Cytogenetic Toxicity of Cisplatin in Bone Marrow Cells of Swiss Mice

Choudhury, Ramesh C.; Jagdale, M.B.; Misra, Sunil

doi:10.1179/joc.2000.12.2.173

Cited by 31 publications

(10 citation statements)

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“…In chromosomal aberration measurements, chromatid and isochromatid breaks were present more frequently, however gaps and complex exchanges were also observed. This evidence was supported by the previous studies, in which rat and mouse bone marrow cells were used (Edelweiss et al, 1995;Choudhury et al, 2000;Sendao et al, 2006). Gulkac et al (2004) have found that antineoplastic, doxorubicin produced an increased frequency of cells with chromosomal aberrations.…”

Section: Discussionsupporting

confidence: 76%

“…It has been reported that cisplatin has a prominent clastogenity effect on the bone marrow cells from Wistar rats (Edelweiss et al, 1995). In a previous study, Choudhury et al (2000) found that single dose of cisplatin (5 mg/kg) led to an increase in the number of mitotic metaphase chromosomal aberrations and they have also concluded that the mitotic index did not change at 24 hours, which suggests that it is non-mitotoxic at given dose. Likewise, Mora et al (2002) have reported that single dose of cisplatin produced an increased frequency of cells with chromosomal aberrations and abnormal metaphases observed at 24th hour.…”

Section: Discussionmentioning

confidence: 95%

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Anticlastogenic effect of caffeic acid phenethyl ester on cisplatin-induced chromosome aberrations in rat bone marrow cells

Yılmaz

Altunbaşak

et al. 2009

Toxicol Ind Health

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Caffeic acid phenethyl ester (CAPE) is an antioxidant that can scavenge free radicals and protect cellular macromolecules, including DNA and proteins, from oxidative damage induced by various agents. The protective effect of CAPE on cisplatin-induced chromosome aberrations has been determined in rat bone marrow cells. The animals were pretreated with a single dose of CAPE (10 micromol/kg body weight [b.w.]) injected intraperitoneally (i.p.) 24 hours before the administration of cisplatin and then sacrificed 24 hours after the cisplatin administration. Cisplatin was administered to rats either alone (5 mg/kg b.w., i.p.) or after CAPE treatment. CAPE has led to a statistically significant decrease in the total number of chromosomal aberrations and abnormal metaphases induced by cisplatin when compared with only cisplatin given groups. We have concluded that CAPE could prevent cisplatin-induced chromosome aberrations by establishing a potent free radical scavenger effect.

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Section: Discussionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 95%

Anticlastogenic effect of caffeic acid phenethyl ester on cisplatin-induced chromosome aberrations in rat bone marrow cells

Yılmaz

Altunbaşak

et al. 2009

Toxicol Ind Health

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“…Antitumor platinum drugs induced intra-and interstrand cross-linking effects, chromosomal aberrations, SCE, and increased MN frequencies in a number of experimental systems in vitro and in vivo as well as in human cells [13,[31][32][33][34][35][36]. In addition, the activation of apoptotic cell death was described as a key defense mechanism by cisplatin to remove cells with severe DNA damage [26][27][28].…”

Section: Discussionmentioning

confidence: 99%

Genotoxic Action of Cycloplatam, a New Platinum Antitumor Drug, on Mammalian Cells in vivo and in vitro

Nersesyan¹,

Perrone

Roggieri

et al. 2003

Chemotherapy

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Cycloplatam (CP), a new antitumor platinum compound of the second generation, was first synthesized in Russia. This drug shows less toxicity in vivo than the widely used cisplatin and carboplatin and a higher antitumor activity than carboplatin. CP is not nephrotoxic with respect to the platinum-based antitumor agents. CP is actually studied in clinical phase II trials in Russia and Armenia. Promising results were obtained in patients with lung, ovary, and prostate cancers. The aim of this work was to study the micronuclei (MN) inducing effect of CP in vivo in murine bone marrow cells and in human lymphocytes in vitro. The mutagenic activity of CP in bone marrow of mice was significantly lower than that of cisplatin at equitoxic doses. In human lymphocytes CP induced a dose-dependent increase of MN, beginning at a very low dose (0.1 µM). Our results showed that CP is much less toxic and MN inducing in vivo in murine bone marrow than cisplatin. In vitro data evidenced that CP is more toxic and genotoxic to human cells than cisplatin. The evidence of a MN-induced activity of an antitumor drug suggests a potential risk for long-time survivors.

