Effects of dietary fish oil on the depletion of carcinogenic PAH-DNA adduct levels in the liver of B6C3F1 mouse.
Effects of dietary fish oil on the depletion of carcinogenic PAH-DNA adduct levels in the liver of B6C3F1 mouse.
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DOI：
10.1371/journal.pone.0026589
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发表时间：
2011
期刊：
影响因子：
3.7
通讯作者：
Moorthy B
中科院分区：
文献类型：
--
作者：
Zhou GD;Zhu H;Phillips TD;Wang J;Wang SZ;Wang F;Amendt BA;Couroucli XI;Donnelly KC;Moorthy B
许多致癌的多环芳烃 (PAH) 及其代谢物可以与 DNA 共价结合。致癌物-DNA 加合物可能导致关键基因突变，最终导致癌症。在这项研究中，我们报告鱼油 (FO) 通过 PAH 解毒来阻止 DNA 加合物的形成。 B6C3F1 雄性小鼠以 FO 或玉米油 (CO) 饮食喂养 30 天。然后，通过单次腹膜内注射，用包括苯并（a）芘（BaP）在内的七种致癌多环芳烃（BaP）对动物进行两种剂量中的一种治疗。治疗后1、3或7天处死动物。通过 32P 标记后测定分析 DNA 加合物的水平。我们的结果表明，与 CO 组相比，FO 组的总肝 DNA 加合物水平显着降低，但 3 d 时低 PAH 剂量除外（P = 0.067）。 7 d 时，高剂量 PAH 组 109 个核苷酸的总加合物水平分别为 41.36±6.48（平均值±SEM）和 78.72±8.03（P = 0.011）。用低剂量（低 2.5 倍）PAH 治疗的动物表现出类似的趋势。 FO组的总加合物水平为12.21±2.33，CO组的总加合物水平为24.07±1.99，P = 0.008。高剂量PAHs治疗7 d后109个核苷酸的BPDE-dG加合物值分别为32.34±1.94（CO组）和21.82±3.37（FO组），P值为0.035。低剂量组在两个饮食组中显示出相似的 BPDE-dG 加合物趋势。 FO 显着增强高剂量和低剂量 PAH 组中 Cyp1a1 的基因表达。与 CO 组相比，低剂量 PAH 组中的 Gstt1 在 FO 中表现出较高水平，P 值为 0.014。组织学观察表明，FO在早期发挥了保肝作用。我们的结果表明 FO 有潜力被开发为癌症化学预防剂。
Many carcinogenic polycyclic aromatic hydrocarbons (PAHs) and their metabolites can bind covalently to DNA. Carcinogen-DNA adducts may lead to mutations in critical genes, eventually leading to cancer. In this study we report that fish oil (FO) blocks the formation of DNA adducts by detoxification of PAHs. B6C3F1 male mice were fed a FO or corn oil (CO) diet for 30 days. The animals were then treated with seven carcinogenic PAHs including benzo(a)pyrene (BaP) with one of two doses via a single intraperitoneal injection. Animals were terminated at 1, 3, or 7 d after treatment. The levels of DNA adducts were analyzed by the 32P-postlabeling assay. Our results showed that the levels of total hepatic DNA adducts were significantly decreased in FO groups compared to CO groups with an exception of low PAH dose at 3 d (P = 0.067). Total adduct levels in the high dose PAH groups were 41.36±6.48 (Mean±SEM) and 78.72±8.03 in 109 nucleotides (P = 0.011), respectively, for the FO and CO groups at 7 d. Animals treated with the low dose (2.5 fold lower) PAHs displayed similar trends. Total adduct levels were 12.21±2.33 in the FO group and 24.07±1.99 in the CO group, P = 0.008. BPDE-dG adduct values at 7 d after treatment of high dose PAHs were 32.34±1.94 (CO group) and 21.82±3.37 (FO group) in 109 nucleotides with P value being 0.035. Low dose groups showed similar trends for BPDE-dG adduct in the two diet groups. FO significantly enhanced gene expression of Cyp1a1 in both the high and low dose PAH groups. Gstt1 at low dose of PAHs showed high levels in FO compared to CO groups with P values being 0.014. Histological observations indicated that FO played a hepatoprotective role during the early stages. Our results suggest that FO has a potential to be developed as a cancer chemopreventive agent.
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影响因子：
5.7
作者：
Lim K;Han C;Dai Y;Shen M;Wu T
通讯作者：
Wu T
DOI：
10.1158/1940-6207.capr-10-0368
发表时间：
2011-08
期刊：
Cancer prevention research (Philadelphia, Pa.)
影响因子：
--
作者：
Fan YY;Ran Q;Toyokuni S;Okazaki Y;Callaway ES;Lupton JR;Chapkin RS
通讯作者：
Chapkin RS
DOI：
10.1073/pnas.81.22.6943
发表时间：
1984-01-01
期刊：
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES
影响因子：
--
作者：
GUPTA, RC
通讯作者：
GUPTA, RC
DOI：
10.1158/1940-6207.capr-09-0044
发表时间：
2010-02
期刊：
Cancer prevention research (Philadelphia, Pa.)
影响因子：
--
作者：
Katiyar SK;Vaid M;van Steeg H;Meeran SM
通讯作者：
Meeran SM
影响因子：
4.7
作者：
Gunter, Marc J.;Divi, Rao L.;Sinha, Rashmi
通讯作者：
Sinha, Rashmi