Investigation of DNA damage of glycidol and glycidol fatty acid esters using Fpg-modified comet assay

Inagaki, Ryo; Uchino, Kohei; Shimamura, Yuko; Masuda, S.

doi:10.2131/fts.6.9

Cited by 6 publications

(5 citation statements)

References 14 publications

(20 reference statements)

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“…The glycidol induce ROS by damaging DNA and proteins in the cells as the epoxide group of the glycidol may react with the macromolecules in the cells (Sevim et al, 2021). The epoxide group of the glycidol have the ability to react with the nucleophilic biomolecules such as protein in the cells that may triggers ROS production (Inagaki et al, 2019). ROS level of treated 116 cells with R-and S-glycidol (Figure 2) had shown that both chemicals are able to induce oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Selective Cytotoxicity Effects of R-Glycidol and S-Glycidol on Vero and HCT 116 Cells in Evaluating the Incidence of Glycidyl Esters in Edible Oils and Fats

NOR MAHIRAN1

2023

JOPR

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Despite their feasibility as food flavouring, glycidol is classified as a probable carcinogen under group 2A by WHO. The cytotoxicity effects of isomers of R-and S-glycidol on African green monkey kidney normal cell lines (Vero) and human colon cancer cell line (HCT 116) remain unclear. Cell viability of the treated Vero and HCT 116 cells was determined using the AlamarBlue® assay. Dichlorodihydrofluorescein diacetate (DCFDA) was used to evaluate reactive oxygen species (ROS) activity. Protein expressions of ERK ½, p-ERK, Bcl-2 and caspase-3 were investigated using western blotting technique. The findings indicated that R-and S-glycidol (1.16 µg/mL) exposure dramatically reduced the cell viability of the treated HCT cells but was slightly cytotoxic to Vero cells, hence triggering ROS activity. R-and S-glycidol cause down-regulation of ERK ½, p-ERK, and BCL-2 protein expression at 48 h of treatment. Furthermore, bothR-and S-glycidol possess close interaction in proximity to 3D-structure of human ERK and p-ERK protein receptors. In conclusion, Rand S-glycidol potentially triggered oxidative stress and affected ERK protein phosphorylation, leading to caspase-3 independent cell death of the treated HCT 166 cells, suggesting that lower doses (<1.16 µg/mL) of Rand S-glycidol are safe for human consumption.

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Section: Discussionmentioning

confidence: 99%

Selective Cytotoxicity Effects of R-Glycidol and S-Glycidol on Vero and HCT 116 Cells in Evaluating the Incidence of Glycidyl Esters in Edible Oils and Fats

NOR MAHIRAN1

2023

JOPR

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“…Micronucleus induction has been confirmed in the bone marrow cells of ICR mice exposed to glycidol using micronucleus test [ 4 ]. Oxidative DNA damaging potency of glycidol in the comet assay was reported using Fpg-modified comet assay [ 5 ]. Therefore, diHOPrVal, the Hb adduct of glycidol, has been used as a biomarker that can assess exposure to GEs and glycidol [ 10 , 11 , 12 , 13 ].…”

Section: Discussionmentioning

confidence: 99%

“…GEs, which have fatty acid in their structure, are degraded by lipase, a lipolytic enzyme, consequently producing glycidol (2,3-epoxy-1-propanol) when ingested by the body through the diet ( Figure 1 ) [ 2 ]. Glycidol is known as a genotoxic epoxide compound and has been reported to induce carcinogenicity [ 3 , 4 , 5 ], chromosomal aberration induction, neurotoxicity, and mutagenicity [ 6 , 7 , 8 , 9 ]. In view of the genotoxic and carcinogenic potential of glycidol, it is important to assess the exposure of GEs to humans from the food and environment for public health perspective.…”

Section: Introductionmentioning

confidence: 99%

Potential Role of Lipase Activity on the Internal Exposure Assessment of Glycidol Released from Its Fatty Acid Esters

