食品中杂环胺在机体中的代谢机制和减控措施的研究进展

王珠琳1*,袁莉2,武红1

1(山西工商学院 健康管理学院,山西 太原,030006)

2(陕西师范大学 食品工程与营养科学学院,陕西 西安,710119)

摘 要 杂环胺作为一类热诱导形成的有害物,广泛存在于富含蛋白质的高温加工食品中。经体内代谢活化后具有较强的致癌和致突变性,可对机体造成严重危害。该文详细综述了杂环胺的分类、在不同食品中的含量及检测方法、代谢机制、毒性作用及其减控措施,以充分揭示食品有害物杂环胺发挥毒性作用的机理,以期为其毒性控制和探索新型减控措施提供参考。

关键词 杂环胺;检测方法;代谢机制;毒性作用;减控措施

1 杂环胺概述

杂环芳香胺(heterocyclic aromatic amines,HAAs)起初是从热加工高蛋白质食物中分离出来的一类致癌、致突变性的有害物质[1-2]。后来,它们从各种环境来源中分离出来,如河水、汽车尾气颗粒、香烟烟雾、人类排泄物和雨水等。HAAs是由2~5个含氮杂环和环外氨基组成的低分子有机胺类化合物,以游离态和结合态2种不同的形式存在[3]。目前在热加工食品中已经鉴定出了30多种HAA,主要分为两大类(表1):一类是氨基咪唑氮杂芳烃类杂环胺(amino-imidazo-azaarenes,AIAs),是在加热温度为100~250 ℃,由碳水化合物、氨基酸和肌酐生成的,主要包括喹啉类(IQ)、喹喔啉类(IQx)、吡啶类(PhIP)、吡啶呋喃类(IFP)等,另一类是氨基咔类杂环胺(amino-carbolines,ACs),是在加热温度高于250 ℃,通过谷氨酸或色氨酸直接热裂解形成的,主要包括α-咔啉类、β-咔啉类、γ-咔啉类、δ-咔啉类等[4-6],常见HAA结构如图1所示。HAAs由于其分子中含有苯环或其他芳香基团,因此具有芳香性[7]。另外,由于其分子中含有多种官能团,同时具有较高的反应活性[8]

图1 常见HAAs的化学结构式
Fig.1 Chemical formula of common HAAs

表1 HAAs的分类
Table 1 Classification of HAAs

类型中文名称英文名称英文缩写AIAs喹啉类喹喔啉类吡啶类吡啶呋喃类2-氨基-3甲基咪唑并[4,5-f]喹啉2-amino-3-methylimidazo[4,5-f]quinolineIQ2-氨基-3,4-二甲基咪唑并[4,5-f]喹啉2-amino-3-dimethylimidazo[4,5-f]quinolineMeIQ2-氨基-3-甲基咪唑并[4,5-f]喹喔啉2-amino-3-methylimidazo[4,5-f]quinoxalineIQx2-氨基-3-二甲基咪唑并[4,5-f]喹喔啉2-amino-3-dimethylimidazo[4,5-f]quinoxalineMeIQx2-氨基-1-甲基-6-苯基咪唑并[4,5-b]吡啶2-amino-1-methyl-6-phenyl-imidazo[4,5-b]pyridinePhIP2-氨基-1,6-二甲基吠喃并[4,5-b]吡啶2-amino-1,6-dimethyl-furo[3,2-e]imidazo[4,5-b]pyridineIFPACsα-咔啉类β-咔啉类γ-咔啉类2-氨基-9H-吡啶并[2,3-b]吲哚2-amino-9H-pyrido[2,3-b]indoleAαC2-氨基-3-甲基-9H-吡啶并[2,3-b]吲哚2-amino-3-methyl-9H-pyrido[2,3-b]indoleMeAαC9H-吡啶并[2,3-b]吲哚9H-pyrido[2,3-b]indoleNorharman1-甲基-9H-吡啶并[2,3-b]吲哚1-methyl-9H-pyrido[2,3-b]indoleHarman3-氨基-1,4-二甲基-5H-吡啶并[4,3-b]吲哚3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indoleTr-P-13-氨基-1-甲基-5H-吡啶并[4,3-b]吲哚3-amino-1-methyl-5H-pyrido[4,3-b]indoleTr-P-2δ-咔啉类2-氨基-6-甲基二吡啶并[1,2-a:3’,2’-d]咪唑2-amino-6-methyldipyrido[1,2-a:3’,2’-d]imidazoleGlu-P-12-氨基-二吡啶并[1,2-a:3’,2’-d]咪唑2-amino-dipyrido[1,2-a:3’,2’-d]imidazoleGlu-P-2

