为改善食品的质量和风味,并延长食品保质期,人们通常使用热处理技术加工某些食品,传统热加工方式包括:煎、煮、蒸、炒、烧烤、烘干和油炸等[1]。在高温处理下,食物中的脂质氧化、蛋白质变性,发生美拉德反应,产生令人愉悦的香气并形成独特食品质地的同时,也产生许多有害物质,如丙烯酰胺、杂环胺、反式脂肪酸和多环芳烃等[2]。丙烯酰胺是一种白色晶体,食物中的丙烯酰胺主要由富含碳水化合物和氨基酸的食物在高温加热过程中通过美拉德反应产生[2]。1994年,国际癌症研究机构(International Agency for Research on Cancer, IARC)将丙烯酰胺列为2A类“人类可能的致癌物”[3];2002年,瑞典国家食品局(Swedish National Food Agency,SNFA)在各种油炸和焙烤食品中检测到大量丙烯酰胺[4];2015年,欧洲食品安全局(European Food Safety Authority,EFSA)将食品中丙烯酰胺的存在确定为公共卫生问题[5]。已有的动物实验和细胞实验证明,丙烯酰胺具有致癌性,可能导致DNA损伤[6],并产生生殖、神经和发育毒性[7]。大量的流行病学研究显示,较高的丙烯酰胺暴露与心血管疾病[8]、乳腺癌[9]、子宫内膜癌症[9]、卵巢癌[9]等发病风险呈正相关。鉴于丙烯酰胺的潜在危害和毒性对人类健康的严重威胁,优化食品配方、开发新型技术有效控制热加工食品中丙烯酰胺的含量,减少人群丙烯酰胺的暴露量至关重要。目前,食品科学领域主要从优化热加工工艺、添加外源性食品添加剂两方面对丙烯酰胺进行预防和控制。本文重点阐述食品热加工过程中丙烯酰胺的形成途径、膳食暴露、体内代谢、健康危害以及防控手段,为食品行业丙烯酰胺的控制提供新的见解,促进食品安全相关标准的完善,降低日常膳食丙烯酰胺暴露,从而保障人类健康。

1 热加工过程中丙烯酰胺的形成途径

当温度高于120 ℃时,蛋白质或氨基酸的氨基残基与还原糖(碳水化合物)的羰基之间发生美拉德反应,从而形成丙烯酰胺。丙烯酰胺的形成途径主要为天冬酰胺途径和丙烯醛途径[10]。

1.1 天冬酰胺途径

与美拉德反应相关联的天冬酰胺途径的具体机理见图1。天冬酰胺与羰基化合物在高于120 ℃的条件下反应生成N-糖基化物,N-糖基化物脱水生成不稳定的席夫碱(Schiff base),席夫碱可能转化为Amadori化合物或脱羧生成亚甲胺叶立德(azomethine ylide),进一步脱羧水解最终生成丙烯酰胺[11]。

图1 天冬酰胺途径生成丙烯酰胺的机制
Fig.1 Mechanisms for formation of acrylamide via asparagine pathway

1.2 丙烯醛途径

丙烯醛途径被认为与油脂氧化相关[12],机理见图2。甘油、脂肪酸发生热降解生成丙烯醛,丙烯醛通过氧化反应形成丙烯酸,丙烯酸脱去羟基与氨反应生成丙烯酰胺[13]。

图2 丙烯醛途径生成丙烯酰胺的机制
Fig.2 Mechanisms for formation of acrylamide via acrolein pathway

图3 食品热加工来源丙烯酰胺的体内代谢途径
Fig.3 In vivo metabolic pathway of acrylamide derived from food hot processing

2 热加工来源的丙烯酰胺膳食暴露和体内代谢

2.1 丙烯酰胺的膳食暴露

丙烯酰胺主要存在于富含碳水化合物和天冬酰胺的食品中,如饼干、面包、薯片、咖啡等,其中油炸、烘烤类的食品丙烯酰胺含量相对较高[14]。欧盟、世界卫生组织(World Health Organization,WHO)、EFSA建立了不同种类食品中丙烯酰胺含量的数据库,部分数据见表1[14-17]。