Shimamura

Inagaki

Oike

et al. 2023

Toxics

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Glycidyl fatty acid esters (GEs) can be found in food, and they can be converted into genotoxic animal carcinogen glycidol in vivo by the action of lipase. This study examined whether human ingestion of charbroiled pork containing high levels of GEs (300 µg/day) increased glycidol–hemoglobin adduct (diHOPrVal), a marker of internal exposure to glycidol using LC-MS/MS. Contrary to expectation, the diHOPrVal value before ingesting charbroiled pork was 3.11 ± 1.10 pmol/g globin, which slightly decreased to 2.48 ± 0.47 pmol/g globin after 5 days of consumption. The decrease in lipase activity caused by the continuous consumption of lipid-rich foods such as meat in humans might decrease internal exposure to glycidol released from its esters. Thus, lipase activity was measured in C57/BL6J mice fed a high-fat diet (HFD) for 8 weeks, and diHOPrVal formation was measured after the administration of glycidyl oleate. Lipase activity was significantly lower in the HFD group than in the normal diet group. The amount of diHOPrVal was reduced in the HFD group. Therefore, the lipase activity was reduced by HFD, thereby decreasing the degradation of glycidol from glycidyl oleate. These results indicate that changes in lipase activity depending on the amount of lipids in the diet may affect the assessment of GEs exposure, and monitoring the lipase activity would provide a comprehensive understanding of exposure assessment.

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“…Glycidyl esters (GE or GEs) are thermal processing hazards that are mainly formed from diacylglycerol during deodorization of refined vegetable oils due to high temperature (>200 °C). , When ingested with edible oil, GEs can be rapidly digested by the gastrointestinal tract to form glycidol, which has been classified as a “group 2A” carcinogen (probably carcinogenic to humans) by the International Agency for Research on Cancer (IARC) . Recently, GEs have also been confirmed that they present a significant genetic damage in the kidney, liver, and blood of mice . It has been well known that GEs are widely found in refined vegetable oils, particularly in palm oil and rice oil, and even also detected in infant formula and baby food products containing refined vegetable oils. , Consequently, more and more researchers have been focusing on studying the formation and inhibition of GEs in refined vegetable oils in recent years.…”

Section: Introductionmentioning

confidence: 99%

“…4 Recently, GEs have also been confirmed that they present a significant genetic damage in the kidney, liver, and blood of mice. 5 It has been well known that GEs are widely found in refined vegetable oils, particularly in palm oil and rice oil, 6 and even also detected in infant formula and baby food products containing refined vegetable oils. 7,8 Consequently, more and more researchers have been focusing on studying the formation and inhibition of GEs in refined vegetable oils in recent years.…”

Section: ■ Introductionmentioning

confidence: 99%

Kinetic Study and Degradation Mechanism of Glycidyl Esters in both Palm Oil and Chemical Models during High-Temperature Heating

Cheng

Liu

Guo

et al. 2020

J. Agric. Food Chem.

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A kinetic model for glycidyl ester (GE) formation in both palm oil and chemical models during high-temperature heating was built to investigate the formation and degradation mechanisms of GEs in refined palm oil. The results showed that the formation and degradation of GEs followed pseudo-first-order reactions, and the rate constants of reaction kinetics followed the Arrhenius equation. The estimated activation energy of the GE degradation reaction (12.87 kJ/mol) was significantly lower than that of the GE formation reaction (34.58 kJ/mol), suggesting that GE degradation occurred more readily than formation. The Fourier transform infrared (FTIR) band intensities of epoxy and ester carboxyl groups decreased over heating time, while no band assigned to the cyclic acyloxonium group was found. Furthermore, no 5,5-dimethyl-1-pyrroline N-oxide (DMPO)-cyclic acyloxonium radical adduct was detected by quadrupole time-of-flight mass spectrometry (Q-TOF-MS). The above findings indicated that GEs were decomposed, fatty acid was also liberated, and GE degradation did not involve a cyclic acyloxonium intermediate. GEs were primarily decomposed into monoacylglycerol via ring-opening reaction during heating followed by fatty acid and glycerol via hydrolysis reaction.

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Investigation of DNA damage of glycidol and glycidol fatty acid esters using Fpg-modified comet assay

Cited by 6 publications

References 14 publications

Selective Cytotoxicity Effects of R-Glycidol and S-Glycidol on Vero and HCT 116 Cells in Evaluating the Incidence of Glycidyl Esters in Edible Oils and Fats

Selective Cytotoxicity Effects of R-Glycidol and S-Glycidol on Vero and HCT 116 Cells in Evaluating the Incidence of Glycidyl Esters in Edible Oils and Fats

Potential Role of Lipase Activity on the Internal Exposure Assessment of Glycidol Released from Its Fatty Acid Esters

Kinetic Study and Degradation Mechanism of Glycidyl Esters in both Palm Oil and Chemical Models during High-Temperature Heating

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