2 杂环胺在食品中的含量及检测方法

目前检测HAA的方法主要有高效液相色谱法、高效液相色谱-质谱联用法、气相色谱-质谱联用法、荧光免疫检测、酶联免疫吸附测定法等。由于食品中HAA含量较低,较难检出,并存在耗时、消耗大量有机试剂的问题。因此研究快速、简便、安全的检测方法至关重要。不同食品中HAA的含量及检测方法如表2所示。

表2 不同食品中HAA的含量及检测方法
Table 2 HAA content and detection methodsin different foods

食品类型HAA类型含量/(ng/g)检测方法检测限参考文献熟骆驼肉MeIQx2.47±0.10PhIP4.89±0.82高效液相色谱-质谱联用法0.01~0.03 ng/g[9]炭烤羊肉IQ2.62±0.04MeIQx2.65±0.08Harman2.38±0.24Norharman6.70±0.50高效液相色谱-质谱联用法0.01~0.70 ng/g[10]烤鸭总含量41.62±5.99猪肉丸总含量22.37±3.06烤鱼总含量396.08±18.55煎牛排总含量20.87±2.04烤鸡总含量10.13±1.27荧光免疫检测0.01~0.014 μg/kg[11]焙烤花生总含量11.45~38.90高效液相色谱-质谱联用法0.009~0.046 ng/g[12]芝麻油Norharman164.91~391.79Harman164.44~228.01高效液相色谱-荧光检测法0.35 μg/kg0.28 μg/kg[13]煎香肠PhIP0.26~0.32Norharman0.86~6.82Harman1.10~2.68超高效液相色谱-串联四极杆质谱法-[14]烤马友鱼IQ0.29±0.00harman15.77±0.06气相色谱-离子迁移谱分析-[15]

续表2

食品类型HAA类型含量/(ng/g)检测方法检测限参考文献烘烤猪肉IQ0.83±0.01IQx0.71±0.02MeIQx4.27±0.04PhIP5.59±0.05Harman1.47±0.01高效液相色谱-质谱联用法-[16]红烧乳鸽MeIQx0.10~0.46PhIP0.10~0.53超高效液相色谱-四极轨道高分辨质谱0.03~0.60 μg/kg[17]炸鱼片IQ1.69±0.18MeIQx1.87±0.32PhIP2.63±0.46超高效液相色谱-质谱法0.31 ng/mL0.14 ng/mL0.36 ng/mL[18]

3 杂环胺在机体中的代谢机制

通常食品中HAA的含量以ng/g为单位进行计量,但长期摄入会对人体造成极大威胁,因此研究HAA在机体中的代谢对其毒性控制具有重要意义。根据已有研究报道,膳食摄入的不同类型HAA在机体中通过多种酶代谢,包括细胞色素 P450酶(cytochrome P450s,CYPs)、过氧化物酶(peroxidase,POD)、N-乙酰转移酶(N-acetyltransferases,NATs)、磺基转移酶(sulfotransferases,SULTs),尿甘二磷酸葡醛酸转移酶(uridine diphosphate-glucuronosyltransferases,UGTs)以及谷胱甘肽S转移酶(glutathione S-transferases,GSTs),它们的主要代谢物会进一步与DNA、蛋白质、脂肪结合,从而产生毒性作用,或通过尿液和粪便的形式排出体外[18]。以MeIQx为例,其代谢途径如图2所示。

