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丁基羟基茴香醚、丁基羟基甲苯及其他抗氧化剂在N,N-二丁基亚硝胺诱发大鼠食管癌和前胃癌过程中的不同修饰反应

Different modifying response of butylated hydroxyanisole, butylated hydroxytoluene, and other antioxidants in N,N-dibutylnitrosamine esophagus and forestomach carcinogenesis of rats.

作者信息

Fukushima S, Sakata T, Tagawa Y, Shibata M A, Hirose M, Ito N

出版信息

Cancer Res. 1987 Apr 15;47(8):2113-6.

PMID:3829000
Abstract

The modifying effects of antioxidants were examined in a carcinogenesis system after N,N-dibutylnitrosamine treatment. Male F344 rats were given 0.05% N,N-dibutylnitrosamine in their drinking water for 4 wk and then treated with basal diet containing 2% butylated hydroxyanisole (BHA), 1% butylated hydroxytoluene (BHT) with 7 ppm vitamin K, 0.8% ethoxyquin, 5% sodium L-ascorbate, 5% sodium erythorbate, or no added chemical for 32 wk. BHA enhanced forestomach carcinogenesis but did not enhance esophageal carcinogenesis. BHT enhanced esophageal carcinogenesis but did not enhance forestomach carcinogenesis. Ethoxyquin significantly enhanced esophageal tumorigenesis. Neither esophageal nor forestomach carcinogenesis was affected by the other antioxidants evaluated. BHA significantly increased DNA synthesis of the forestomach epithelium, whereas BHT tended to increase that of the esophageal epithelium. Thus, BHA and BHT showed different modifying responses in carcinogenesis of the esophagus and forestomach.

摘要

在N,N - 二丁基亚硝胺处理后的致癌系统中研究了抗氧化剂的修饰作用。给雄性F344大鼠饮用含0.05% N,N - 二丁基亚硝胺的水4周,然后用含2%丁基化羟基茴香醚(BHA)、1%丁基化羟基甲苯(BHT)与7 ppm维生素K、0.8%乙氧喹、5% L - 抗坏血酸钠、5%异抗坏血酸钠的基础饲料或不添加化学物质的基础饲料处理32周。BHA增强了前胃致癌作用,但未增强食管癌发生。BHT增强了食管癌发生,但未增强前胃致癌作用。乙氧喹显著增强了食管肿瘤发生。所评估的其他抗氧化剂均未影响食管癌和前胃癌发生。BHA显著增加了前胃上皮的DNA合成,而BHT则倾向于增加食管上皮的DNA合成。因此,BHA和BHT在食管和前胃的致癌作用中表现出不同的修饰反应。

相似文献

1
Different modifying response of butylated hydroxyanisole, butylated hydroxytoluene, and other antioxidants in N,N-dibutylnitrosamine esophagus and forestomach carcinogenesis of rats.丁基羟基茴香醚、丁基羟基甲苯及其他抗氧化剂在N,N-二丁基亚硝胺诱发大鼠食管癌和前胃癌过程中的不同修饰反应
Cancer Res. 1987 Apr 15;47(8):2113-6.
2
Effects of butylated hydroxyanisole, butylated hydroxytoluene, and NaCl on gastric carcinogenesis initiated with N-methyl-N'-nitro-N-nitrosoguanidine in F344 rats.丁基羟基茴香醚、丁基羟基甲苯和氯化钠对用N-甲基-N'-硝基-N-亚硝基胍引发F344大鼠胃癌发生的影响。
J Natl Cancer Inst. 1984 May;72(5):1189-98.
3
Modification of chemical carcinogenesis by antioxidants.抗氧化剂对化学致癌作用的修饰。
Princess Takamatsu Symp. 1983;14:381-9.
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Carcinogenicity and modification of the carcinogenic response by BHA, BHT, and other antioxidants.丁基羟基茴香醚(BHA)、二丁基羟基甲苯(BHT)及其他抗氧化剂的致癌性与致癌反应的改变
Crit Rev Toxicol. 1985;15(2):109-50. doi: 10.3109/10408448509029322.
5
Promoting activities of butylated hydroxyanisole, butylated hydroxytoluene and sodium L-ascorbate on forestomach and urinary bladder carcinogenesis initiated with methylnitrosourea in F344 male rats.丁基羟基茴香醚、丁基羟基甲苯和L-抗坏血酸钠对F344雄性大鼠经甲基亚硝基脲引发的前胃癌和膀胱癌发生的促进作用。
Gan. 1984 Sep;75(9):769-75.
6
Modifying effects of concomitant treatment with butylated hydroxyanisole or butylated hydroxytoluene on N,N-dibutylnitrosamine-induced liver, forestomach and urinary bladder carcinogenesis in F344 male rats.叔丁基对苯二酚或叔丁基羟基甲苯联合处理对F344雄性大鼠中N,N-二丁基亚硝胺诱导的肝脏、前胃和膀胱癌发生的修饰作用。
Cancer Lett. 1988 Dec 15;43(3):167-72. doi: 10.1016/0304-3835(88)90166-8.
7
Studies on antioxidants: their carcinogenic and modifying effects on chemical carcinogenesis.抗氧化剂研究:其致癌作用及对化学致癌的修饰作用
Food Chem Toxicol. 1986 Oct-Nov;24(10-11):1071-82. doi: 10.1016/0278-6915(86)90291-7.
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Induction of forestomach lesions in rats by oral administrations of naturally occurring antioxidants for 4 weeks.通过口服天然抗氧化剂4周诱导大鼠前胃病变。
Jpn J Cancer Res. 1987 Apr;78(4):317-21.
9
Effects of butylated hydroxyanisole pretreatment on low dose N-methyl-N'-nitro-N-nitrosoguanidine- or N,N-dibutylnitrosamine-induced rat forestomach or esophageal carcinogenesis.丁基羟基茴香醚预处理对低剂量N-甲基-N'-硝基-N-亚硝基胍或N,N-二丁基亚硝胺诱导的大鼠前胃或食管癌发生的影响。
Carcinogenesis. 1991 Oct;12(10):1773-6. doi: 10.1093/carcin/12.10.1773.
10
Histologic and autoradiographic studies on the forestomach of hamsters treated with 2-tert-butylated hydroxyanisole, 3-tert-butylated hydroxyanisole, crude butylated hydroxyanisole, or butylated hydroxytoluene.对用2-叔丁基化羟基茴香醚、3-叔丁基化羟基茴香醚、粗制丁基化羟基茴香醚或丁基化羟基甲苯处理的仓鼠前胃进行的组织学和放射自显影研究。
J Natl Cancer Inst. 1986 Jan;76(1):143-9.

