Palm oil supply chain factors impacting chlorinated precursors of 3-MCPD esters

Tiong, Soon Huat; Nair, Anusha; Wahid, Siti Aishah Abd; Saparin, Norliza; Karim, Nur Azwani Ab; Sabri, Maizatul Putri Ahmad; Zain, Mohd Zairey Md; Teh, Huey Fang; Adni, Ahmad Sarwani; Tan, Chin Ping; Lai, Oi Ming; Cheah, See Siang; Appleton, David R.

doi:10.1080/19440049.2021.1960430

Cited by 6 publications

(5 citation statements)

References 27 publications

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“…Under high temperatures, hydrochloric acid reacts with glycerol, which is hydrolyzed by triglycerides to form 3-MCPD (26). 3-MCPD has reproductive, renal and neurotoxic effects and may also have carcinogenic and mutagenic effects (26). To the best of our knowledge, however, whether 3-MCDP induces cell damage via ferroptosis in HUVECs has not been previously reported.…”

Section: Discussionmentioning

confidence: 94%

Activating autophagy and ferroptosis of 3‑Chloropropane‑1,2‑diol induces injury of human umbilical vein endothelial cells via AMPK/mTOR/ULK1

Xiao

Liu

2023

Mol Med Rep

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3-Chloropropane-1,2-diol (3-MCPD) is an internationally recognized food pollutant. 3-MCPD has reproductive, renal and neurotoxic properties. However, whether 3-MCPD induces human umbilical vein endothelial cell (HUVEC) injury has not been previously reported. In the present study, HUVECs were treated using 2 µg/ml 3-MCPD for 24 h at 37˚C. The effects of 3-MCPD on HUVEC proliferation and cell cycle arrest, death and senescence were then assessed using Cell Counting Kit-8 (CCK-8), flow cytometry and β-galactosidase staining, respectively. Whether 3-MCPD induced ferroptosis was evaluated using JC-1 and FerroOrange staining and transmission electron microscopy. A small interfering RNA targeting AMPK was used to assess whether 3-MCPD promoted ferroptosis via AMPK signaling. The results demonstrated that 3-MCPD inhibited HUVEC proliferation in a dose-dependent manner and induced cell cycle arrest. Furthermore, 3-MCPD promoted senescence in HUVECs with elevated DNA damage and cell death. The CCK-8 results demonstrated that ferroptosis and autophagy inhibitors significantly reversed cell death caused by 3-MCPD. Moreover, 3-MCPD increased mitochondrial membrane potential, which indicated that 3-MCPD contributed to mitochondrial dysfunction. 3-MCPD also markedly increased intracellular Fe 2+ levels and lipid peroxidation in HUVECs. The present study assessed the underlying mechanism by which 3-MCPD activated autophagy and ferroptosis in HUVECs. The data demonstrated that 3-MCPD significantly increased phosphorylation levels of AMPK and unc-51 like autophagy activating kinase (ULK1) but significantly decreased phosphorylation of mTOR in HUVECs. Furthermore, silencing of AMPK significantly reversed the increase in autophagy, lipid peroxidation and Fe 2+ induced by 3-MCPD. In conclusion, 3-MCPD demonstrated a significant damaging effect on HUVECs via induction of autophagy and ferroptosis; such effects may be mediated by AMPK/mTOR/ULK1 signaling. To the best of our knowledge, the present study was the first to demonstrate the mechanism of 3-MCPD-induced vascular endothelial cell injury and lays a molecular foundation for the prevention of 3-MCPD-related vascular diseases.

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Section: Discussionmentioning

confidence: 94%

Activating autophagy and ferroptosis of 3‑Chloropropane‑1,2‑diol induces injury of human umbilical vein endothelial cells via AMPK/mTOR/ULK1

Xiao

Liu

2023

Mol Med Rep

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“…Chloropropanol esters were a class of compounds formed during the processing of refined vegetable oils and are abundant in palm oil 57 . There were a number of factors that affected chloropropanol ester production, mainly including the use of inorganic chlorinated fertilizers, fruit bruising and degradation, the recycling of sterilized condensate during milling and washing, and different refining conditions 58 . It has been shown that chloropropanol esters were detected in 125 samples of edible vegetable oils.…”

Section: Discussionmentioning

confidence: 99%

“…57 There were a number of factors that affected chloropropanol ester production, mainly including the use of inorganic chlorinated fertilizers, fruit bruising and degradation, the recycling of sterilized condensate during milling and washing, and different refining conditions. 58 It has been shown that chloropropanol esters were detected in 125 samples of edible vegetable oils. The health risks caused by chloropropanol esters cannot be ignored.…”

