School of Food Science and Technology, National Engineering Laboratory for Cereal Fermentation Technology, Collaborative Innovation Center of Food Safety and Quality Control in Jiangsu Province, Jiangnan University, 1800 Lihu Road, Wuxi, 214122, Jiangsu, People's Republic of China.
Shandong LuHua group co., LTD, Laiyang, 265200, People's Republic of China.
Lipids Health Dis. 2019 Feb 1;18(1):37. doi: 10.1186/s12944-019-0980-0.
Recently, the harmful effects of frying oil on health have been gradually realized. However, as main components of frying oils, biochemical effects of total polar compounds (TPC) on a cellular level were underestimated.
The effects of total polar compounds (TPC) in the frying oil on the lipid metabolism, oxidative stress and cytotoxicity of HepG2 cells were investigated through a series of biochemical methods, such as oil red staining, real-time polymerase chain reaction (RT-PCR), cell apoptosis and cell arrest.
Herein, we found that the survival rate of HepG2 cells treated with TPC decreased in a time and dose dependent manner, and thereby presented significant lipid deposition over the concentration of 0.5 mg/mL. TPC were also found to suppress the expression levels of PPARα, CPT1 and ACOX, elevate the expression level of MTP and cause the disorder of lipid metabolism. TPC ranged from 0 to 2 mg/mL could significantly elevate the amounts of reactive oxygen species (ROS) in HepG2 cells, and simultaneously increase the malondialdehyde (MDA) content from 21.21 ± 2.62 to 65.71 ± 4.20 μmol/mg of protein (p < 0.05) at 24 h. On the contrary, antioxidant enzymes superoxide dismutase (SOD), glutathione (GSH), and catalase (CAT) respectively decreased by 0.52-, 0.56- and 0.28-fold, when HepG2 cells were exposed to 2 mg/mL TPC for 24 h. In addition, TPC could at least partially induce the apoptosis of HepG2 cells, and the transition from G0/G1 to G2 phase in HepG2 cells was impeded.
TPC could progressively cause lipid deposition, oxidative stress and cytotoxicity, providing the theoretical support for the detrimental health effects of TPC.
最近，人们逐渐认识到食用油在高温加热过程中产生的有害物质对健康的危害。然而，作为食用油的主要成分，总极性化合物（TPC）对细胞水平的生化作用却被低估了。
通过一系列生化方法，如油红染色、实时聚合酶链反应（RT-PCR）、细胞凋亡和细胞阻滞，研究了煎炸油中的总极性化合物（TPC）对 HepG2 细胞的脂质代谢、氧化应激和细胞毒性的影响。
在这里，我们发现 TPC 处理的 HepG2 细胞的存活率随时间和剂量呈依赖性下降，当浓度为 0.5mg/mL 时，细胞表现出明显的脂质沉积。TPC 还被发现抑制了 PPARα、CPT1 和 ACOX 的表达水平，提高了 MTP 的表达水平，导致脂质代谢紊乱。浓度范围为 0 至 2mg/mL 的 TPC 可显著增加 HepG2 细胞内活性氧（ROS）的含量，并同时使丙二醛（MDA）含量从 21.21±2.62μmol/mg 蛋白增加到 65.71±4.20μmol/mg 蛋白（p<0.05）24h。相反，当 HepG2 细胞暴露于 2mg/mL TPC 24h 时，抗氧化酶超氧化物歧化酶（SOD）、谷胱甘肽（GSH）和过氧化氢酶（CAT）分别减少了 0.52、0.56 和 0.28 倍。此外，TPC 至少可以部分诱导 HepG2 细胞凋亡，并阻止 HepG2 细胞从 G0/G1 期向 G2 期的过渡。
TPC 可导致脂质沉积、氧化应激和细胞毒性，为 TPC 对健康的有害影响提供了理论依据。