表1 不同类别食品中丙烯酰胺的含量

Tab.1 Acrylamide content in different types of food μg/kg

食品类别调查量/种中位数平均值第95百分位水平基准水平面包和饼干类小麦面包302153812050其他面包992546203100饼干和威化饼682103201810350薄饼162183231590400酥脆面包4378989428350姜饼6931551551600800咖啡类烘焙咖啡566203203563400速溶咖啡1166206201333850马铃薯制品类炸薯片3781961961115500薯片和小吃8003893891841750其他麸皮制品和全谷物151135135413300非全谷物或非麸皮小麦和黑麦产品33140140-300非全谷物或非麸皮玉米、燕麦、斯佩尔特小麦大麦和大米产品1495050230150以谷类为基础的婴儿食品394151520040巧克力粉27575--鱼和海鲜、碎屑、捣碎产品43535--烤坚果和水果1452525--

由表1可知,咖啡和马铃薯制品中的丙烯酰胺含量较高。鉴于饮食的个体差异和多样性,整合评估不同地域丙烯酰胺的膳食暴露量显得尤为重要。高菲[18]分别统计评估了不同国家及中国不同区域的丙烯酰胺膳食暴露量。研究发现,中国人群的丙烯酰胺日均摄入量较低,这可能与我国烹饪方式与饮食习惯相关[19]。农村区域每日人均丙烯酰胺膳食暴露量高于城市区域,我国辽宁省、黑龙江省的薯类食物摄入量远高于其他地区,每日人均丙烯酰胺膳食暴露量相对较高,第六次中国总膳食研究评估了12种食物对丙烯酰胺总体膳食暴露的累加,计算所得的暴露边界值(margin of exposure, MOE)为1142,远低于EFSA的结论值[19]。该研究结果表明,丙烯酰胺对人类潜在的健康危害仍然显著,采用合理的方法对热加工来源的丙烯酰胺进行监测防控显得尤为重要。

2.2 丙烯酰胺的体内代谢

经口摄入的丙烯酰胺会被机体迅速吸收,在肝脏、心脏、肾脏、大脑、胎盘及乳汁中均有丙烯酰胺检出[20]。丙烯酰胺在人体内的代谢途径主要包括两种,见图 3。丙烯酰胺进入人体后,在细胞色素P450酶系的作用下,转化为环氧丙酰胺(glycidamide, GA),GA通过环氧化物水解酶转化成无毒的甘油酰胺,这一步通常被认为是丙烯酰胺的解毒途径[21]。在谷胱甘肽-S-转移酶(glutathione S-transferase, GST)的作用下,AA或GA可以与谷胱甘肽(glutathione, GSH)偶联,通过后续降解过程转化为巯基尿酸加合物,包括N-乙酰-S-(2-氨基甲酰乙基)-L-半胱氨酸(AAMA)、N-乙酰-S-(2-氨基甲酰乙基)-L-半胱氨酰亚砜(AAMA-sul)、N-(R,S)-乙酰-S-(2-氨基甲酰-2-羟乙基)-L-半胱氨酸(GAMA)以及N-乙酰-S-(1-氨基甲酰-2-羟乙基)-L-半胱氨酸(iso-GAMA),通过尿液排出体外; AA和GA也能够与DNA上的鸟嘌呤形成特定加合物,导致基因突变和损伤。AA形成的DNA加合物主要有N1-(2-羧基-2-羟乙基)-2′-脱氧腺苷(N1-GA-dA)、N3-(2-氨基甲酰-2-羟乙基)腺嘌呤(N3-GA-Ade)、N7-(2-氨基甲酰-2-羟乙基)鸟嘌呤(N7-GA-Gua)以及N6-(2-羧基-2-羟乙基)-2′-脱氧腺苷(N6-GA-dA)[22];除此以外,AA和GA可与血红蛋白(Hb)末端的缬氨酸结合,形成稳定的加合物(HbAA和HbGA),这被视做人群暴露的重要生物标志物[21]。

3 丙烯酰胺的毒性及危害

食物来源的丙烯酰胺与健康危害密切相关,以往的研究揭示了丙烯酰胺的经口半数致死量,大鼠、小鼠和兔急性毒性实验显示丙烯酰胺经口LD50为 150～180 mg/kg[23]。人类经口急性中毒后,多表现为胃肠道和中枢神经系统功能障碍,以及行走困难、痛触觉减退等周围神经损伤表现。其主要健康危害可归纳为神经毒性、生殖毒性、遗传毒性。

