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在植入致瘤剂量1,6-二硝基芘的F344大鼠中DNA加合物的形成及T淋巴细胞突变诱导

DNA adduct formation and T-lymphocyte mutation induction in F344 rats implanted with tumorigenic doses of 1,6-dinitropyrene.

作者信息

Smith B A, Fullerton N F, Heflich R H, Beland F A

机构信息

National Center for Toxicological Research, Jefferson, Arkansas 72079, USA.

出版信息

Cancer Res. 1995 Jun 1;55(11):2316-24.

PMID:7757982
Abstract

Diesel emissions are known to induce tumors in experimental animals and are suspected of being carcinogenic in humans. Of the compounds associated with diesel exhaust, 1,6-dinitropyrene is a particularly potent mutagen and carcinogen. In these experiments, we have investigated the use of DNA adducts and T-lymphocyte mutations of 1,6-dinitropyrene as biomarkers for exposure to diesel emissions. 1,6-Dinitropyrene (0-150 micrograms) was applied directly to the lungs of male F344 rats according to a protocol known to induce lung tumors. In target (lung) and surrogate (liver, WBC, and spleen lymphocytes) tissues, one major DNA adduct, N-(deoxyguanosin-8-yl)-1-amino-6-nitropyrene, was detected by HPLC and/or 32P-postlabeling analyses. The levels of this adduct reached a maximum 1-7 days following treatment and decreased to 13-50% of the peak values by 28 days after dosing. In the lung, a 2-fold increase in dose resulted in a 2-fold increase in DNA binding up to the 30-micrograms dose; in the liver the same relationship was observed up to 10 micrograms 1,6-dinitropyrene. At higher doses, the extent of adduct formation still increased, but the rate was much lower than that occurring at lower doses. A limiting dilution clonal assay was used to measure mutation induction at the hypoxanthine-guanine phosphoribosyltranferase locus in spleen T lymphocytes. Following treatment, the mutant frequency increased until 21 weeks, remained constant until week 40, and then began to decrease. Mutant induction was dose related, with the increase in mutant frequency being significant at doses > or = 1 microgram 1,6-dinitropyrene. These data indicate that 1,6-dinitropyrene, a constituent of diesel emissions, is metabolically activated by nitroreduction to give DNA adducts in target and surrogate tissues. They further suggest that T-lymphocyte mutations may be a more sensitive and longer-lived biomarker than DNA adducts for assessing previous exposures to nitropolycyclic aromatic hydrocarbons.

摘要

已知柴油排放物会在实验动物中诱发肿瘤,并且怀疑对人类具有致癌性。在与柴油废气相关的化合物中,1,6 - 二硝基芘是一种特别强效的诱变剂和致癌物。在这些实验中,我们研究了使用1,6 - 二硝基芘的DNA加合物和T淋巴细胞突变作为接触柴油排放物的生物标志物。根据已知可诱发肺部肿瘤的方案,将1,6 - 二硝基芘(0 - 150微克)直接施用于雄性F344大鼠的肺部。在靶组织(肺)和替代组织(肝脏、白细胞和脾淋巴细胞)中,通过高效液相色谱法(HPLC)和/或32P后标记分析检测到一种主要的DNA加合物,即N - (脱氧鸟苷 - 8 - 基)-1 - 氨基 - 6 - 硝基芘。该加合物的水平在处理后1 - 7天达到最高,给药后28天降至峰值的13 - 50%。在肺中,剂量增加2倍导致DNA结合增加2倍,直至30微克剂量;在肝脏中,直至10微克1,6 - 二硝基芘时观察到相同的关系。在更高剂量下,加合物形成的程度仍会增加,但速率远低于低剂量时的情况。使用极限稀释克隆测定法来测量脾T淋巴细胞中次黄嘌呤 - 鸟嘌呤磷酸核糖转移酶位点的突变诱导情况。处理后,突变频率在21周前增加,在40周前保持恒定,然后开始下降。突变诱导与剂量相关,当剂量≥1微克1,6 - 二硝基芘时,突变频率的增加具有显著性。这些数据表明,柴油排放物的成分1,6 - 二硝基芘通过硝基还原代谢活化,在靶组织和替代组织中产生DNA加合物。它们进一步表明,对于评估先前接触硝基多环芳烃的情况,T淋巴细胞突变可能是比DNA加合物更敏感且寿命更长的生物标志物。

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