图2 MeIQx的代谢途径
Fig.2 Metabolic pathway of MeIQx

HAAs的代谢主要包括解毒和活化[19]。首先是Ⅰ相酶的代谢,HAAs在CYPs催化作用下环外氨基的N发生氧化反应形成氮-羟基-杂环胺(N-OH-HAAs)衍生物[20]。N-OH-HAAs是一种具有遗传毒性的代谢物,它与DNA共价结合形成易于突变的DNA加合物[21]。肝脏中CYP1A2、CYP1A1和CYP1B1是催化人类HAA 环外氨基N氧化的主要CYP[22]。一项药物动力学研究,CYP1A2在人体中参与了91%的MeIQx代谢和70%的PhIP代谢[23]。PhIP被CYP1A2代谢的主要途径是通过N氧化形成具有遗传毒性的N-OH-PhIP,而MeIQx被CYP1A2代谢的主要途径是通过8-甲基氧化形成解毒产物IQx-8-COOH[24]。在啮齿类动物、非人灵长类动物和人类中,CYP对HAAs的代谢存在种间差异,这主要归因于CYP表达水平的不同、催化活性的差异以及CYP对HAA的区位选择性[25-26]

II期酶在HAAs代谢中具有双重作用,有助于解毒和生物活化[9]。II期酶(包括NATs、SULTs和UGTs)会与一些HAA环外氨基直接结合进行解毒[27]。NAT1和NAT2是两种不同的N-乙酰转移酶同工酶。NAT2主要在肝脏中表达,而NAT1主要在肝外组织中表达。许多具有致癌芳香胺结构的物质会经过NATs的代谢,例如Glu-P-1和AαC会经历NATs的N-乙酰化,而AIAs则不会被NATs代谢[28]。人体中SULTs属于一个基因超家族,分为两个亚家族:苯酚磺基转移酶(SULT1)和羟基类固醇磺基转移酶(SULT2)[29]。IQ和MeIQx在大鼠体内由SULT1A1催化形成氨基磺酸衍生物,是主要的解毒代谢物[30]。在人尿中也检测到MeIQx-N2-SO3H,也证实了SULTs的解毒作用[31]。而其他HAAs在啮齿类动物或人类中则不发生磺化作用。UGTs在机体中会参与环境中的化学物质、致癌物等葡萄糖醛酸结合反应,从而清除或灭活外源和内源性化合物。有研究报道,UGTs会通过催化IQ、PhIP、AαC等环外氨基葡萄糖醛酸化发挥解毒作用[32]。另外,II期酶也会发挥生物活化作用。在啮齿动物和非人灵长类动物体内N-OH-HAAs会被NATs或SULTs催化酯化形成活化产物,进一步异裂生成易与大分子物质(如蛋白质、DNA等)形成加合物的芳基氮离子中间物,最终导致癌症的发生[21]。大多数N-OH-HAAs可被NAT2生物激活,例如HONH-MeIQx、HONH-IQ、HONH-AαC等, SULT1A1、SULT1A2可以催化IQ、PhIP、AαC 等N-羟基代谢产物结合DNA形成加成物[33]

4 杂环胺的毒性作用

4.1 致突变作用

在人体中,HAA可激活CYP1A1和1A2的氧化作用,形成N-羟基衍生物,而这一类物质可与DNA形成加合物,从而导致 DNA受损,如DNA中的链式氢键断裂、位点突变以及DNA中的缺失和插入等,对人体的肝脏、淋巴组织等器官产生致突变性[34]。与食品中的其他诱变剂相比,HAAs具有较强的致突变性,其致突变性比黄曲霉毒素 B1高100倍,比苯并芘高2 000倍[35]。不同类型HAA的致突变能力不同,据TOTSUKA等[36]报道,AIA是高温加工肉食中存在的主要诱变剂,并证明了AIA 是沙门氏菌中迄今为止最有效的诱变剂。王一然等[37]通过Ames 氏预培养法对采用不同烹调方法的高蛋白食物进行致突变检测,发现采用不同烹调方法的食物致突变性不同,烹调温度、加热时间与致突变性成正比。LYNCH等[38]通过对Muta小鼠持续4天经口灌胃0.2、2 和 20 mg/kg剂量的PhIP,来研究PhIP在体内的致突变性,发现PhIP仅在20 mg/kg剂量时对小鼠大肠和肝脏具有致突变性。GI等[39]持续4周给雄性 F344 gpt delta 转基因大鼠分别灌胃0、0.1、1、10 或 100 mg/kg剂量的IQ,结果发现在10 和 100 mg/kg 组中,肝脏中gpt转基因突变的频率显着增加。此外,突变频率在 1、10 和 100 mg/kg组中呈剂量依赖性。