3.1 神经毒性

近年来,丙烯酰胺能够诱导产生神经毒性已被充分证实,流行病学研究显示,高剂量AA职业暴露人群出现较为明显的神经毒性作用[24]。LoPachin等[25]将大鼠暴露于丙烯酰胺,发现较低和较高的丙烯酰胺暴露剂量都使大鼠产生神经功能障碍,较高丙烯酰胺暴露组的大鼠染毒约8 d后产生中度神经毒性,较低丙烯酰胺暴露组的大鼠约在26 d后产生中度神经毒性。以往的研究也表明,丙烯酰胺会通过血脑屏障进入脑组织引发神经毒性。Yao等[26]检查了血脑脊液屏障的通透性,以及它分泌转甲状腺素蛋白和运输暴露于丙烯酰胺 7、14、21、28 d的大鼠瘦素的能力,最终的结果表明丙烯酰胺暴露会损害血脑脊液屏障并损害分泌和运输功能,这些损伤可能是丙烯酰胺诱导神经毒性的基础。随着研究的深入,丙烯酰胺诱导神经毒性的机制主要归纳为氧化应激、细胞凋亡、细胞自噬、肠道稳态等方面[27]。

3.1.1 氧化应激

丙烯酰胺或环氧丙酰胺与谷胱甘肽结合,导致谷胱甘肽损失和细胞氧化还原状态的紊乱,从而过量产生活性氧(reactive oxygen species, ROS)[27]。ROS作为氧化应激的主要诱导物,正常情况下会被机体中的超氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase, GPx)和过氧化氢酶(catalase, CAT)或谷胱甘肽(glutathione, GSH)、黄酮类化合物、多酚类化合物(儿茶素、酚酸)、抗坏血酸(维生素C)或α-生育酚等抗氧化物清除[28]。丙烯酰胺通过激活多种信号通路,导致GSH消耗、ROS积累,进而产生氧化损伤导致神经毒性。

丝裂原活化蛋白激酶(mitogen-activated protein kinase, MAPK),包括应激激活的p38 丝裂原活化蛋白激酶(p38 mitogen-activated protein kinase, p38 MAPK)、细胞外信号调节激酶(extracellular signal-regulated kinase, ERK)和c-Jun N末端激酶(c-Jun N-terminal kinase,JNK)。MAPK通路在各种刺激诱导的细胞增殖和凋亡中起着重要作用。Nan等[29]对HepG2 细胞进行处理,发现丙烯酰胺在HepG2 细胞中诱导氧化应激和内质网应激反应,并伴有MAPK信号通路的激活。Nan等[30]还发现在Kupffer细胞中,丙烯酰胺诱导活性氧过度产生,伴随着MAPK通路激活,导致NLRP3 炎症小体形成,并最终增加IL-1β和IL-18的释放。

核因子红细胞系2相关因子2(Nrf 2)是细胞抗氧化的重要因子,Keap 1/Nrf 2轴是细胞抗氧化应激的主要防御机制之一[31]。Davuljigari等[31]发现暴露于丙烯酰胺的小鼠产生神经毒性,出现后肢功能障碍、单胺能轴突变性以及肝毒性,但通过萝卜硫素干预后,Nrf 2 信号通路被激活,进而减轻丙烯酰胺的毒性作用。

NF-κB通路可以调节炎症反应、氧化应激和细胞凋亡,在神经毒性中起着至关重要的作用。Qiang等[32]发现长期高脂饮食加剧了丙烯酰胺暴露小鼠的运动功能障碍和脊髓运动神经元的损伤;丙烯酰胺暴露和高脂饮食共同导致脊髓神经元线粒体的形态变化,并且高脂饮食显著加剧了丙烯酰胺诱导的NF-κB、NLRP 3炎症小体和cGAS-STING通路的激活。

PI3K/Akt信号通路与细胞增殖、凋亡和细胞防御相关[33]。Thabet等[33]通过动物实验证明PI3K/Akt/GSK-3β/Nrf 2途径的激活提供了对丙烯酰胺或γ-辐射诱导的神经毒性的保护作用。

3.1.2 细胞自噬

自噬-溶酶体途径包括相关基因的启动,将细胞质溶酶体与自噬体融合,以及自溶酶体的降解,其对于维持细胞稳态、预防丙烯酰胺诱导的神经毒性作用至关重要[34]。Yang等[34]发现丙烯酰胺诱导的自噬激活伴随着自噬底物P62 的积累,以及自噬-溶酶体途径失调可能会导致丙烯酰胺诱导的细胞凋亡和NLRP3 炎症体通路激活发生。Pang等[35]的研究结果显示,丙烯酰胺暴露导致了溶酶体功能障碍,减少了LAMP1和成熟组织蛋白酶D的数量,并导致泛素化蛋白的积累。此外,丙烯酰胺还通过降低Bcl-2表达、增加Bax和裂解的caspase-3表达以及提高凋亡率来增加细胞凋亡。

