应用氢呼气试验测定食物口-结肠转运时间

目的建立测定食物口结肠转运时间（ＯＣＴＴ）的方法。方法采用氢呼气试验（ＢＨＴ），以乳果糖为对照，测定１３名健康成人对５组富含碳水化合物食物的口结肠转运时间。结果乳果糖糖浆９０．０ｍｉｎ±５０．６ｍｉｎ，红薯２３７．３ｍｉｎ±６４．９ｍｉｎ，馒头３４１．３ｍｉｎ±７７．９ｍｉｎ，玉米粉３５２．５ｍｉｎ±５９．５ｍｉｎ，大米组出现产氢人数少，肉末米饭组未出现氢值升高，故这两组均不能判断ＯＣＴＴ值；ＯＣＴＴ值与最高氢峰值呈负相关（ｒ＝－０．６６２５），与最高氢峰值出现的时间和吸收率呈正相关（ｒ分别是０７６６８和０．８７９０）。结论用氢呼气试验法测定食物的口结肠转运时间是简便、可靠、安全、可行的方法。     

谷氨酰胺和丙氨酰-谷氨酰胺双肽影响人回结肠粘膜增殖的离体实验

背景／目的：谷氨酰胺（Glu)对危重患小肠上皮有一 定营养作用。在肠外营养时由于其不够稳定而限制了它的应用，但此不足可以通过使用稳定的丙氨酰－谷氨酰肽双肽（Ala-Gln）而克服。本研究目的是验证如下假设，即谷氨酰胺或丙氨酰－谷氨酰胺双肽不但可以刺激回肠细胞增殖，而且可以刺激结肠细胞增殖，维护肠屏障功能。方法：将正常人回肠、近段结肠、乙状结肠及直活检标本分别加入谷氨酰胺（2mmol/L）、丙氨酰－谷氨酰胺双肽（2mmol/L）、生理盐水（对照），孵育4小时。S期的细胞用5溴－2脱氧尿苷标记。对被标记的腺管纵向切片和静止期细胞进行记数。结果：谷氨酰胺和丙氨酰－谷氨酰胺双肽可以刺激回肠细胞、近段结肠、乙状结肠及直肠腺管细胞的增殖。在回肠标本、整个腺管的细胞增被较好的标记，而在结肠则主要对腺管的基底部分有营养作用。结论：谷氨酰胺和丙氨酰－谷氨酰胺双肽不但对肠细胞，而且对结肠细胞有营养作用，从而可阻止肠外营养时肠粘膜萎缩，维护肠屏障功能。     

文摘

文摘２３９英国聚丙烯生产工人患结肠直肠癌的危险度〔英〕／ＢｏｕｓｋｊｉｌｌＪ／／ＯｃｃｕｐＥｎｖｉｒｏｎＭｅｄ．－１９９４，５１（１１）．－７８６为探讨接触聚丙烯与结肠直肠癌危险度之间的关系，对英国柴郡卡灵顿市两家聚丙烯工厂的生产工人进行了研究。这两...     

简讯及其它

简讯及其它３４５国际生命科学学会欧洲分会结肠微生物体系：营养与健康专题研讨会［英］／ｅｄｉｔｏｒ∥ＩＬＳＩＥｕｒＮｅｗｓｌｅｔｔ．－１９９４，（１８）．－１～２为了搞清人结肠微生物体系（ｍｉｃｒｏｆｌｏｒａ）在吸收代谢、免疫调节、肠道生理学与疾病等方...     

