Reduced cytochrome P4501A activity and recovery from oxidative stress during subchronic benzo[a]pyrene and benzo[e]pyrene treatment of rainbow trout.
Reduced cytochrome P4501A activity and recovery from oxidative stress during subchronic benzo[a]pyrene and benzo[e]pyrene treatment of rainbow trout.
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DOI：
10.1016/j.taap.2011.04.015
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发表时间：
2011-07-01
影响因子：
3.8
通讯作者：
Hahn ME
中科院分区：
文献类型：
--
作者：
Curtis LR;Garzon CB;Arkoosh M;Collier T;Myers MS;Buzitis J;Hahn ME
本研究评估了芳烃受体（AHR）亲和力和细胞色素P4501A （CYP1A）蛋白及其活性在多芳烃（PAH）诱导的氧化应激中的作用。在1 ~ 100 nM浓度范围内，苯并[a]芘（BaP）而非苯并[e]芘（BeP）竞争性取代虹鳟AHR2α中2 nM [3H] 2,3,7,8 -四氯二苯并-对二恶英。在饲喂3 μg BaP或BeP/g鱼/天的3、7、14、28或50天内，虹鳟鱼的胆汁中出现了荧光芳香族化合物，虹鳟鱼的肝脏很容易以接近稳定的速率排出这些多芳香族烃（PAHs）及其代谢物。CYP1A蛋白催化虹鳟鱼肝脏微粒体中98%以上的乙氧基间苯二酚- o -去乙基酶（EROD）活性。饲喂两种多环芳烃50 d后，肝脏微粒体EROD活性先升高后降低。肝脏免疫组化证实CYP1A蛋白在饲喂两种多环芳烃3天后升高，并持续升高至28天。在饲喂这些多环芳烃50天的任何时候，BaP和BeP都没有增加肝脏DNA加合物的浓度。在喂食两种多环芳烃14天后，血液细胞的彗星测定显示出明显的DNA损伤，而在喂食50天后则不明显。随着时间的推移，两种多环芳烃肝脏EROD活性与血细胞DNA损伤之间存在很强的正相关。在3、7、14和28天后，BaP或BeP均未显著改变肾主干的CYP1A蛋白和3-硝基酪氨酸（氧化应激的生物标志物）免疫染色。AHR2α亲和力与BaP和bep诱导的氧化应激无明显关联。
This study assessed the role of aryl hydrocarbon receptor (AHR) affinity, and cytochrome P4501A (CYP1A) protein and activity in polyaromatic hydrocarbon (PAH)-induced oxidative stress. In the 1–100 nM concentration range benzo[a]pyrene (BaP) but not benzo[e]pyrene (BeP) competitively displaced 2 nM [3H]2, 3, 7, 8-tetrachloro-dibenzo-p-dioxin from rainbow trout AHR2α. Based on appearance of fluorescent aromatic compounds in bile over 3, 7, 14, 28 or 50 days of feeding 3 μg of BaP or BeP/g fish/day, rainbow trout liver readily excreted these polyaromatic hydrocarbons (PAHs) and their metabolites at near steady state rates. CYP1A proteins catalyzed more than 98% of ethoxyresorufin-O-deethylase (EROD) activity in rainbow trout hepatic microsomes. EROD activity of hepatic microsomes initially increased and then decreased to control activities after 50 days of feeding both PAHs. Immunohistochemistry of liver confirmed CYP1A protein increased in fish fed both PAHs after 3 days and remained elevated for up to 28 days. Neither BaP nor BeP increased hepatic DNA adduct concentrations at any time up to 50 days of feeding these PAHs. Comet assays of blood cells demonstrated marked DNA damage after 14 days of feeding both PAHs that was not significant after 50 days. There was a strong positive correlation between hepatic EROD activity and DNA damage in blood cells over time for both PAHs. Neither CYP1A protein nor 3-nitrotyrosine (a biomarker for oxidative stress) immunostaining in trunk kidney were significantly altered by BaP or BeP after 3, 7, 14, or 28 days. There was no clear association between AHR2α affinity and BaP and BeP-induced oxidative stress.
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影响因子：
4.8
作者：
Karchner, SI;Powell, WH;Hahn, ME
通讯作者：
Hahn, ME
DOI：
10.1006/faat.1993.1039
发表时间：
1993-04-01
期刊：
FUNDAMENTAL AND APPLIED TOXICOLOGY
影响因子：
--
作者：
GILROY, DJ;CARPENTER, HM;CURTIS, LR
通讯作者：
CURTIS, LR
影响因子：
13.6
作者：
Jonsson, Sofia;Persson, Ylva;Tysklind, Mats
通讯作者：
Tysklind, Mats
DOI：
10.1016/0027-5107(94)90300-x
发表时间：
1994-05-01
期刊：
MUTATION RESEARCH
影响因子：
--
作者：
ANDERSON, D;YU, TW;SCHMEZER, P
通讯作者：
SCHMEZER, P
DOI：
10.1073/pnas.93.21.11853
发表时间：
1996-10-15
影响因子：
11.1
作者：
MacMillanCrow, LA;Crow, JP;Thompson, JA
通讯作者：
Thompson, JA