3.1.3 肠道稳态

以往的研究显示肠道微生物群结构的改变与认知功能、焦虑、抑郁和孤独症谱系障碍密切相关[36]。Tan等[37]通过小鼠实验证明丙烯酰胺通过影响肠屏障的完整性和增加循环LPS、IL-1和TNF-α的水平来刺激脑部炎症反应。Ye等[36]的研究发现,丙烯酰胺会诱导青春期小鼠产生认知和情绪障碍,而α-硫辛酸显著影响了与孤独症和抑郁症相关的细菌的数量,同时提高了粪便样本中的短链脂肪酸水平,并诱导了血清氨基酸浓度的变化从而改善由丙烯酰胺引起的认知缺陷。

3.2 生殖毒性

早期研究显示,丙烯酰胺及其代谢物缩水甘油酰胺与多巴胺受体和精子细胞精蛋白结合,抑制驱动蛋白和动力蛋白的活性,干扰神经元细胞内运输和精子运动;低剂量的丙烯酰胺会减少啮齿动物同窝仔数,较高剂量的丙烯酰胺会影响精子形态和运动能力从而降低交配频率[38]。最新的研究显示,在检测皱叶欧芹甲醇提取物对丙烯酰胺诱导的雄性大鼠生殖功能障碍的保护作用的过程中,发现丙烯酰胺降低睾酮水平,提高睾丸丙二醛水平,降低超氧化物歧化酶活性,并对精子造成损伤[39]。此外,丙烯酰胺诱导TNF-α水平升高,类固醇生成急性调节蛋白和细胞色素P450scc水平降低,并上调NF-κB P65 的表达,下调驱动蛋白的表达,说明丙烯酰胺也能通过氧化损伤和炎症途径产生生殖毒性。

3.3 遗传毒性

已有的研究表明,丙烯酰胺长期暴露会导致染色体和微核畸变,从而诱导DNA损伤,进而导致肿瘤。Baum等[40]比较了V79 细胞中,丙烯酰胺和环氧丙酰胺的诱变潜力,发现环氧丙酰胺在浓度为800 μmol/L或更高时显示出对突变的浓度依赖性诱导,但在丙烯酰胺浓度高达6 000 μmol/L时未发现显著的遗传毒性或致突变性。Puppel等[41]在高浓度丙烯酰胺(6 mmol/L)中孵育24 h后,在V79和Caco-2细胞中观察到DNA显著增加的轻微损伤。

4 丙烯酰胺的防控

尽管检测技术在日常监控丙烯酰胺含量方面发挥了重要作用,但要降低食品中丙烯酰胺含量,仍需从源头入手,采用有效的防控手段保障食品安全。目前常用的控制措施主要包括选择合适的原料、改进加工工艺以及添加外源性物质。

选择还原糖含量、游离氨基酸含量和天冬酰胺含量相对较低的食品原料可以在一定程度上从源头降低丙烯酰胺的含量。Becalski等[42]的研究发现,选择还原糖含量低的原料能够有效控制薯片中的丙烯酰胺含量。

加工工艺层面对丙烯酰胺进行控制包括原料预处理、控制加工温度和时间。对食物进行微波预处理,可以让食物短时间达到较高的温度,减少了加热时间,有效降低丙烯酰胺的生成[10]。Tuta等[43]证明微波预解冻冷冻能明显降低油炸薯条中丙烯酰胺的含量。除此以外,热烫有助于降低原料中还原糖的含量,在一定程度上抑制美拉德反应。Viklund等[44]研究了焯水对马铃薯中还原糖、天冬酰胺浓度和丙烯酰胺含量的影响,最终发现焯水可使丙烯酰胺含量降低51%～73%。热处理的时间和温度也对丙烯酰胺的形成至关重要。Tepe等[45]研究了不同加热温度和加热时间组合下丙烯酰胺含量的动力学参数,发现随着油炸温度和时间的增加,两个马铃薯品种中丙烯酰胺的形成增加。

已有的研究表明,香辛料提取物、植物多酚、氨基酸和一些亲水胶体都可有效抑制丙烯酰胺的生成[46]。王来钊[47]的研究显示,表儿茶素(EC)和表没食子儿茶素没食子酸酯(EGCG)在丙烯酰胺形成阶段抑制作用显著。章宇[48]以富含生物黄酮的竹叶抗氧化物(AOB)和绿茶提取物(EGT)两种植物黄酮制剂为研究对象,证明其对油炸薯片、炸鸡翅和油条中丙烯酰胺的抑制作用。程军等[49]研究了包括杨梅素、山柰酚、槲皮素、芦丁在内的6种黄酮醇对美拉德反应中丙烯酰胺形成的抑制作用和量效关系,得出抑制丙烯酰胺形成的最佳作用浓度。除此以外,近年来也有研究使用微生物来源的酶对丙烯酰胺进行缓解控制。Dias等[50]从米曲霉中获取了高效的L-天冬酰胺酶,可以减少炸薯条中72%丙烯酰胺的生成。