溃疡性结肠炎患者基质金属蛋白酶-1表达测定的意义

目的检测基质金属蛋白酶-1（MMP-1）在溃疡性结肠炎（UC）患者结肠组织中的表达，探讨MMP-1在溃疡形成过程中的作用以及与病情严重程度之间的关系。方法采用逆转录-聚合酶链反应（RT—PCR）和免疫组织化学染色法在40例UC患者的结肠黏膜溃疡区、炎症区以及相对正常区取活组织在mRNA水平及蛋白水平上测定MMP-1表达，以10例正常人的结肠组织（正常对照组）作为对照，分析MMP-1的表达与病情严重程度之间的关系。结果在mRNA水平上，MMP-1在溃疡区、炎症区结肠组织中的表达较相对正常区明显增加（P〈0．01），较正常对照组也明显增加（P〈0．01）；在蛋白水平上，MMP-1在溃疡区、炎症区的表达较相对正常区明显增加（P〈0．05），较正常对照组也明显增加（P〈0．05）；相对正常区与正常对照组之间的表达无论在mRNA水平还是在蛋白水平差异均无统计学意义；MMP-1的表达在溃疡区、炎症区、相对正常区及正常对照组结肠组织中的阳性率分别为85％、82％、58％、40％；MMP-1与UC病情严重程度具有相关性（r=0．406，P〈0．05）。结论UC病变结肠组织中MMP-1的表达增加，并且与UC的组织损伤程度有关，MMP-1可以作为评价UC病情严重程度的生物学指标；应用外源性基质金属蛋白酶抑制剂治疗可能会成为UC治疗的新途径。     

空肠弯曲菌、结肠弯曲菌检验方法团体标准解读

空肠弯曲菌和结肠弯曲菌是重要的食源性病原菌，是导致人类弯曲菌病的重要菌种。病原菌的培养、鉴定是食品污染以及人和动物感染诊断的“金标准”。中国CDC传染病预防控制所和国家食品安全风险评估中心等单位撰写了《空肠弯曲菌、结肠弯曲菌检验方法（T/CPMA 006－2019）》团体标准。标准以“科学性、规范性、适用性和可行性”为基本原则，提出从不同种类的标本、样品中空肠弯曲菌和结肠弯曲菌的分离培养以及鉴定的方法，用于指导和规范我国不同种类的标本以及样本中两种弯曲菌的检测过程、检测步骤和鉴定方法，提高空肠弯曲菌、结肠弯曲菌的检测水平。     

妇科肿瘤患者血清中细胞因子的表达及意义

目的：研究妇科肿瘤患者血清中细胞因子的变化，探索与发病机理的相关性。方法：以双抗体夹心ＥＬＩＳＡ法对７９例妇科肿瘤患者血清中肿瘤坏死因子（ＴＮＦ－α）、白细胞介素－６（ＩＬ－６）、白细胞介素－８（ＩＬ－８）和白细胞介素－１０（ＩＬ－１０）水平进行了监测。结果：妇科恶性肿瘤组ＴＮＦ－α、ＩＬ－６、ＩＬ－８和ＩＬ－１０水平均明显高于正常对照组和妇科良性肿瘤组（Ｐ＜０．０１），其中尤以卵巢癌增高最为明显，其次为子宫内膜癌和滋养细胞肿瘤。结论：说明ＴＮＦ－α、ＩＬ－６、ＩＬ－８和ＩＬ－１０细胞因子可能参与肿瘤的形成和发展过程，并对妇科良、恶性肿瘤的鉴别诊断有一定意义。     

镜下微波治疗大肠息肉63例报导

我院于1994年11月至1996年11月应用国产微波仪经纤维结肠镇治疗大肠息肉63例，摘除息肉79枚，疗效满意，现报告如下。1临床资料1．1男性48例，女性15例；年龄6－67岁，平均43岁；病程2个月至10年；临床表现腹泻、腹胀与血便；63例均系本院经纤维结肠镜检发现的病例。直肠用枚，乙状结肠25枚，降结肠18枚，根结肠5枚，升结肠3枚；其中单发50例，多发13例（10例2枚、3例3枚）；息肉直径小于0．scm27枚，0.5－1cm30枚，1.1－2cm15枚。大于2cm7枚；广基54枚，亚蒂10枚，带蒂15枚。病理检出炎性息肉35例，腺癌性28例。1．2仪器纤维结肠镜（肠镜）…     