4.2 致癌作用

流行病学研究调查表明,膳食摄入HAAs与结肠癌、食道癌、胃癌、胰腺癌、前列腺癌、乳腺癌和其他癌症的风险增加相关[40]。结直肠癌的发病率取决于生活方式、环境因素、遗传和饮食[41]。接触食品源性 HAA被认为是结直肠癌发生的一个重要因素。研究发现,MeIQx与结直肠癌风险之间存在统计学上存在显著的正相关关系[42]。食道癌被认为是全世界最常见的癌症类型之一[43]。在 CROSS 等[44]的研究中,食用肉类中两种高浓度的 HAA(MeIQx 和 PhIP)与食道癌风险增加相关。另外,越来越多的证据表明饮食习惯也会影响前列腺癌的发病率[9]。在动物模型中,杂环胺与前列腺癌的风险呈正相关[45]。然而,与流行病学研究的结果并不一致,在SANDER等[45]研究发现,HAA摄入量或大量食用熟肉与前列腺癌之间不存在相关性。BOGEN等[46]研究中,在接受根治性前列腺切除术的男性中,前列腺肿瘤细胞中有较高水平的PhIP-DNA加合物,并且PhIP 增加前列腺特异性抗原水平。过度煮熟的食物产生的杂环胺在许多体外和体内测试系统中具有极强的致突变性,其中一种诱变剂PhIP可诱发大鼠乳腺肿瘤,饮食流行病学研究表明它也会增加人类患乳腺癌的风险[47-48]

4.3 神经毒性

目前大多数神经退行性疾病没有有效的治疗方法,识别和预防导致病因的可改变危险因素是减少神经退行性疾病的关键方法[49]。流行病学研究发现HAA与神经退行性疾病风险之间的存在关联性[50-51],因此研究HAA神经毒性机制具有重要意义。相关研究发现HAA主要会通过造成特定神经元群的功能障碍、活性氧的形成、氧化应激、线粒体生物能受损、线粒体功能障碍和DNA损伤等增加神经退行性疾病的患病风险[52-55]。HAA神经毒性的研究主要集中在β-咔啉类(Harman及其衍生物)。据报道,在震颤和帕金森病患者中,血液中Harman及其衍生物的浓度显着升高[56-57]。Harman会在特发性震颤患者的大脑中积聚,表明它可以穿过血脑屏障进入大脑,从而造成神经退行性疾病[58]。另外,有研究表明AIA类中 PhIP及其代谢物和其他 HAA 也具有神经毒性[59-60]。SYEDA等[49]研究团队发现HAA的暴露在细胞和动物模型中会产生与帕金森病和阿尔茨海默病相关的神经毒性。

4.4 心肌毒性

HAA除了具有致突变、致癌、神经毒性作用外,它还会造成心肌毒性,但相关研究较少[61]。DAVIS等[62]通过10 d给大鼠灌胃剂量为100 mg/kg IQ或PhIP,发现与对照组大鼠对比,IQ或PhIP处理组大鼠的心脏异常,伴有慢性炎症病灶、肌细胞坏死、肌原纤维溶解和紊乱等症状。另外,他们研究团队还发现将大鼠心肌细胞暴露N-OH-IQ或N-OH-PhIP后,心肌细胞显示异常,如肌丝损失、肌浆网肿胀和线粒体异常等[63]。这些结果表明,HAA可能在心脏退化中发挥作用。HAA毒性作用具体见图3。

