Vinblastine treatment induces dose-dependent increases in the frequency of micronuclei in mouse bone marrow

Jagetia, Ganesh Chandra; Jacob, Preenu Sunil

doi:10.1016/0165-1218(92)90003-i

Cited by 33 publications

(4 citation statements)

References 18 publications

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“…In the present study, the statistically significant (p ≤ 0.01) induction of MN per thousand PCEs with its dose-dependent increase (table 3) is in agreement with earlier reports [53, 54]. In comparison to the size of MNs induced by CTX, in the VBL-treated groups of mice a good number of MN were very large in size.…”

Section: Discussionsupporting

confidence: 81%

“…The MI study 24 h after treatment with VBL, however, did not show any significant difference in the percentage of dividing cells from that of the vehicle control group of mice (table 2). This observation gains support from earlier reports on the dose-dependent decline in the MI and anaphases in the bone marrow of mice treated with vincristine [42, 52]and VBL [53]. Besides, there are earlier reports on the dose-dependent delay in the cell cycle and the prolongation of S-phase after VBL treatment [19, 39].…”

Section: Discussionsupporting

confidence: 75%

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Cytogenetic Consequences of Vinblastine Treatment in Mouse Bone Marrow

Choudhury¹,

Palo²,

Padhy³

2004

Chemotherapy

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Background: Vinblastine (VBL), a vinca alkaloid, has very often been included in different cancer chemotherapeutic treatment regimens. Chemotherapy cures certain cancers and, at least, increases the life expectancy of cancer patients. However, in cancer survivors, a second malignancy frequently occurs after chemotherapy, which warrants detailed genotoxicity testing of the chemotherapeutic agents. The available genotoxicity test reports on VBL are self-contradictory and inconclusive. Thus, following a suitable experimental protocol, it is necessary to test the cytogenetic consequences of VBL treatment in mammals. Methods: Swiss mice received 1 of 3 different doses of VBL (0.5, 1.0 and 1.5 mg/kg body weight) as a single intraperitoneal injection. The cytogenetic toxicity of VBL was assessed from the induced aberrant metaphases, chromosomal aberrations (CAs) excluding gaps and the mitotic index (MI) 24 h after treatment, and micronuclei (MN) 30 h after treatment. Results: All 3 doses of VBL induced statistically significant (p ≤ 0.01) percentages of aberrant metaphases and CAs, but there was no significant change in the MI. The induced percentage of aberrant metaphases and CAs were decreased with the increase in the dose of VBL. On the other hand, there was a dose-dependent and significant (p ≤ 0.01) increase in MN induction. Conclusions: The results of this study indicate the clastogenic potential of VBL in the mouse bone marrow. In the present study, the induction of numerous relatively large-sized MN by VBL is in agreement with the reported aneugenic action of the drug. Although VBL is cytotoxic and is a spindle poison, the mechanism(s) involved in bringing about its clastogenic effects is yet to be elucidated.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionsupporting

confidence: 75%

Cytogenetic Consequences of Vinblastine Treatment in Mouse Bone Marrow

Choudhury¹,

Palo²,

Padhy³

2004

Chemotherapy

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“…33 Vinblastine has been reported to induce clastogenic effect by producing micronuclei in the bone marrow cells of mice. 34 Likewise, other antimitotic agent taxol also increased the micronuclei in V79 cells. 30 The micronuclei formation was consistently detected in mononucleate cells in both the Naringin and Naringin + Vinblastine groups.…”

Section: Discussionmentioning

confidence: 95%

Grapefruit flavonoid naringin protects v79 cells against the vinblastine-induced DNA damage in vitr

Jagetia

2023

MOJAP

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Vinblastine an antimitotic agent is used to treat hematological malignancies and in combination cancer chemotherapy. Vinblastine produces second malignancies in the survivors which can be reduced/prevented in cancer patients by intervention with natural products. Naringin a grapefruit bioflavonoid was tested for its chemoprotective activity in cultured V79 cells. The V79 cells were treated with 1, 2, 5, 10, 25, 50, 100, and 200 µg/mL of naringin 1 h before exposure to 10 µg/mL of vinblastine. The DNA damage was evaluated by micronucleus assay at 22 h after vinblastine exposure in mononucleate, binucleate, and trinucleate cells. Vinblastine treatment increased the frequency of micronuclei significantly in both the mononucleate and binucleate V79 cells whereas different concentrations of naringin significantly reduced the formation of vinblastine-induced micronuclei. A maximum reduction in micronuclei formation was recorded at 200 µg/mL naringin in both mononucleate and binucleate cells. The determination of cell proliferation indicates that naringin treatment impacted the cell proliferation, especially at 2 to 25 µg/mL which increased at 200 µg/mL in both the naringin and Naringin+Vinblastine groupsgroup as indicated by a rise in binucleate and trinucleate cell numbers. The present study indicates that naringin protects the V79 cells against vinblastine-induced DNA damage indicated by significant attrition in micronuclei formation and 200 µg/mL naringin was highly effective.

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“…Anemia, infection, and a variety of other illnesses can all be diagnosed with complete blood picture. 8 , 9 In medicine, there is a lack of understanding of hematological indices and the changes caused by various gamma-radiation dosages.…”

Section: Introductionmentioning

confidence: 99%

Beneficial Effect of Rosuvastatin Therapy on Spleen Injury Induced by Gamma Irradiation in Rats: Targeting Nrf2/EPRE Pathway

et al. 2023

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Purpose The present study investigates the new approach of rosuvastatin (RUV) administration as a drug for the management of spleen injury induced by gamma irradiation. Main Methods Forty rats were used and divided equally into 4 groups: control group, irradiated group, IRR + rosuvastatin group (10 mg/Kg b. wt), and IRR + rosuvastatin group (20 mg/kg b. wt) for 7 days orally. Results The possible curative effect can be illustrated via the improvement of hematopoietic cell count (Hb, RBCs, and WBCs) and oxidative stress markers (MDA and GST) in addition to biochemical parameters including [heme oxigenase-1 (HO-1), nuclear erythroid 2-related factor (Nrf2), NOD-, LRR- and pyrin domain- containing protein 3 (NLRP3) inflammasome] and immune assay of nuclear factor kappa beta (NF-kB P65) and inducible nitric oxide synthase (iNOS). Histological pictures emphasize the biochemical findings. Rosuvastatin treatments by using two different doses improve the tested parameters. High-dose administration of RUV (20 mg/kg p.o.) recorded better results than the low dose (10 mg/kg p.o.). Conclusion Our results suggested that rosuvastatin reversed the radiation-induced spleen-damaging effects. So, RUV can be introduced to the market as a new therapy for the management of spleen damages.

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Vinblastine treatment induces dose-dependent increases in the frequency of micronuclei in mouse bone marrow

Cited by 33 publications

References 18 publications

Cytogenetic Consequences of Vinblastine Treatment in Mouse Bone Marrow

Cytogenetic Consequences of Vinblastine Treatment in Mouse Bone Marrow

Grapefruit flavonoid naringin protects v79 cells against the vinblastine-induced DNA damage in vitr

Beneficial Effect of Rosuvastatin Therapy on Spleen Injury Induced by Gamma Irradiation in Rats: Targeting Nrf2/EPRE Pathway

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