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亚慢性苯处理雄性小鼠外周血正色素红细胞中微核的持续性

Persistence of micronuclei in peripheral blood normochromatic erythrocytes of subchronically benzene-treated male mice.

作者信息

Rithidech K, Au W W, Ramanujam V M, Whorton E B, Legator M S

机构信息

Department of Preventive Medicine and Community Health, University of Texas Medical Branch, Galveston.

出版信息

Environ Mol Mutagen. 1988;12(3):319-29. doi: 10.1002/em.2860120306.

Abstract

The kinetics of micronucleus (MN) induction and decline in blood normochromatic erythrocytes (NCE) of mice subchronically exposed to benzene was investigated during and after exposure. Swiss (ICR) male mice (10/group) were given 0.0, 36.6, 73.2, and 146.4 mg/kg body weight benzene by gavage daily for 14 days, except for days 5 and 10. The frequency of MN increased significantly (P less than .001) during benzene treatment as a function of both concentration and time. Eleven days after exposure the levels of MN were higher than those observed at the end of exposure. After an initial rapid decline in the frequency of MN from 11 to 18 days postexposure, the decline became linear with time through 60 days postexposure. Using linear regression analysis, the MN level in each treatment group was predicted to reach control levels by approximately 85 days post-treatment. Dose-dependent suppression and recovery of erythropoiesis, estimated by polychromatic erythrocyte frequency, were observed in the 1st and 2nd weeks of exposure, respectively. Red blood cell (RBC) production was markedly increased in the first 3 weeks after benzene treatment. At later times the rate of production of the RBC returned to normal and may account for the linear decline observed in MN frequency. This research indicates that the frequency of MN is dose and duration dependent, while the decline in MN frequency after the end of benzene exposure can be related to changes in the kinetics of erythropoiesis.

摘要

研究了亚慢性暴露于苯的小鼠血液正色素红细胞(NCE)中微核(MN)诱导和消退的动力学,观察时间为暴露期间及暴露后。将瑞士(ICR)雄性小鼠(每组10只)每天经口灌胃给予0.0、36.6、73.2和146.4 mg/kg体重的苯,共14天,第5天和第10天除外。在苯处理期间,微核频率随浓度和时间显著增加(P小于0.001)。暴露11天后,微核水平高于暴露结束时观察到的水平。暴露后11至18天微核频率最初迅速下降,之后至暴露后第60天下降呈线性。通过线性回归分析预测,各处理组的微核水平在处理后约85天达到对照水平。分别在暴露的第1周和第2周观察到,通过多色红细胞频率估计的红细胞生成受到剂量依赖性抑制和恢复。苯处理后的前3周红细胞(RBC)生成显著增加。在之后的时间里,RBC生成速率恢复正常,这可能是微核频率呈线性下降的原因。本研究表明,微核频率与剂量和持续时间有关,而苯暴露结束后微核频率的下降可能与红细胞生成动力学的变化有关。

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