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甲基化苯并[a]芘和苯并[e]芘的紫外线光照射导致脂质过氧化的诱导。

UVA photoirradiation of methylated benzo[a]pyrene and benzo[e]pyrene leading to induction of lipid peroxidation.

作者信息

Sáenz Diógenes Herreño, Xia Qingsu, Fu Peter P

机构信息

Department of Pharmacology and Toxicology, School of Medicine, University of Puerto Rico, San Juan, Puerto Rico 00936-5067.

出版信息

Int J Environ Res Public Health. 2007 Jun;4(2):153-7. doi: 10.3390/ijerph2007040010.

DOI:10.3390/ijerph2007040010
PMID:17617679
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3728581/
Abstract

Polycyclic aromatic hydrocarbons (PAHs) are widespread genotoxic environmental pollutants and potentially pose a health risk to humans. Although the biological and toxicological activities, including metabolism, mutagenicity and carcinogenicity of PAHs have been thoroughly studied, their phototoxicity and photo-induced biological activities have not been well examined. In this research, we studied the photoirradiation of isomeric methylbenzo[a]pyrene (MBaP) and methylbenzo[e]pyrene (MBeP) by UVA light in the presence of a lipid, methyl linoleate, and evaluated the potential of these compounds to induce lipid peroxidation. The compounds chosen for study included BaP, 3-MBaP, 4-MBaP, 6-MBaP, 7-MBaP, 10-MBaP, BeP, 4-MBeP, and 9-MBeP. The results indicate that upon photoirradiation by UVA at 7 and 21 J/cm2, these compounds induced lipid peroxidation. The levels of the induced lipid peroxidation were similar among BaP and the isomeric MBaPs, and among the BeP and MBePs, with the BaP group higher than the BeP group. There was also a co-relation between the UV A light dose and the level of lipid peroxidation induced. Lipid peroxide formation was inhibited by NaN3 (singlet oxygen and free radical scavenger) and was enhanced by the presence of deuterium oxide (D2O) (extends singlet oxygen lifetime). These results suggest that photoirradiation of MBaPs and MBePs by UVA light generates reactive oxygen species (ROS), which induce lipid peroxidation.

摘要

多环芳烃(PAHs)是广泛存在的具有基因毒性的环境污染物,可能对人类健康构成风险。尽管PAHs的生物学和毒理学活性,包括其代谢、致突变性和致癌性已得到充分研究,但其光毒性和光诱导的生物学活性尚未得到充分研究。在本研究中,我们研究了在脂质亚油酸甲酯存在的情况下,用紫外线A(UVA)光照射同分异构体甲基苯并[a]芘(MBaP)和甲基苯并[e]芘(MBeP),并评估了这些化合物诱导脂质过氧化的潜力。选择用于研究的化合物包括苯并[a]芘(BaP)、3-甲基苯并[a]芘(3-MBaP)、4-甲基苯并[a]芘(4-MBaP)、6-甲基苯并[a]芘(6-MBaP)、7-甲基苯并[a]芘(7-MBaP)、10-甲基苯并[a]芘(10-MBaP)、苯并[e]芘(BeP)、4-甲基苯并[e]芘(4-MBeP)和9-甲基苯并[e]芘(9-MBeP)。结果表明,在7和21 J/cm²的UVA光照射下,这些化合物诱导了脂质过氧化。BaP和同分异构体MBaP之间以及BeP和MBeP之间诱导的脂质过氧化水平相似,BaP组高于BeP组。UVA光剂量与诱导的脂质过氧化水平之间也存在相关性。脂质过氧化物的形成受到叠氮化钠(单线态氧和自由基清除剂)的抑制,并因重水(D₂O)的存在而增强(延长单线态氧寿命)。这些结果表明,UVA光照射MBaP和MBeP会产生活性氧(ROS),从而诱导脂质过氧化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fdf/3728581/e3cbc1c81067/ijerph-04-00153f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fdf/3728581/42f3d477dc55/ijerph-04-00153f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fdf/3728581/d20e4863a28b/ijerph-04-00153f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fdf/3728581/6dabbcf480b2/ijerph-04-00153f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fdf/3728581/e3cbc1c81067/ijerph-04-00153f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fdf/3728581/42f3d477dc55/ijerph-04-00153f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fdf/3728581/d20e4863a28b/ijerph-04-00153f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fdf/3728581/6dabbcf480b2/ijerph-04-00153f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fdf/3728581/e3cbc1c81067/ijerph-04-00153f4.jpg

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