Clastogenic effects of cis-diamminedichloroplatinum II. Induction of chromosomal aberrations in primary spermatocytes and spermatogonial stem cells of mice

Adler, I.‐D.; Tarras, A. El

doi:10.1016/0165-7992(90)90087-z

Cited by 29 publications

(20 citation statements)

References 14 publications

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“…Bone marrow cells are susceptible to oxidative damage and sensitive to clastogenic chemicals so, it has been commonly used for screening of mutagenicity and/or antimutagenicity property of chemicals (Umegaki et al, 1997). The results of present investigation showed development of these mutagenic parameters after cisplatin alone or combination treatment of tumor-bearing mice and supports the earlier findings of its genotoxic properties (Adler and El-Tarras, 1989;Brozovic et al, 2011). The chromosomal aberration pattern revealed that chromatid breaks and fragments occurred more frequently after cisplatin treatment (Fig.…”

Section: Discussionsupporting

confidence: 78%

“…The clastogenicity of cisplatin in humans and experimental animals has been well documented. Cisplatin induces formation of micronuclei in bone marrow cells and chromosomal aberrations in the germinal cells of mice (Kliesch and Adler, 1987;Adler and El-Tarras, 1989) and also the micronuclei in peripheral blood lymphocytes of testicular patients with various types of cancers (Osanto et al, 1991;Elsendoorn et al, 2001). It is imperative to reduce the drug-induced genotoxicity, a goal that have been tried experimentally by administration of free radical scavengers such as antioxidants (Antunes et al, 1999(Antunes et al, , 2000aAttia, 2010;Dos Santos et al, 2012) with varying degree of success.…”

Section: Introductionmentioning

confidence: 99%

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Ascorbic Acid (Vitamin C)-Mediated Protection on Mutagenic Potentials of Cisplatin in Mice Bearing Ascites Dalton ’s Lymphoma

Amenla¹,

Prasad²

2016

Research J. of Mutagenesis

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Cisplatin is a potent anticancer drug which has been in use against a variety of cancers for a long time. The present study was carried out to assess the protective ability of ascorbic acid on cisplatin-induced mutagenic effects in tumor-bearing mice. The increase in the frequency of chromosomal aberrations, micronuclei and sperm abnormality were studied as markers of mutagenicity. Indicators of oxidative stress relatives like lipid peroxidation, reduced glutathione and the activities of enzymes such as catalase, glutathione-S-transferase and glutathione reductase were also studied to understand the possible mechanism(s) underlying this amelioration. Pre-treatment with ascorbic acid in combination group significantly reduced cisplatin-induced mutagenicity, markedly decreased lipid peroxidation along with increased level of glutathione and activities of antioxidant enzymes particularly in the liver of mice. The overall studies suggest that ascorbic acid with its antioxidant and free radical scavenging properties may play a part in its protective role in the abatement of cisplatin-induced mutagenesis and oxidative damage in the normal tissues of mice.

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Section: Discussionsupporting

confidence: 78%

Section: Introductionmentioning

confidence: 99%

Ascorbic Acid (Vitamin C)-Mediated Protection on Mutagenic Potentials of Cisplatin in Mice Bearing Ascites Dalton ’s Lymphoma

Amenla¹,

Prasad²

2016

Research J. of Mutagenesis

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“…Kliesch and Adler (1987) observed an increase in the number of polychromatic erythrocytes with micronuclei in the bone marrow cells of mice treated with DDP. Chromosomal aberrations were also observed in bone marrow cells and differentiating spermatogonia of mice treated with 2.5 mg of DDP/kg bw (Adler and El-Tarras, 1989).…”

