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高温烹饪条件下食用油油烟中杂环胺前体物对颗粒物生成的影响及其对人肺细胞炎症反应的作用。

The effect of PhIP precursors on the generation of particulate matter in cooking oil fumes at high cooking temperatures and the inflammation response in human lung cells.

机构信息

Department of Mechanical Systems Engineering, Sookmyung Women's University, 100, Cheongpa-ro 47-gil, Yongsan-gu, Seoul, Republic of Korea.

Department of Mechanical Systems Engineering, Sookmyung Women's University, 100, Cheongpa-ro 47-gil, Yongsan-gu, Seoul, Republic of Korea.

出版信息

J Hazard Mater. 2023 Jan 5;441:129792. doi: 10.1016/j.jhazmat.2022.129792. Epub 2022 Aug 23.

DOI:10.1016/j.jhazmat.2022.129792
PMID:36084470
Abstract

Cooking Oil Fumes (COFs) contain carcinogenic organic substances such as polycyclic aromatic hydrocarbons (PAHs) and heterocyclic amines (HCAs), of which 2-Amino-1-methyl-6-phenylimidazo(4,5-b)pyridine (PhIP) is known as mainly meat-borne carcinogens. In this work, to identify the mechanisms to induce the inflammation response in human lung cells (A549) exposed to COFs, we investigated the physicochemical and biological characteristics of COFs generated with PhIP precursors (L-phenylalanine, creatinine, and glucose) at high cooking temperatures (300 °C and 600 °C). Interestingly, we found that PhIP was not formed both at 300 °C and 600 °C, while a large number of carbon nanoparticles were generated from soybean oil containing the PhIP precursors at 600 °C. From the biological analysis, COFs generated with the PhIP precursors at 600 °C induced the most significant pro-inflammatory cytokine (IL-6). This result indicates that the particulate matter in COFs generated with the PhIP precursors above the smoke temperature is the primary factor directly affecting the lung inflammatory response rather than PhIP. This study demonstrates for the first time a novel principle of the inflammatory response that the PhIP precursors can aggravate lung injury by affecting the physical properties of COFs depending on cooking temperature. Therefore, our finding is a significant result of overcoming the bias in previous studies focusing only on the chemical toxicity of PhIP in the inflammatory response of COFs.

摘要

食用油油烟(COFs)中含有致癌的有机物质,如多环芳烃(PAHs)和杂环胺(HCAs),其中 2-氨基-1-甲基-6-苯基咪唑并(4,5-b)吡啶(PhIP)被认为是主要的肉类来源的致癌物质。在这项工作中,为了确定暴露于 COFs 中的人肺细胞(A549)中炎症反应的诱导机制,我们研究了在高温烹饪条件下(300°C 和 600°C)用 PhIP 前体(L-苯丙氨酸、肌酸和葡萄糖)生成的 COFs 的物理化学和生物学特性。有趣的是,我们发现 PhIP 既不在 300°C 也不在 600°C 下形成,而在 600°C 时,含有 PhIP 前体的大豆油会产生大量的碳纳米颗粒。从生物学分析来看,用 PhIP 前体在 600°C 下生成的 COFs 会诱导产生最显著的促炎细胞因子(IL-6)。这一结果表明,高于烟雾温度的 PhIP 前体生成的 COFs 中的颗粒物质是直接影响肺部炎症反应的主要因素,而不是 PhIP。本研究首次证明了一个新的炎症反应原理,即 PhIP 前体可以通过影响 COFs 的物理性质,根据烹饪温度加重肺损伤。因此,我们的发现是克服以往研究仅关注 COFs 中 PhIP 的化学毒性的炎症反应的偏见的一个重要结果。

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