图3 HAA的毒性作用
Fig.3 Toxic effects of HAA

5 杂环胺的减控措施

目前,已有研究发现加工温度、加工时间以及加工方式会在不同程度上影响食物中HAA的形成。另外,通过添加天然或合成的外源物,也会在一定程度上减少食物中HAA的含量[64]。根据相关报道,多种癌症与HAAs有关,因此应在食品加工过程中有效减少HAAs的形成,并从膳食摄入中加以控制,以促进人体健康[40]

5.1 改善加工条件

在食品加工过程中,加工温度和时间是两个关键因素,直接影响HAAs的产生和加工食品的感官属性[64]。已有研究表明,加工温度和时间与HAAs的形成呈线性正相关,通过控制加工温度和加工时间是降低食品中HAAs含量的有效途径[65]。早期毒理学研究表明,控制预先设计的加工温度和时间,可以降低从培根样品中提取的HAAs的致突变活性[66]。此外,通过热加工前微波预处理也可以降低HAAs含量。早期的研究报道,微波预处理降低了炸牛肉饼中HAA前体(包括脂肪、肌酸、肌酐、各种氨基酸和葡萄糖)的浓度,使其致突变性远低于未接受预处理的牛肉饼[67]。最近一项研究发现,在烧烤前使用微波处理相比未经微波处理,显著降低了HAA浓度,其原因可能是微波处理过程中造成水分损失,使小分子前体无法到达肉表面,无法作为HAA形成的反应物质[68]。另外,杨钊宇等[69]研究了不同种类植物油(大豆油、葵花籽油、高油酸葵花籽油、花生油、菜籽油、棕榈油)对油炸鸡肉中HAA的含量的影响,发现在相同加工温度及时间条件下,大豆油对HAA形成的促进作用大于其他5种植物油。

5.2 添加外源物

5.2.1 益生菌

在食品中添加益生菌可以起到发酵作用,提高食品品质,以及利用各种机制,如活的菌株产生特定酶、菌株细胞壁的吸附特性等去除食品中产生的有毒污染物,从而降低有毒污染物对人类身体健康的风险[70]。乳酸菌菌株作为众所周知的益生菌,可以作为抗致癌化合物的良好食品添加剂。有研究通过胃肠道模型、动物试验和临床研究发现,一些乳酸菌菌株细胞壁的肽聚糖可以通过直接物理结合,从介质环境中去除致癌化合物,并避免致癌化合物降解产生有毒次级代谢产物的再度污染。王惠汀等[71]研究结果表明,乳酸菌主要通过细胞壁上各种官能团物理吸附PhIP,并探究了乳酸菌吸附效果最佳条件为菌株浓度1010CFU/mL、pH 6、温度37 ℃、吸附时间1.5 h。

5.2.2 调味料

食品调味料经常在食品加工过程中使用,调味料的使用不仅可以提高感官属性和消费者接受度,而且有助于减少加工过程中HAAs。一些常用调味料,如黑胡椒粉、洋葱、大蒜、生姜、辣椒粉、八角和迷迭香等,已被证明可以减轻HAAs的形成。JINAP等[72]已证明当生姜添加量为4% (4 g/100 g牛肉)时可以有效地抑制烤牛肉中MeIQx和IQ的水平。王可心等[15]也研究了生姜对HAA形成的影响,发现生姜添加量为1.5%对烘烤猪肉中HAA形成抑制率最大。张漫漫[73]研究发现当八角、良姜和黑胡椒的添加量为1.5%时,对Norharman的抑制率分别为 66%、66%和 63%,可有效减少山黑猪叉烧肉中HAAs含量。华玲等[74]研究,发现添加黑胡椒可显著降低烤草鱼中HAA的生成量,但黑胡椒的添加量与其对HAA的抑制效果不存在相关性。另外,李星雨等[75]探究了5种香辛料(丁香、桂皮、花椒、草果、黑胡椒)及其主效成分对煎制猪肉中杂环胺生成的影响,发现丁香水提物及其主效成分的抑制效果最为显著,且发现香辛料对HAA的抑制作用与与其主效成分有关,但其影响程度各不相同,可能是与其他成分共同作用,抑制HAA的形成。

