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大鼠体内暴露于黄曲霉毒素B1和N-亚硝基非那西丁后淋巴细胞细胞遗传损伤的序贯监测。

Sequential monitoring of cytogenetic damage in rat lymphocytes following in vivo exposure to aflatoxin B1 and N-nitrosophenacetin.

作者信息

Li S Y, Lin J K

机构信息

Institute of Biochemistry, Medical College, National Taiwan University, Taipei, Republic of China.

出版信息

Mutat Res. 1990 Nov;242(3):219-24. doi: 10.1016/0165-1218(90)90087-i.

Abstract

Rats were treated intraperitoneally with different concentrations of aflatoxin B1 (AFB1) or N-nitrosophenacetin (NP). Blood was sequentially drawn by venous puncture at 6, 24, 72, 120 h and 14 days after a single injection of AFB1 or NP. After AFB1 the frequency of SCEs and chromosome aberrations increased progressively and reached a maximum level after 24 h and then decreased with time. By 2 weeks post treatment, the SCE and chromosome aberration values were within the control range. A small but significant SCE induction was observed when rats were treated with NP, but no chromosome breakage was induced even at the highest dose (20 mg/kg). We suggest that the elimination of DNA damage by repair mechanisms and lymphocyte turnover is responsible for the reduction of SCEs and chromosome aberrations with time. This assay seems promising for sequential monitoring of cytogenetic damage in rat lymphocytes following in vivo exposure to genotoxicants.

摘要

给大鼠腹腔注射不同浓度的黄曲霉毒素B1(AFB1)或N-亚硝基非那西丁(NP)。单次注射AFB1或NP后,分别于6、24、72、120小时和14天通过静脉穿刺依次采血。注射AFB1后,姐妹染色单体交换(SCE)频率和染色体畸变率逐渐增加,24小时后达到最高水平,随后随时间下降。治疗后2周,SCE和染色体畸变值在对照范围内。用NP处理大鼠时观察到轻微但显著的SCE诱导,但即使在最高剂量(20mg/kg)下也未诱导染色体断裂。我们认为,修复机制和淋巴细胞更新对DNA损伤的消除是SCE和染色体畸变随时间减少的原因。该试验似乎有望用于体内暴露于遗传毒性剂后对大鼠淋巴细胞细胞遗传损伤的连续监测。

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