Section: Molecular Docking Analysis Of 13-dcp and Nrf2mentioning

confidence: 99%

1,3‐Dichloro‐2‐propanol induced ferroptosis through Nrf2/ARE signaling pathway in hepatocytes

Guan

Zhang

Meng

et al. 2022

Environmental Toxicology

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1,3-Dichloro-2-propanol (1,3-DCP) is a representative chloropropane environmental contaminant with multiple toxicities. Ferroptosis is a novel iron-dependent form of regulated cell death that is closely associated with the accumulation of lipid peroxides, Fe 2+ and reactive oxygen species (ROS). In this study, we found that 1,3-DCP could induce mouse liver injury via ferroptosis. Administrating of C57BL/6J mice with 12.5, 25, and 50 mg/kg 1,3-DCP for 4 weeks via oral gavage, the data showed that 1,3-DCP exposure led to the pathological changes in mouse livers, remarkably induced accumulation of malondialdehyde (MDA) and Iron, reduction of glutathione (GSH), and changed in the expression of ferroptosis marker proteins glutathione peroxidase 4 (GPX4) and acyl-CoA synthetase-4 (ACSL4). Then, we also proved the results with HepG2 cells in vitro. The data showed that treatment 1,3-DCP significantly triggered the ferroptosis in vitro. Furthermore, we found that the ferroptosisrelated signal pathways were significantly activated in mice livers and HepG2 cells in response to 1,3-DCP exposure. The data showed that 1,3-DCP induced ferroptosis by inhibiting nuclear factor erythroid 2-related factor 2 (Nrf2) translocation into nuclear and thereby suppressing the expression of its downstream target proteins including GPX4, ferritin heavy chain (FTH), ferroportin (FPN), cystine/glutamate transporter xCT (SLC7A11), and heme oxygenase 1 (HO-1). Taken together, our findings confirmed that 1,3-DCP induced ferroptosis via the Nrf2/ARE signaling pathway in hepatocytes. Our works provide new toxicity mechanisms of 1,3-DCP with ferroptosis on hepatocytes injury.

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“…Neutralizing the FFA in crude oil using hydrogen carbonates or alkaline carbonate before deodorization can reduce the 3-MCPDE production. In addition, the bruising of oil palm fruits accelerated the action of lipase leading to an increase in DAG and FFA content in palm oil, therefore eliminating damaged fruits before the oil extraction was also effective in reducing the production of 3-MCPDE.…”

Section: Hot Research Topics On 3-mcpdementioning

confidence: 99%

Bibliometric Analysis of Research Trends on 3-Monochloropropane-1,2-Diol Esters in Foods

Wei

Liu

Zheng

et al. 2022

J. Agric. Food Chem.

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3-Monochloropropane-1,2-diol esters (3-MCPDE) are common food contaminants mainly formed in the edible oil refining process. Due to their potential hazards, 3-MCPDE has become a widespread food safety concern. In this study, CiteSpace and VOSviewer were used to conduct a bibliometric analysis on the 3-MCPDE research papers collected in the Web of Science Core Collection from 1998 to 2022. The results showed that the number of research publications on 3-MCPDE has increased rapidly since 2010. Analysis of the hotspots in 3-MCPDE studies showed that more attention has been paid to the exposure assessment, formation mechanism, detection methods, mitigation methods and toxicity, and toxicology of 3-MCPDE. Finally, the future trends of research on 3-MCPDE were analyzed and proposed. The mitigation methods and toxicology studies of 3-MCPDE are still the research hotspots in the future. In addition, nutritional intervention for 3-MCPDE toxicity will be an emerging trend.

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Palm oil supply chain factors impacting chlorinated precursors of 3-MCPD esters

Cited by 6 publications

References 27 publications

Activating autophagy and ferroptosis of 3‑Chloropropane‑1,2‑diol induces injury of human umbilical vein endothelial cells via AMPK/mTOR/ULK1

Activating autophagy and ferroptosis of 3‑Chloropropane‑1,2‑diol induces injury of human umbilical vein endothelial cells via AMPK/mTOR/ULK1

1,3‐Dichloro‐2‐propanol induced ferroptosis through Nrf2/ARE signaling pathway in hepatocytes

Bibliometric Analysis of Research Trends on 3-Monochloropropane-1,2-Diol Esters in Foods

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