依布硒啉及苯半异硒唑酮氨基酸衍生物的体外抗肿瘤活性

采用ＳＲＢ活细胞染色法，研究了９个新合成的苯并异硒啉对体外培养的三种不同组织人肿瘤细胞生长的抑制作用。结果表明：这类化合物对人肝癌细胞Ｂｅｌ－７４０２，结肠癌细胞ＨＣＴ－８和表皮癌细胞Ａ４３１的生长的抑制作用与其化学结构密切相关。     

先天性巨结肠术后患儿远期行为问题探讨

目的：探讨先天性巨结肠术后患儿远期心理行为问题及发生原因。方法：利用自制的一般情况调查表和Achenbach儿童行为量表（CBCL）对46例先天性巨结肠根治术后的患儿和138例对照进行调查，研究其行为问题。结果：（1）病例组行为问题的发生率（23．91％）较对照组（10．14％）高（P＜0．05），6－11岁男性儿童病例组违纪问题较对照组高（P＜0．05）；（2）长段型和全结肠型行为问题的发生率较短段型和普通型的高（P＜0．05）。结论：先天性巨结肠患者术后较对照组儿童有着较多的心理行为问题，主要原因是病变本身及病变类型影响了患儿的排便功能，采取针对性措施改善先天性巨结肠术后患儿远期心理行为发育状况是必要的。     

Tea as a potential chemopreventive agent in PhIP carcinogenesis: effects of green tea and black tea on PhIP-DNA adduct formation in female F-344 rats

The heterocyclic amine 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is formed during the cooking of proteinaceous animal foods (meat, chicken, and fish). PhIP is a carcinogen in the Fischer 344 (F-344) rat; it induces mammary tumors in female rats and lymphomas and colon and prostate tumors in male rats. In F-344 rats, PhIP forms DNA adducts in various organs, including the target organs. Inhibition of PhIP-DNA adduct formation is likely to lead to inhibition of PhIP tumorigenicity. We have examined the chemopreventive properties of green tea and black tea in PhIP carcinogenesis by evaluating their effects on PhIP-DNA adduct formation in the female F-344 rat. Young adult animals were maintained on powdered AIN-76A diet while receiving regular drinking water or 2% (wt/vol) infusions of green tea or black tea for a total of six weeks. During Weeks 3, 4, and 5, all animals received PhIP by gavage (1 mg/kg/day). Three rats per group were euthanized on Days 1 and 8 after termination of PhIP exposure. DNA was isolated from a number of organs and analyzed for PhIP-DNA adducts by 32P-postlabeling assays. Compared with animals on regular drinking water, PhIP-DNA adduct formation was inhibited in small intestine, colon, liver, and mammary epithelial cells (MECs) of animals receiving green tea or black tea as the sole source of drinking fluid. Green tea inhibited adduct formation in colon, liver, and MECs (33.3-80.0%) on both days, but only on Day 8 (54.4%) in small intestine. Black tea inhibited adduct formation on both days in liver (71.4-80.0%), on Day 1 in colon (40.0%), and on Day 8 in small intestine (81.8%); it had no effect on MEC adducts. Neither green tea nor black tea had an effect on adduct levels in pancreas, lungs, white blood cells, heart, kidneys, spleen, cecum, or stomach. Similarly, these teas did not affect the rate of adduct removal (percent change from Day 1 to Day 8) in any organ. It is concluded that green tea and black tea are potential chemopreventive agents in PhIP-induced tumorigenesis in the F-344 rat.     

