Le Bon A M, Roy C, Dupont C, Suschetet M
Unité de Toxicologie Nutritionnelle, INRA, Dijon, France.
Cancer Lett. 1997 Mar 19;114(1-2):131-4. doi: 10.1016/s0304-3835(97)04642-9.
The effects of dietary administration of diallyl sulfide (DAS), diallyl disulfide (DADS) and allyl mercaptan (AM) on the genotoxicity of different chemicals were studied in two experimental systems: (i) measurement of hepatic DNA single-strand breaks induced in rats by aflatoxin B1 (AFB1), N-nitrosodimethylamine (NDMA) or methylnitrosourea (MNU); (ii) mutagenicity of AFB1 or NDMA on Salmonella typhimurium TA100 using hepatic S9 from rats fed allyl sulfides as the activation system. All compounds strongly reduced hepatic DNA breaks induced by AFB1 and NDMA but did not modify the genotoxicity of MNU. In the Ames test, the mutagenicity of NDMA was strongly inhibited by hepatic S9 from rats fed either compound. The mutagenicity of AFB1 was also reduced but to a lesser extent. Such effects are likely related to the modulation of drug-metabolizing enzymes which play a key role in metabolic activation as well as detoxication of NDMA and AFB1.
在两个实验系统中研究了膳食给予二烯丙基硫醚（DAS）、二烯丙基二硫醚（DADS）和烯丙基硫醇（AM）对不同化学物质遗传毒性的影响：（i）测量黄曲霉毒素B1（AFB1）、N-亚硝基二甲胺（NDMA）或甲基亚硝基脲（MNU）诱导大鼠肝脏DNA单链断裂的情况；（ii）以喂食烯丙基硫化物的大鼠肝脏S9作为活化系统，检测AFB1或NDMA对鼠伤寒沙门氏菌TA100的致突变性。所有化合物均能显著减少AFB1和NDMA诱导的肝脏DNA断裂，但不改变MNU的遗传毒性。在艾姆斯试验中，喂食任何一种化合物的大鼠肝脏S9均强烈抑制NDMA的致突变性。AFB1的致突变性也有所降低，但程度较小。这些作用可能与药物代谢酶的调节有关，药物代谢酶在NDMA和AFB1的代谢活化以及解毒过程中起关键作用。
