Nadathur S R, Gould S J, Bakalinsky A T
Department of Food Science and Technology, Oregon State University, Corvallis 97331-6602.
Mutat Res. 1995 Apr;334(2):213-24. doi: 10.1016/0165-1161(95)90014-4.
Reconstituted non-fat dry milk powder, fermented by a mixture of Streptococcus thermophilus CH3 and Lactobacillus bulgaricus 191R to produce yogurt, was freeze-dried and extracted in acetone. After evaporation of the acetone, the extract was dissolved in dimethyl sulfoxide (DMSO) and tested for antimutagenicity. In the Ames test, significant dose-dependent activity was observed against N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), 4-nitro-quinoline-N-oxide (4NQO), 3,2'-dimethyl-4-aminobiphenyl (DMAB), 9,10-dimethyl-1,2-benz[a]anthracene (DMBA), and 3-amino-1-methyl-5H-pyrido[4,3-b]indole acetate (Trp-P-2). Weak activity was observed against 1,2,7,8-diepoxyoctane (DEO), and no activity was observed against methyl methanesulfonate (MMS), ethyl methanesulfonate (EMS), or aflatoxin B1 (AFB1). In a related assay (Saccharomyces cerevisiae D7), significant antimutagenic activity was detected against MNNG and 4NQO. Activity against the experimental colon carcinogens MNNG and DMAB was examined further, as assayed in the Ames test (Salmonella typhimurium TA100). Compounds responsible for both activities were less soluble in aqueous solutions than in DMSO. Adjustment of yogurt pH to 3, 7.6, or 13 prior to freeze-drying and acetone extraction did not significantly alter the amount of anti-MNNG activity recovered. In contrast, extractability of anti-DMAB activity was significantly greater at acidic pH. Conjugated linoleic acid, a known dairy anticarcinogen, failed to inhibit mutagenesis caused by either mutagen, suggesting that other yogurt-derived compound(s) are responsible. Unfermented milk was treated with lactic acid, yogurt bacteria without subsequent growth, or both, to determine if formation of antimutagenic activity required bacterial growth. Extracts of the milk treatments exhibited the same weak antimutagenicity observed in unfermented milk, approximately 2.5-fold less than in the yogurt extracts, suggesting that antimutagenic activity is associated with bacterial growth.
将由嗜热链球菌CH3和保加利亚乳杆菌191R混合发酵制成酸奶的复原脱脂奶粉进行冷冻干燥,然后用丙酮萃取。丙酮蒸发后,提取物溶解于二甲基亚砜(DMSO)中并进行抗诱变活性测试。在艾姆斯试验中,观察到对N-甲基-N'-硝基-N-亚硝基胍(MNNG)、4-硝基喹啉-N-氧化物(4NQO)、3,2'-二甲基-4-氨基联苯(DMAB)、9,10-二甲基-1,2-苯并[a]蒽(DMBA)和3-氨基-1-甲基-5H-吡啶并[4,3-b]吲哚乙酸(Trp-P-2)有显著的剂量依赖性活性。对1,2,7,8-二环氧辛烷(DEO)观察到较弱的活性,而对甲磺酸甲酯(MMS)、乙磺酸乙酯(EMS)或黄曲霉毒素B1(AFB1)未观察到活性。在一项相关试验(酿酒酵母D7)中,检测到对MNNG和4NQO有显著的抗诱变活性。如在艾姆斯试验(鼠伤寒沙门氏菌TA100)中所测定的,进一步研究了对实验性结肠致癌物MNNG和DMAB的活性。具有这两种活性的化合物在水溶液中的溶解度低于在DMSO中的溶解度。在冷冻干燥和丙酮萃取之前将酸奶的pH值调节至3、7.6或13,并未显著改变回收的抗MNNG活性的量。相比之下,在酸性pH下抗DMAB活性的可萃取性显著更高。共轭亚油酸是一种已知的乳制品抗癌剂,未能抑制由任何一种诱变剂引起的诱变作用,这表明其他源自酸奶的化合物起了作用。用乳酸、未后续生长的酸奶细菌或两者处理未发酵牛奶,以确定抗诱变活性的形成是否需要细菌生长。牛奶处理提取物表现出与未发酵牛奶中观察到的相同的弱抗诱变活性,比酸奶提取物中的活性低约2.5倍,这表明抗诱变活性与细菌生长有关。