Effects of dietary conjugated linoleic acid on DNA adduct formation of PhIP and IQ after bolus administration to female F344 rats

Meats cooked at high temperatures contain mutagenic heterocyclic amines such as 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) and 2-amino-3-methylimidazo[4,5-f]quinoline (IQ). In female Fischer 344 rats, IQ is a multiorgan carcinogen, whereas PhIP induces mammary adenocarcinomas. For IQ and PhIP, N-hydroxylation, catalyzed by microsomal cytochrome P-450 1A1 and/or 1A2, and then esterification, especially O-acetylation, are the principal steps leading to DNA adduct formation. Conjugated linoleic acid (CLA) is a mixture of conjugated linoleic acid isomers found in various meat and dairy products. We have examined the effect of dietary CLA on DNA adduct formation by PhIP and IQ in female Fischer 344 rats. Four-week-old animals were maintained on AIN-76A diet without or with CLA (4% wt/wt) and treated with IQ or PhIP (50 mg/kg by gavage) after two weeks. Animals were killed (4/group) one, four, and eight days later. DNA isolated from mammary epithelial cells, liver, colon, and white blood cells was analyzed for carcinogen-DNA adducts by 32P-postlabeling assays. On Day 1, dietary CLA significantly inhibited adduct formation (82.0%) in mammary epithelial cells in IQ--but not in PhIP-treated rats. In the colon, dietary CLA significantly inhibited PhIP-DNA adduct formation (18.7%) on Day 8 but increased IQ-DNA adduct formation (30.5%) on Day 8. Dietary CLA had no effect on adduct levels in liver or white blood cells. Calf thymus DNA was incubated with N-hydroxy-PhIP or -IQ in the presence of acetyl-CoA. Enzymatic activation was catalyzed by liver or mammary cytosol. A two-week pretreatment with 2% (wt/wt) dietary CLA had no effect on O-acetyltransferase-catalyzed IQ- or PhIP-DNA adduct formation. It is concluded, under certain conditions, that dietary CLA can lower IQ- and PhIP-DNA adduct formation. Overall, however, the major mode of action of CLA is probably by a mechanism other than the inhibition of the N-hydroxylation and subsequent O-acetylation of PhIP or IQ.     

Inhibition of DNA adduct formation of PhIP in female F344 rats by dietary conjugated linoleic acid

The dietary mutagen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is a mammary carcinogen in the female Fischer (F344) rat and a colon carcinogen in the male F344 rat. To exert its carcinogenicity, it is believed that PhIP needs to form adducts with DNA, a process requiring N-hydroxylation of PhIP by cytochromes P-450 1A1 and/or 1A2 (CYP 1A1 and/or 1A2), as well as further esterification of the hydroxylamine thus formed. Dietary conjugated linoleic acid (CLA) inhibits chemical carcinogenesis in various experimental models. We have examined the effect of dietary CLA on PhIP-DNA adduct formation in female F344 rats. Four-week-old animals were maintained on AIN-76A diet without or with CLA (1%, 0.5%, and 0.1% wt/wt) for 57 days. PhIP was added to the diets (0.04% wt/wt) from Days 14-42. Animals were killed (4/group) on Days 43, 50, and 57. DNA isolated from liver, mammary epithelial cells (MEC), colon, and white blood cells (WBC) was analyzed for PhIP-DNA adducts by 32P-postlabeling assays. On Day 43, CLA inhibited adduct formation in the liver (up to 58%) in a dose-dependent manner. CLA also inhibited hepatic adduct levels (29-39%) on Day 50 (at 1.0% and 0.5% CLA) and on Day 57 (53% at 0.5% CLA). CLA significantly reduced adduct levels in the WBC on Day 50 (63-70%). Adducts in MEC and the colon were not affected by dietary CLA. On Day 57, adduct levels in MEC, liver, colon, and WBC were 0-30.3%, 8.6-41.7%, 21.5-50.7%, and 7.5-11.8%, respectively, of those on Day 43. Northern blot analysis of liver RNA showed that dietary CLA did not affect steady-state levels of CYP 1A1 or 1A2 mRNA. It is concluded that dietary CLA inhibits PhIP-DNA adduct formation in liver and WBC but that those in MEC and the colon are unaffected when a low-level dietary regimen of carcinogen and inhibitor was used. In inhibiting PhIP-DNA adduct formation, CLA does not appear to act by inhibiting CYP 1A1 or 1A2 expression.     