5.2.3 天然活性物质

多酚广泛存在于植物性食物中,具有良好的抗氧化及抗菌等生物活性,具有极高的潜在应用价值[76]。DING等[77]通过研究绿原酸、表儿茶素、芦丁、槲皮素和奎宁酸对炭烤羊肉中 HAA形成的抑制作用,发现绿原酸和表儿茶素通过与HAA前体物(葡萄糖、核糖、果糖、异亮氨酸、缬氨酸和赖氨酸)发生竞争性化学反应,极大地抑制了IQ、MeIQx、Norharman、Harman和PhIP的形成,且表儿茶素的抑制效果优于绿原酸。绿茶中富含酚类化合物,可以起到抗衰老和抗癌等作用。杨爍等[78]通过研究发现0.5%绿茶提取物对炸羊肉丸中PhIP、IQ、MeIQx、4,8-DiMeIQx有显著抑制作用,但对Harman、Norharman表现出促进作用,另外,随着绿茶提取物添加量的增加,HAA前体物的含量呈下降趋势,表明绿茶提取物可前体物的转化,抑制HAA的形成。光皮木瓜中也富含多酚,其中原花青素所占比例最高,具有强抗氧化活性。孔婉青[79]探究了光皮木瓜原花青素对煎炸鸡肉和豆腐中HAA的抑制作用,结果表明原花青素可以通过减缓食物脂质氧化,降低葡萄糖、肌酸以及氨基酸等前体物质的消耗对杂环胺的抑制呈剂量依赖性。周娜等[80]研究发现矢车菊-3-O-葡萄糖苷及其代谢物原儿茶酸可以通过减少DNA损伤和细胞凋亡修复IQ和PhIP诱导的细胞损伤,细胞损伤特别严重时则可促进细胞凋亡,减少癌变,抑制HAA毒性作用的发挥。基于桑叶中富含多种多酚化合物,XU等[81]研究了桑叶提取物对红烧番鸭中HAA形成的影响,发现酚类化合物显著抑制HAA的形成。其中,四羟基异黄酮对游离HAA具有显著抑制作用,抑制率为64.43%。另外,有研究发现山药提取物的添加也可以阻碍前体物向HAA的转化,降低烤马友鱼过程中脂肪氧化及蛋白氧化[14]。具体见表3。

表3 添加外源物对HAA毒性作用的影响
Table 3 Effect of adding foreign substances on toxicity of HAA

类型外源物名称添加量实验对象吸附率/抑制率(效果)参考文献益生菌植物乳杆菌(37X-6)1×1010CFU/mLPhIP (50 mg/L)(80.43±1.42)%戊糖片球菌(37X-15)1×1010CFU/mLPhIP (50 mg/L)(83.36±1.25)%弯曲乳杆菌(X3-1B)1×1010CFU/mLPhIP (50 mg/L)(76.96+1.04)%[71]调味料生姜八角良姜黑胡椒黑胡椒水提物4%牛肉1.5%烘烤猪肉饼55.45%1.5%山黑猪叉烧(Norharman)66%1.5%山黑猪叉烧(Norharman)66%1.5%山黑猪叉烧(Norharman)63%1.5%烤草鱼(8-MeIQx)46.91%1%烤草鱼(4,8-Di MeIQx)47.69%1.5%烤草鱼(Harman)28.97%0.05%~0.30%煎制猪肉MeIQx无明显抑制作用4,8-DiMeIQx抑制作用较弱Harman抑制作用较弱Norharman抑制作用显著(最高74.55%)PhIP未检测到[15][73][74][75]