5 展 望

既往研究表明,丙烯酰胺的危害及防控已成为食品安全领域的重要课题。通过优化食品加工工艺、改进烹饪方法以及选择合适的原料,可以有效降低食品中丙烯酰胺的含量。尽管随着研究的深入,近年来热加工食品中丙烯酰胺的含量已得到有效的控制,但未来仍需时刻关注丙烯酰胺的防控,如利用生物技术改良原料作物以减少丙烯酰胺前体物质的形成,开发新型食品添加剂以阻断丙烯酰胺的生成途径,以及应用先进的食品加工技术,例如非热加工技术,以减少加工过程中丙烯酰胺的生成。此外,还需进一步开展丙烯酰胺的膳食暴露评估和体内代谢研究,建立更为完善的膳食暴露评估模型,结合不同人群的饮食习惯和代谢特征,更准确地评估丙烯酰胺对健康的影响,为风险评估和个性化防控策略的制定提供重要依据。最后,综合性防控措施的研究与应用仍需重视,通过多种手段的结合,探索能够有效降低食品中丙烯酰胺含量的综合性防控策略,并将防控手段实际应用到生产,在显著降低食品中丙烯酰胺含量的同时,保持或提升食品的营养价值和感官特性,推动食品工业健康发展。

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Research Progress on Source, Hazards, and Prevention and Control of Acrylamide From Thermal Processed Food

ZHANG Yu, ZENG Jia, WAN Xuzhi

(College of Biosystems Engineering and Food Science,Zhejiang University,Hangzhou 310058,China)

Abstract：Acrylamide is a typical food contaminant widely present in fried, baked, and other thermal processed foods. Dietary exposure to acrylamide is closely associated with the risk of diseases such as cardiovascular diseases and breast cancer. The International Agency for Research on Cancer has classified it as a Group 2A “probable human carcinogen”. Considering the potential harm and toxic threats of acrylamide posed to human health, it was crucial to optimize food formulations and develop new technologies to effectively control acrylamide levels in thermal processed foods and reduce human exposure. The research progress on acrylamide formation pathways during food heat processing, dietary exposure, metabolism in the body, health risks, and prevention and control measures were summarized. Acrylamide was primarily formed through the Maillard reaction under high-temperature conditions, especially in foods rich in reducing sugars and amino acids. Its content was significantly influenced by food composition and processing conditions. The main formation pathways of acrylamide were the asparagine pathway and the acrolein pathway.Acrylamide from food sources was closely related to health risks. Due to its complex metabolic pathways in the human body, it might cause neurotoxicity, reproductive toxicity, and genotoxicity and was potentially associated with cancer development. In the field of food science, preventive and control measures for acrylamide mainly focus on optimizing thermal processing techniques and adding exogenous food additives.By integrating raw material selection, process optimization, and the addition of exogenous substances, effective strategies for reducing acrylamide levels were explored and analyzes key directions for future research were analyzed in this study. The goal was to provide a scientific basis for inhibiting acrylamide formation during food processing, supporting the healthy development of the food industry, and ensuring consumer dietary safety.

Keywords：acrylamide; formation mechanism; dietary exposure; toxicological mechanism; prevention and control strategies

doi：10.12301/spxb202400494

文章编号：2095-6002(2024)06-0015-10

引用格式：章宇,曾嘉,万旭志.热加工食品中丙烯酰胺的来源、危害及防控措施研究进展[J]. 食品科学技术学报,2024,42(6):15-24.

ZHANG Yu,ZENG Jia,WAN Xuzhi. Research progress on source, hazards, and prevention and control of acrylamide from thermal processed food[J]. Journal of Food Science and Technology, 2024,42(6):15-24.

中图分类号：TS201.2

文献标志码：A

收稿日期：2024-07-30

基金项目：国家重点研发计划项目(2023YFF1105300)。

Foundation： National Key Research and Development Program of China (2023YFF1105300).

第一作者：章 宇,男,教授,博士生导师,主要从事食品加工来源污染物危害控制方面的研究。

(责任编辑：李 宁)