Effect of dietary constituents with chemopreventive potential on adduct formation of a low dose of the heterocyclic amines PhIP and IQ and phase II hepatic enzymes

We conducted a study to evaluate dietary chemopreventive strategies to reduce genotoxic effects of the carcinogens 2-amino-1-methyl-6-phenyl-imidazo[4,5-b]pyridine (PhIP) and 2-amino-3-methylimidazo[4,5-f]quinoline (IQ). PhIP and IQ are heterocyclic amines (HCAs) that are found in cooked meat and may be risk factors for cancer. Typical chemoprevention studies have used carcinogen doses many thousand-fold higher than usual human daily intake. Therefore, we administered a low dose of [14C]PhIP and [3H]IQ and utilized accelerator mass spectrometry to quantify PhIP adducts in the liver, colon, prostate, and blood plasma and IQ adducts in the liver and blood plasma with high sensitivity. Diets supplemented with phenethylisothiocyanate (PEITC), genistein, chlorophyllin, or lycopene were evaluated for their ability to decrease adduct formation of [14C]PhIP and [3H]IQ in rats. We also examined the effect of treatments on the activity of the phase II detoxification enzymes glutathione S-transferase (GST), UDP-glucuronyltransferase (UGT), phenol sulfotransferase (SULT) and quinone reductase (QR). PEITC and chlorophyllin significantly decreased PhIP-DNA adduct levels in all tissues examined, which was reflected by similar changes in PhIP binding to albumin in the blood. In contrast, genistein and lycopene tended to increase PhIP adduct levels. The treatments did not significantly alter the level of IQ-DNA or -protein adducts in the liver. With the exception of lycopene, the treatments had some effect on the activity of one or more hepatic phase II detoxification enzymes. We conclude that PEITC and chlorophyllin are protective of PhIP-induced genotoxicity after a low exposure dose of carcinogen, possibly through modification of HCA metabolism.     

Comparison of white tea, green tea, epigallocatechin-3-gallate, and caffeine as inhibitors of PhIP-induced colonic aberrant crypts

There is growing interest in the possible health benefits of tea. We reported previously on the inhibition by white tea of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-induced colonic aberrant crypt foci (ACF) in the rat (4). To distinguish between blocking and suppressing effects, and thus provide mechanistic insights into prevention during the initiation versus post-initiation phases of carcinogenesis, white tea, and green tea were administered at 2% (w/v) as the sole source of drinking fluid either 2 wk before and 2 wk during PhIP dosing (100 mg/kg, every other day by oral gavage), or starting 1 wk after the carcinogen and continued until the study was terminated at 16 wk. In the former protocol, each tea produced marginal inhibition of colonic ACF, despite evidence for changes in several hepatic enzymes involved in heterocyclic amine metabolism. Post-initiation, however, the data were as follows (ACF/colon, mean +/- SE): PhIP/water 12.2 +/- 1.5; PhIP/white tea 5.9 +/- 0.9 (** P < 0.01); PhIP/caffeine 5.9 +/- 1.5 (** P < 0.01); PhIP/EGCG 3.5 +/- 0.8 (***P < 0.001); PhIP/green tea 8.9 +/- 1.2 (P = 0.22, not significant). In the latter study, apoptosis was determined using in situ oligo ligation and cleaved caspase-3 assays, whereas cell proliferation was assessed via bromodeoxyuridine (BrdU) incorporation. No consistent changes were seen in apoptosis assays, but BrdU labeling was as follows (percent of cells positive/colonic crypt, mean +/- SE): PhIP/water 10.4 +/- 0.6; PhIP/white tea 8.6 +/- 0.2 (*P < 0.05); PhIP/EGCG 6.0 +/- 0.85 (** P < 0.01); PhIP/caffeine 8.75 +/- 0.45 (*P < 0.05); PhIP/green tea 9.5 +/- 0.4 (P > 0.05, not significant). The data imply that white tea, caffeine, and EGCG may be most effective post-initiation, via the inhibition of cell proliferation in the colon and through the suppression of early lesions.     