续表3

类型外源物名称添加量实验对象吸附率/抑制率(效果)参考文献调味料丁香水提物桂皮水提物花椒水提物草果水提物0.05%~0.30%煎制猪肉MeIQx无抑制作用4,8-DiMeIQx抑制作用显著(最高51.58%)Harman抑制作用显著Norharman抑制作用显著PhIP抑制作用显著(最高89.35%)0.05%~0.30%煎制猪肉MeIQx无明显抑制作用4,8-DiMeIQx抑制作用显著(最高72.68%)Harman抑制作用显著Norharman抑制作用显著PhIP抑制作用显著(最高100%)0.05%~0.30%煎制猪肉MeIQx抑制作用显著(最高33.85%)4,8-DiMeIQx促进作用Harman无明显抑制作用Norharman无明显抑制作用PhIP无明显抑制作用0.05%~0.30%煎制猪肉MeIQx无明显抑制作用4,8-DiMeIQx抑制作用显著(22.94%)Harman抑制作用显著(53.98%)Norharman促进作用PhIP未检测到[75][75][75][75]天然活性物质绿原酸0.025~0.625 mmol/L表儿茶素0.025~0.625 mmol/L绿茶提取物0.5%光皮木瓜原花青素0.04%桑叶提取物0.3 mg/L山药提取物1%炭烤羊肉Harman 73.53~89.92%Norharman59.85~94.18%PhIP66.32~100% IQx13.74~36.64%8-MeIQx49.81~55.85%炭烤羊肉Harman 81.51~84.87%Norharman80.45~88.66%PhIP94.74~100% IQx41.98~51.53%8-MeIQx48.68~50.57%炸羊肉丸PhIP52%IQ60%MeIQx12%4, 8-DiMeIQx24%煎炸40次豆腐(总HAA)3.85%煎炸40次鸡肉(总HAA)15.89%红烧番鸭43.44%烤马友鱼Norharman59.08%Harman47.99%[77][77][78][79][81][14]矢车菊-3-O-葡萄糖苷及其代谢物原儿茶酸0~500 μmol/L500 μmol/L IQ和125 μmol/L PhIP干预HepG2细胞修复IQ和PhIP造成的细胞损伤[80]

6 总结与展望

本文详细综述了杂环胺的分类、在不同食品中的含量及检测方法、代谢机制、毒性作用及其减控措施,为未来杂环胺相关研究提供参考。由于食品中HAA的含量微少较难测得,相关检测技术仍需进一步改进,以提高灵敏度和分析结果准确度,为其相关研究奠定基础。通过改善加工条件和添加外源抑制物都可有效抑制或减少有害物生成量,未来可以继续挖掘新型抑制剂,并探究其对HAAs的形成和代谢的影响,深入研究相关机理,为开发新型减控措施提供参考。在日常饮食中,我们除了要合理膳食、均衡营养外,还需根据食物的特性选取合适的加工方式,以减少有害物的形成,避免有害物对人体产生危害。

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Research progress on metabolism mechanism and control measures of heterocyclic aromatic amines in food

WANG Zhulin1*, YUAN Li2, WU Hong1

1(Shanxi Technology and Business University, Institute of Health Management, Taiyuan, 030006, China)2(College of Food Engineering and Nutritional Science, Shaanxi Normal University, Xi’an 710119)

ABSTRACT Heterocyclic aromatic amines, as a kind of harmful substance formed by heat induction, are widely present in high-temperature processed foods rich in protein.After metabolic activation in vivo, it is highly carcinogenic and mutagenic, causing serious harm to the body.In this paper, the classification, content, and detection methods of heterocyclic aromatic amines in different foods, metabolic mechanism, toxic effects, and reduction and control measures of heterocyclic aromatic amines were reviewed in detail, to fully reveal the mechanism of toxic effects of heterocyclic aromatic amines in food and provide references for toxicity control and exploration of new reduction and control measures.

Key words heterocyclic aromatic amines;detection method;metabolic mechanism;toxic effect;control reduction measure

DOI:10.13995/j.cnki.11-1802/ts.037922

引用格式:王珠琳,袁莉,武红.食品中杂环胺在机体中的代谢机制和减控措施的研究进展[J].食品与发酵工业,2024,50(17):414-424.WANG Zhulin, YUAN Li, WU Hong.Research progress on metabolism mechanism and control measures of heterocyclic aromatic amines in food[J].Food and Fermentation Industries,2024,50(17):414-424.

第一作者:硕士,助教(通信作者, E-mail:w1115796990@163.com)

基金项目:校对重点案例研发项目(2024A1005)

收稿日期:2023-11-11,改回日期:2023-12-12