Section: Resultsmentioning

confidence: 86%

“…However, the use of DDP is limited because of its toxicity to normal tissues (Rosenberg, 1985). DDP is highty mutagenic, causing sister-chromatid exchange and chromosomal aberrations in cultured mammalian cells, mouse bone marrow cells, and peripheral blood lymphocytes of patients (Kliesch and Adler, 1987;Adler and El-Tarras, 1989;Ohe et al, 1990;Osanto et al, 1991;Krishnaswamy and Dewey, 1993). The generation of free radicals is believed to be an important mechanism in the development of DDP toxicity (Masuda et al, 1994;Baliga et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Anticlastogenic effect of vitamin C on cisplatin in vivo

1999

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The ability of vitamin C (VC) to protect against the clastogenic action of the chemotherapeutic agent cisplatin (DDP, cis-diamminedichloroplatinun II) in rat bone marrow cells was evaluated. DDP was administered to Wistar rats either alone or after treatment with VC. The rats were treated with VC (50, 100 or 200 mg/kg body weight) by gavage 10 min before the administration of DDP (5 mg/kg body weight, ip) and then sacrificed 24 h after treatment. VC significantly reduced (by about 70%) the clastogenicity of DDP in rat bone marrow cells. The antioxidant action of VC presumably modulates the clastogenic action of DDP.
Neste estudo foi avaliado o efeito protetor da vitamina C (VC) sobre a ação clastogênica da cisplatina (DDP) em células da medula óssea de ratos. A DDP, um agente quimioterápico, foi injetada em ratos Wistar sozinha ou após o tratamento com a VC. Os animais foram tratados com VC (50, 100 or 200 mg/kg de peso corporal) por gavagem 10 min antes da administração intraperitoneal de DDP (5 mg/kg de peso corporal). Os resultados obtidos mostraram que a VC foi efetiva na redução estatisticamente significativa da clastogenicidade da DDP em ratos Wistar (aproximadamente 70%). O efeito antioxidante da VC foi proposto para explicar a modulação da ação clastogênica da DDP

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“…It has been reported that preleptotene͞leptotene spermatocytes are much more sensitive to CP-induced chromosome aberrations than are spermatocytes at the zygotene or pachytene stages (ref. 27; preleptotene spermatocytes require about 4 days to progress to pachynema), but it is not clear that these clastogenic events are the same that would stimulate crossing-over. Recent evidence from mice suggests that by the early to midpachytene stage, events have progressed to a point where they can be resolved rapidly into chiasmata (28).…”

Section: Resultsmentioning

confidence: 99%

Cisplatin increases meiotic crossing-over in mice

Hanneman

Legare²,

Sweeney³

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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Genetic mapping of traits and mutations in mammals is dependent upon linkage analysis. The resolution achieved by this method is related to the number of offspring that can be scored and position of crossovers near a gene. Higher precision mapping is obtained by expanding the collection of progeny from an appropriate cross, which in turn increases the number of potentially informative recombinants. A more efficient approach would be to increase the frequency of recombination, rather than the number of progeny. The anticancer drug cisplatin, which causes DNA strand breakage and is highly recombinogenic in some model organisms, was tested for its ability to induce germ-line recombination in mice. Males were exposed to cisplatin and mated at various times thereafter to monitor the number of crossovers inherited by offspring. We observed a striking increase on all three chromosomes examined and established a regimen that nearly doubled crossover frequency. The timing of the response indicated that the crossovers were induced at the early pachytene stage of meiosis I. The ability to increase recombination should facilitate genetic mapping and positional cloning in mice.

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Clastogenic effects of cis-diamminedichloroplatinum II. Induction of chromosomal aberrations in primary spermatocytes and spermatogonial stem cells of mice

Cited by 29 publications

References 14 publications

Ascorbic Acid (Vitamin C)-Mediated Protection on Mutagenic Potentials of Cisplatin in Mice Bearing Ascites Dalton ’s Lymphoma

Ascorbic Acid (Vitamin C)-Mediated Protection on Mutagenic Potentials of Cisplatin in Mice Bearing Ascites Dalton ’s Lymphoma

Anticlastogenic effect of vitamin C on cisplatin in vivo

Cisplatin increases meiotic crossing-over in mice

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