Inhibition by white tea of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine-induced colonic aberrant crypts in the F344 rat

There is growing interest in the potential health benefits of tea, including the anticarcinogenic properties. We report here that white tea, the least processed form of tea, is a potent inhibitor of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-induced colonic aberrant crypts in the rat. Male Fischer 344 rats were treated for 8 wk with white tea (2% wt/vol) or drinking water alone, and on alternating days in experimental Weeks 3 and 4 the animals were given PhIP (150 mg/kg body wt p.o.) or vehicle alone. At the end of the study there were 5.65 +/- 0.81 and 1.31 +/- 0.27 (SD) aberrant crypt foci per colon in groups given PhIP and PhIP + white tea, respectively (n = 12, P < 0.05). No changes were detected in N-acetyltransferase or arylsulfotransferase activities compared with controls, but there was marked induction of ethoxyresorufin O-deethylase, methoxyresorufin O-demethylase, and UDP-glucuronosyltransferase after treatment with white tea. Western blot revealed corresponding increases in cytochrome P-450 1A1 and 1A2 proteins. Enzyme assays and Western blot also revealed induction of glutathione S-transferase by white tea. There was less parent compound and 4'-hydroxy-PhIP but more PhIP-4'-O-glucuronide and PhIP-4'-O-sulfate in the urine from rats given PhIP + white tea than in urine from animals given carcinogen + drinking water. The results indicate that white tea inhibits PhIP-induced aberrant crypt foci by altering the expression of carcinogen-metabolizing enzymes, such that there is increased ring hydroxylation at the 4' position coupled with enhanced phase 2 conjugation.     

杂环胺代表物PhIP对大鼠不同组织脂质过氧化作用的影响

目的研究杂环胺代表物2-氨基-1-甲基-6-苯基-咪唑并[4,5-b]吡啶(PhIP)对雄性大鼠心、肺、肝、肾组织脂质过氧化作用的影响。方法对大鼠进行PhIP(5、10和15mg/kg)灌胃染毒,24 h后取大鼠心、肺、肝、肾组织,采用生化方法测定这4种组织的脂质过氧化作用相关指标。结果与对照组相比,15 mg/kg的PhIP可显著诱导大鼠心和肺组织超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GPx)活性(P<0.05或P<0.01);而在肝组织中,10和15 mg/kg的PhIP显著抑制了这3种酶的活性(P<0.05或P<0.01)。肾组织中SOD、CAT和GPx活性的变化与对照组相比没有显著性差异。同时,随着PhIP浓度增加,大鼠心、肺、肝、肾组织中丙二醛(MDA)含量也随着增高,呈现浓度-效应关系,在较高浓度下(10和15 mg/kg的PhIP)与对照组相比差异有显著性(P<0.05)。结论 PhIP引起大鼠心、肺、肝、肾脂质过氧化,这种效应存在组织差异性。     

Green tea and cancer prevention

Extracts of green tea and green tea polyphenols have exhibited inhibitory effects against the formation and development of tumors at different organ sites in animals. These include animal models for skin, lung, oral cavity, esophagus, stomach, intestine, colon, liver, pancreas, bladder, mammary gland, and prostate cancers. In addition to suppressing cell proliferation, promoting apoptosis, and modulating signaling transduction, green tea polyphenols, especially (-)-epigallocatechin-3-gallate, also inhibit cell invasion, angiogenesis, and metastasis. This article reviews data on the cancer preventive activities of green tea polyphenols, possible mechanisms involved, and the relationship between green tea consumption and human cancer risk.     

