Apoptosis is induced by sub-acute exposure to 3-MCPD and glycidol on Wistar Albino rat brain cells

Sevim, Çiğdem; Özkaraca, Mustafa; Kara, Mehtap; Ulaş, Nergis; Mendil, Ali Sefa; Margină, Denisa; Tsatsakis, Aristidis

doi:10.1016/j.etap.2021.103735

Cited by 7 publications

(7 citation statements)

References 29 publications

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“…In addition to renal and testicular toxicity, hepatotoxicity, pulmonary toxicity, immunotoxicity, and neurotoxicity caused by 3-MCPDE have also been reported. − The investigation on the absorption, distribution, and metabolism of 3-MCPDE in rats showed that 3-MCPD 1-palmitate can be directly absorbed and metabolized in vivo . In terms of hepatotoxicity, liver function impairment and histopathological changes have been demonstrated by the studies of the 3-MCPDE toxicity.…”

Section: Hot Research Topics On 3-mcpdementioning

confidence: 99%

“…Second, increasing studies have shown that the kidney is not the only target organ of 3-MCPDE. − It is recommended that the toxicity of 3-MCPDE should be further investigated by animal experiments. Moreover, most studies are based on the premise that 3-MCPDE can be fully hydrolyzed into 3-MCPD, which may introduce uncertainty into toxicology studies of 3-MCPDE.…”

Section: Trends In Future Studymentioning

confidence: 99%

“…3-MCPDE can be hydrolyzed to its free form 3-MCPD by lipase in the intestinal tract. By exploring the toxic effects, 3-MCPD and its esters have been demonstrated to be nephrotoxic, testicular toxic, and hepatotoxic, and free 3-MCPD has even been considered to be a nongenotoxic carcinogen (group 2B). − However, at present, the formation of 3-MCPDE in refined edible oils has not been industrially controlled. Therefore, ingestion of 3-MCPDE from the daily diet is inevitable.…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Hot Research Topics On 3-mcpdementioning

confidence: 99%

Section: Trends In Future Studymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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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“…The cytotoxicity of 3-MCPD has been widely reported in different systems (21,(37)(38)(39). For example, 3-MCPD has been reported to trigger the death of 293 cells via the death receptor and the mitochondrial pathway (37).…”

Section: Fundingmentioning

confidence: 99%

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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“…Inappropriate apoptosis or increased rate of apoptosis of endothelial cells has been reported to play a deleterious role in the development of common vascular diseases, including atherosclerosis ( Dimmeler and Zeiher, 2000 ; Hao et al, 2021 ; Hou et al, 2019 ; Mallat and Tedgui, 2000 ; Yao et al, 2021 ). Glycidol has been found to induce apoptosis in Wistar Albino rat brain cells ( Sevim et al, 2021 ). Autophagy is a lysosome-dependent cellular degradation program by which cells utilize lysosomes to degrade their excess or damaged macromolecules and organelles, and the degradation products can be recycled by cells for further use.…”

Section: Introductionmentioning

confidence: 99%

Apigenin and its octoic acid diester attenuated glycidol-induced autophagic-dependent apoptosis via inhibiting the ERK/JNK/p38 signaling pathways in human umbilical vein endothelial cells (HUVECs)

Zhao

Jiang

Guo

et al. 2023

Current Research in Food Science

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Apoptosis is induced by sub-acute exposure to 3-MCPD and glycidol on Wistar Albino rat brain cells

Cited by 7 publications

References 29 publications

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

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

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

Apigenin and its octoic acid diester attenuated glycidol-induced autophagic-dependent apoptosis via inhibiting the ERK/JNK/p38 signaling pathways in human umbilical vein endothelial cells (HUVECs)

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