Induction and elimination of cytogenetic disturbances in lymphocytes of monkeys exposed to thiophosphamide

Kuzin, S. M.; Stukalov, S. V.; Викторов, В. В.; Dshemilev, A. A.; Popandopulo, P. G.

doi:10.1007/bf00840764

Cited by 2 publications

(1 citation statement)

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“…The decrease in the number of SCE during the second mitosis with prolongation of the interval between exposure and fixation suggests that repair is possible without DNA replication. From our results it can be concluded that decreased SCE level in lymphocytes after exposure to mutagens [2,3,6] is due predominantly to substitution of lymphocytes by cells formed in hemopoietic tissue after exposure. Our data provide no unambiguous answer about the mechanisms and intensity of nonreplicative repair of injuries inducing SCE in blood lymphocytes.…”

Section: Resultsmentioning

confidence: 80%

Relationship between the duration and number of cell cycles after mutagenic exposure and the incidence of sister chromatid exchanges

Kuzin

Stukalov

1998

Bull Exp Biol Med

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The incidence of sister chromatid exchanges during the second and third mitoses in Jungar hamster bone marrow cells and human lymphocytes is assessed at different times after mutagenic exposure to thiophosphamide. In the control, the mean number of sister chromatid exchanges in bone marrow cells did not change during three consecutive cycles irrespective of the rate of cell proliferation. Thiophosphamide exposure resulted in replicative or nonreplicative repair of injuries inducing sister chromatid exchanges. About 50-70% of injuries are eliminated during a replicative (mitotic) cycle. Nonreplicative repair is intensive in proliferating bone marrow cells and weakly expressed in blood lymphocytes. Key Words: sister chromatid exchanges; lymphocytes; bone marrow cells; thiophosphamideSister chromatid exchanges (SCE) are formed during DNA replication as realization of primary chromosome injuries. The number of such injuries and, therefore, SCE after mutagenic exposure gradually decreases due to reparative processes and death of cells damaged worst of all [3,6,9]. SCE-inducing injuries can be repaired in proliferating ceils during DNA replication and other phases of mitotic cycle and in nonproliferating cells [1,7,9]. Published data about the contribution of each of these processes to the decrease in the SCE level after mutagenic exposure are contradictory. However, it is the crucial point determining the conditions of SCE test for analysis of mutagenic loading in genetic monitoring.Our purpose was to assess the incidence of SCE during the second and third mitoses at different times after mutagenic exposure of Jungar hamster MATERIALS AND METHODSIn vivo experiments were carried out on 36 Jungar hamsters weighing 35 g. A 50-mg tablet of 5-bromo-2'deoxyuridine (BDU, Sigma), 80% of which was coated with an MK-6 biological glue for decelerating the drug absorption and prolonging its effect, was subcutaneously implanted into each animal. In parallel with this, experimental hamsters were intraperitoneally injected with thiophosphamide (TP) in a dose of 1.5 lag/g dissolved in normal saline. Controls were injected with saline alone. The animals were sacrificed by cervical dislocation after 13-37 h at 6-h intervals. Two hours before sacrifice the animals were injected eolchicine in a dose of 2 ~tg/g intraperitoneally. Bone marrow was collected from femoral bones.For in vitro experiments, human donor blood was incubated for 96 h in the presence of BDU. Blood specimens were treated with TP for 1 h (10

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Section: Resultsmentioning

confidence: 80%

Relationship between the duration and number of cell cycles after mutagenic exposure and the incidence of sister chromatid exchanges

Kuzin

Stukalov

1998

Bull Exp Biol Med

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Peculiar features of bone marrow cell proliferation in Djungarian hamsters with genetic disorders under thiotepa effect

Kuzin¹,

Bogomolov²,

Berechikidze³

et al. 2022

PHAR

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The paper aims to examine the proliferation of bone marrow cell pool in Djungarian hamsters and the subsequent restoration of their genetic stability after the action of thiotepa (TT). The study involved 36 animals, of which 16 were in the control group (injected with 0.25 ml of physiological solution), and 20 in the experimental group (0.25 ml of thiotepa at a dose of 1.5 mg per 1 kg of body weight). The maximum number of cells with CA amounting to 30.0% was observed 13 hours after TT injection (p≤0.05 between the control and experimental groups) and rapidly declined to 5.7% over subsequent periods by the 37th hour of the experiment (p≤0.05). The results suggest that the restoration of cell pool genetic stability is largely associated with the cell selection mechanisms, which confers an advantage over cell proliferation without chromosome anomalies.

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Induction and elimination of cytogenetic disturbances in lymphocytes of monkeys exposed to thiophosphamide

Cited by 2 publications

References 2 publications

Relationship between the duration and number of cell cycles after mutagenic exposure and the incidence of sister chromatid exchanges

Relationship between the duration and number of cell cycles after mutagenic exposure and the incidence of sister chromatid exchanges

Peculiar features of bone marrow cell proliferation in Djungarian hamsters with genetic disorders under thiotepa effect

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Induction and elimination of cytogenetic disturbances in lymphocytes of monkeys exposed to thiophosphamide

Cited by 2 publications

References 2 publications

Relationship between the duration and number of cell cycles after mutagenic exposure and the incidence of sister chromatid exchanges

Relationship between the duration and number of cell cycles after mutagenic exposure and the incidence of sister chromatid exchanges

﻿Peculiar features of bone marrow cell proliferation in Djungarian hamsters with genetic disorders under thiotepa effect

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Peculiar features of bone marrow cell proliferation in Djungarian hamsters with genetic disorders under thiotepa effect