School of Food Science and Engineering, Yangzhou University, Yangzhou 225127, China.
School of Tourism and Cuisine, Yangzhou University, Yangzhou 225127, China.
Food Res Int. 2024 Feb;178:113988. doi: 10.1016/j.foodres.2024.113988. Epub 2024 Jan 7.
Polycyclic aromatic hydrocarbons (PAHs), a widespread class of food pollutants, are commonly exposed to humans along with edible oil. The dietary exposure pattern of PAH4 was simulated to study the toxicity and oxidative stress of oil-based PAH4 on hepatocytes. The findings demonstrated that oil-based PAH4 induced cell viability and mitochondrial membrane potential decreased and promoted apoptosis and oxidative stress in a concentration-dependent manner. Benzo[a]pyrene had the strongest toxicity and HL-7702 cells were more sensitive to toxicity than HepG2 cells, due to differences in induced CYP1A enzyme activity. Oil-based PAH4 had greater cytotoxicity than PAH4, attributed to the synergistic effect of oil and PAH4. Furthermore, oil-based PAH4 induced oxidative stress in HepG2 and HL-7702 cells through the same AHR-Nrf2-KEAP1 pathway, which was elucidated by detecting genes and proteins expression. This study lays the foundation for elucidating the harm of dietary exposure to PAHs and reminds us that food composition may increase the harm of PAHs.
多环芳烃(PAHs)是一类广泛存在的食品污染物,常与食用油一起被人类摄入。本研究模拟了膳食中多环芳烃(PAH4)的暴露模式,以研究油基 PAH4 对肝细胞的毒性和氧化应激作用。结果表明,油基 PAH4 呈浓度依赖性诱导细胞活力和线粒体膜电位降低,并促进细胞凋亡和氧化应激。苯并[a]芘具有最强的毒性,HL-7702 细胞比 HepG2 细胞对毒性更敏感,这归因于诱导的 CYP1A 酶活性的差异。油基 PAH4 的细胞毒性大于 PAH4,这归因于油和 PAH4 的协同作用。此外,油基 PAH4 通过相同的 AHR-Nrf2-KEAP1 通路诱导 HepG2 和 HL-7702 细胞发生氧化应激,这可通过检测基因和蛋白表达来阐明。本研究为阐明膳食暴露多环芳烃的危害奠定了基础,并提醒我们食物成分可能会增加多环芳烃的危害。