引用本文的文献

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Int J Mol Sci. 2022 Apr 20;23(9):4559. doi: 10.3390/ijms23094559.
2
Dose dependence of 1-O-hexyl-2,3,5-trimethylhydroquinone promotion of forestomach carcinogenesis in rats pretreated with N-ethylnitrosourethane.用N-亚硝基乙基脲预处理的大鼠中,1-O-己基-2,3,5-三甲基对苯二酚促进前胃癌发生的剂量依赖性
Jpn J Cancer Res. 1998 May;89(5):475-80. doi: 10.1111/j.1349-7006.1998.tb03286.x.
3
Comparison of reversibility of rat forestomach lesions induced by genotoxic and non-genotoxic carcinogens.
遗传毒性致癌物和非遗传毒性致癌物诱导的大鼠前胃损伤的可逆性比较。
Jpn J Cancer Res. 1993 Nov;84(11):1120-9. doi: 10.1111/j.1349-7006.1993.tb02811.x.
4
Effects of combined treatment with phenolic compounds and sodium nitrite on two-stage carcinogenesis and cell proliferation in the rat stomach.酚类化合物与亚硝酸钠联合处理对大鼠胃两阶段致癌作用及细胞增殖的影响
Jpn J Cancer Res. 1994 Jan;85(1):17-25. doi: 10.1111/j.1349-7006.1994.tb02881.x.
5
Effects of phenobarbital and carbazole on carcinogenesis of the lung, thyroid, kidney, and bladder of rats pretreated with N-bis(2-hydroxypropyl)nitrosamine.苯巴比妥和咔唑对经N-双(2-羟丙基)亚硝胺预处理的大鼠肺、甲状腺、肾脏和膀胱致癌作用的影响。
Jpn J Cancer Res. 1988 Apr;79(4):460-5. doi: 10.1111/j.1349-7006.1988.tb01614.x.
6
Inhibitory effects of antioxidants on N-bis(2-hydroxypropyl)nitrosamine-induced lung carcinogenesis in rats.抗氧化剂对N-双(2-羟丙基)亚硝胺诱导的大鼠肺癌发生的抑制作用。
Jpn J Cancer Res. 1990 Sep;81(9):871-7. doi: 10.1111/j.1349-7006.1990.tb02660.x.
7
Effects of sodium nitrite and catechol or 3-methoxycatechol in combination on rat stomach epithelium.亚硝酸钠与儿茶酚或3-甲氧基儿茶酚联合使用对大鼠胃上皮的影响。
Jpn J Cancer Res. 1990 Sep;81(9):857-61. doi: 10.1111/j.1349-7006.1990.tb02657.x.
8
Effect of butylated hydroxyanisole on the level of DNA adduction by aristolochic acid in the rat forestomach and liver.丁基羟基茴香醚对大鼠前胃和肝脏中马兜铃酸所致DNA加合物水平的影响。
Jpn J Cancer Res. 1990 Mar;81(3):220-4. doi: 10.1111/j.1349-7006.1990.tb02553.x.
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Organ-specific modification of tumor development by low-dose combinations of agents in a rat wide-spectrum carcinogenesis model.大鼠广谱致癌模型中低剂量联合用药对肿瘤发生的器官特异性修饰作用
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Jpn J Cancer Res. 1991 Dec;82(12):1397-405. doi: 10.1111/j.1349-7006.1991.tb01812.x.