleated Normchromatic Erythrocytes (MnNCEs), and also increased PCE/(PCE+NCE) ratio in bone marrow cells. Furthermore, treatment of rats with glucosamine before cisplatin significantly inhibited apoptosis, necrosis and ROS generation in bone marrow cells, and also increased red blood cells count in peripheral blood. Conclusion: This study shows glucosamine to be a new effective chemoprotector against cisplatin-induced DNA damage and apoptosis in rat bone marrow cells. The results of this study may be helpful in reducing the harmful effects of cisplatin-based chemotherapy in the future.

Evaluation of genotoxicity of pan masala employing chromosomal aberration and micronucleus assay in bone marrow cells of the mice

2009 ◽  
Vol 25 (7) ◽  
pp. 467-471 ◽  
Author(s):  
BN Mojidra ◽  
K. Archana ◽  
AK Gautam ◽  
Y. Verma ◽  
BC Lakkad ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Chromosome Aberration ◽  
Chromosomal Aberration ◽  
Bone Marrow Cells ◽  
Micronucleus Assay ◽  
Control Group ◽  
Genotoxic Potential ◽  
Polychromatic Erythrocytes ◽  
Significant Difference ◽  
Marrow Cells

Pan masala is commonly consumed in south-east Asian and other oriental countries as an alternate of tobacco chewing and smoking. Genotoxic potential of pan masala (pan masala plain and pan masala with tobacco known as gutkha) was evaluated employing chromosome aberration (CA) and micronucleus (MN) assay in vivo. Animals were exposed to three different doses (0.5%, 1.5% and 3%) of pan masala plain (PMP) and gutkha (PMT) through feed for a period of 6 months and micronucleus and chromosomal aberrations were studied in the bone marrow cells. Induction of mean micronuclei in polychromatic erythrocytes (MNPCE) and normochromatic erythrocyte (MNNCE) was higher in both types of pan masala treated groups with respect to control group. Both pan masala plain and gutkha treatment significantly induced the frequency of MNPCE and MNNCE in the bone marrow cells, indicating the genotoxic potential. Furthermore, slight decline in the ratio of polychromatic erythrocytes to normochromatic erythrocytes was also noticed, suggesting the cytotoxic potential even though the ratio was statistically non significant. A dose-dependent, significant increase in chromosome aberration was observed in both types of pan masala treated mice with respect to control. However, no significant difference in micronucleus and chromosomal aberration induction was noticed between two types of pan masala exposed (PMP and PMT) groups. Results suggest that both types of pan masala, i.e. plain and gutkha, have genotoxic potential.

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

scholarly journals Antimutagenic and Antiapoptotic Effects of Aqueous Root Extract of Inula racemosa Hook. f. on 4-NQO-Induced Genetic Damage in Mice

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
P. Arumugam ◽  
M. Murugan
Keyword(s):  
Bone Marrow ◽  
Dna Damage ◽  
Bone Marrow Cells ◽  
Annexin V ◽  
Root Extract ◽  
Protective Effects ◽  
Inula Racemosa ◽  
Polychromatic Erythrocytes ◽  
Aqueous Root Extract ◽  
Marrow Cells

The present study was performed as part of an attempt to authenticate the use of Inula racemosa root extract as traditional medicine in India by experimentally investigating their protective effects on 4-nitroquinoline-1-oxide (4-NQO) induced DNA damage and apoptosis in mice bone marrow cells. Aqueous root extract (ARE) of Inula racemosa (100, 200 and 400 mg/kg bw) with and without 4-NQO along with vehicle control (H2O) were administered orally for five consecutive days. 4-NQO (7.5 mg/kg bw) was injected intraperitoneally to the mice on the sixth day. After 24 h, the animals were sacrificed and extracted bone marrow cells were used for micronuclei and apoptotic analysis. Antiapoptotic effect of ARE (400 mg/kg bw) was measured by the use of Annexin V-FITC assay kit. 4-NQO generated the frequency of micronucleated polychromatic erythrocytes (MnPCEs) by about 4.7 times the control value, 14.29 MnPCEs/2500 PCEs. Pretreatment with ARE significantly reduced the MnPCEs frequency (39–72%) with respect to their doses, and increased PCEs/NCEs ratio was observed over the 4-NQO alone. 4-NQO-induced total apoptotic cells were about 12% over the control which was significantly brought down to 3.5% by pretreatment with 400 mg/kg bw of ARE. This was the first report that recorded the protective effects of I. racemosa on 4-NQO-induced DNA damage and apoptosis in mice bone 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 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
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