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“…Interestingly, several studies have clearly shown the deleterious effect of cytotoxic chemotherapy on protein synthesis and DNA replication resulting in diminished bone formation, but the precise mechanism has not been studied yet. 3 Therefore, in this study, we evaluated the effect of cisplatin on the survival of osteoblasts and applied the proteomics technology for identifying protein(s) involved in the action of cisplatin in osteoblasts.…”

mentioning

confidence: 99%

Up-regulation of Nucleophosmin 1 in Cisplatin-induced Death of Mouse Osteoblastic MC3T3-E1 Cells

Kim¹,

Lee²,

Min³

et al. 2008

Bulletin of the Korean Chemical Society

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Cisplatin (cis-diamminedichloroplatinum II, Fig. 1A) is one of the most used chemotherapeutic agents in the management of malignant bone and soft tissue tumors, but its treatment can show the impairment of bone formation. Actually, during the administration of cisplatin, its effect has been reported to be targeted directly on the proliferation and differentiation of bone-forming cells.1 In addition, in the study to elucidate the effect of cisplatin on regenerate bone formation during the distraction and consolidation phases of bone transport osteogenesis, cisplatin-treated dogs had decreased mineralized bone volume, decreased percentage of woven bone volume, decreased percentage of osteoblastcovered bone and increased porosity, suggesting that bone formation and resorption may be uncoupled in cisplatintreated regenerate bone. 2Throughout adult life, bone tissue is subject to a continuous process of turnover, whereby old bone is removed and replaced by new bone by the coupled processes of bone resorption and bone formation. Osteoblasts are the bone lining cells responsible for the production of the matrix constituents such as a collagen and originate from a bone marrow stromal stem cells under the influence of local growth factors. These precursors undergo proliferation and differentiate into preosteoblasts and then into mature osteoblasts. Interestingly, several studies have clearly shown the deleterious effect of cytotoxic chemotherapy on protein synthesis and DNA replication resulting in diminished bone formation, but the precise mechanism has not been studied yet.3 Therefore, in this study, we evaluated the effect of cisplatin on the survival of osteoblasts and applied the proteomics technology for identifying protein(s) involved in the action of cisplatin in osteoblasts.First, the effect of cisplatin on the proliferation of MC3T3-E1 cells was evaluated (Fig. 1B). In a dose-dependent manner, the proliferation of MC3T3-E1 cells was significantly inhibited ~90% and ~54% in 1-day and 4-day culture by the treatment of 100 μM cisplatin, respectively. Since 100 μM of cisplatin significantly inhibited the proliferation of MC3T3-E1 cells in 1-day culture, cells incubated with/ without 100 μM cisplatin for 1 day were used for identifying the differentially expressed protein(s). Using Phoretix 2D image analysis software, the altered spots were compared based on their volume percentages in the total spot volume over the whole gel images. Of over 500 protein spots resolved in a 2-DE gel with silver staining analyzed, 18 spots was above 2-fold increased, whereas 35 spots decreased in cisplatin-treated cells (data not shown). Among these spots, the circle-indicated spot in Figure 2A was increased 2.63-fold in cisplatin-treated cells compared to control. The circle-indicated spot was digested in gel with trypsin and subjected to peptide mass fingerprinting (PMF). The representative MALDI-TOF MS spectrum for the spot was shown in Figure 2B. According to the PMF, the estimated pI and molecular weight (MW) by the 2-DE map, the...

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Cytogenetic Toxicity of Cisplatin in Bone Marrow Cells of Swiss Mice

Cited by 31 publications

References 58 publications

Anticlastogenic effect of caffeic acid phenethyl ester on cisplatin-induced chromosome aberrations in rat bone marrow cells

Anticlastogenic effect of caffeic acid phenethyl ester on cisplatin-induced chromosome aberrations in rat bone marrow cells

Genotoxic Action of Cycloplatam, a New Platinum Antitumor Drug, on Mammalian Cells in vivo and in vitro

Up-regulation of Nucleophosmin 1 in Cisplatin-induced Death of Mouse Osteoblastic MC3T3-E1 Cells

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