Absence of PhIP adducts,p53 and Apc mutations,in rats fed a cooked beef diet containing a high level of heterocyclic amines

Meat cooked at high temperatures contains mutagens and carcinogens known as heterocyclic amines (HCA). Cooking temperature and time determine the amount of HCA produced. The present study examined the DNA of liver, colon, and stomach from rats fed a high level of HCA for 27 weeks. Male Sprague‐Dawley rats were fed a high‐fat AIN‐76A‐based diet containing 60% by weight cooked beef containing a high level of HCA, especially 2‐amino‐l‐methyl‐6‐phenylimidazo[4,5‐b]pyridine (PhIP, 72 ng/g cooked beef), the most abundant HCA in cooked meat products. At the end of 27 weeks the rats were terminated, and small portions of liver, colon, and stomach were quick‐frozen in liquid nitrogen. The DNA was isolated from the thawed tissue by phenol‐chloroform extraction, and the genomic DNA was analyzed for the presence of PhIP adducts by ³²P‐postla‐beling analysis. The DNA was also used in polymerase chain reactions to amplify the rat p53 and Apc genes, then direct dye‐terminator DNA sequencing was carried out. Results showed no PhIP adducts in any tissue. In addition, no signature p53 or Apc gene mutations were seen in colon or stomach DNA. These results indicate that the high level of HCA present in a diet of well‐cooked meat does not cause 1) persistent PhIP adducts similar to those produced by feeding pure PhIP at high doses or 2) p53 and Ape gene mutations in nontumor tissue.     

Effects of dietary conjugated linoleic acid on DNA adduct formation of PhIP and IQ after bolus administration to female F344 rats

Meats cooked at high temperatures contain mutagenic heterocyclic amines such as 2‐amino‐l‐methyl‐6‐phenylimidazo[4,5‐b]pyridine (PhIP) and 2‐amino‐3‐methylimidazo[4,5‐f]quinoline (IQ). In female Fischer 344 rats, IQ is a multiorgan carcinogen, whereas PhIP induces mammary adenocarcinomas. For IQ and PhIP, N‐hydroxylation, catalyzed by microsomal cytochrome P‐450 1A1 and/or 1A2, and then esterification, especially O‐acetylation, are the principal steps leading to DNA adduct formation. Conjugated linoleic acid (CLA) is a mixture of conjugated linoleic acid isomers found in various meat and dairy products. We have examined the effect of dietary CLA on DNA adduct formation by PhIP and IQ in female Fischer 344 rats. Four‐week‐old animals were maintained on AIN‐76A diet without or with CLA (4% wt/wt) and treated with IQ or PhIP (50 mg/kg by gavage) after two weeks. Animals were killed (4/group) one, four, and eight days later. DNA isolated from mammary epithelial cells, liver, colon, and white blood cells was analyzed for carcinogen‐DNA adducts by ³²P‐postla‐beling assays. On Day 1, dietary CLA significantly inhibited adduct formation (82.0%) in mammary epithelial cells in IQ‐but not in PhIP‐treated rats. In the colon, dietary CLA significantly inhibited PhIP‐DNA adduct formation (18.7%) on Day 8 but increased IQ‐DNA adduct formation (30.5%) on Day 8. Dietary CLA had no effect on adduct levels in liver or white blood cells. Calf thymus DNA was incubated with N‐hydroxy‐PhIP or ‐IQ in the presence of acetyl‐CoA. Enzymatic activation was catalyzed by liver or mammary cytosol. A two‐week pretreatment with 2% (wt/wt) dietary CLA had no effect on O‐acetyltransferase‐catalyzed IQ‐ or PhIP‐DNA adduct formation. It is concluded, under certain conditions, that dietary CLA can lower IQ‐ and PhlP‐DNA adduct formation. Overall, however, the major mode of action of CLA is probably by a mechanism other than the inhibition of the N‐hydroxylation and subsequent O‐acetylation of PhIP or IQ.