Characterization of Electron Ionization Mass Spectral (EIMS) Fragmentation Patterns of Chloropropanol Esters of Palmitic Acid Using Isotope Labeling Technique

Rahn, Anja; Yaylayan, Varoujan A.

doi:10.5650/jos.ess14117

Cited by 2 publications

(1 citation statement)

References 11 publications

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“…In recent years, chloropropanol esters can be generated in the frying process at high temperatures and have become a focus of food toxicology. Large quantities of chloropropanol esters have been found in daily food. , Chloropropanols derived from the degradation of chloropropanol esters by intestinal lipase further increase their exposure dose and pose a threat to food safety . Exposure to 1,3-DCP could be more dangerous than previously estimated.…”

Section: Introductionmentioning

confidence: 99%

1,3-Dichloro-2-propanol-Induced Renal Tubular Cell Necroptosis through the ROS/RIPK3/MLKL Pathway

Fan

Lü

et al. 2022

J. Agric. Food Chem.

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1,3-Dichloro-2-propanol (1,3-DCP), as a food pollutant, exists in a variety of foods. Studies have shown that it has nephrotoxicity. In the study, we found that 1,3-DCP caused renal injury with necroptosis in C57BL/6J mice. The mechanism of 1,3-DCP-caused nephrotoxicity was further explored in NRK-52E cells in vitro. We found that 1,3-DCP caused cell necroptosis with the increase in lactate dehydrogenase (LDH) levels and the expressions of RIPK3 and MLKL. But pretreatment with a ROS inhibitor Nacetyl-L-cysteine (NAC), a RIPK3 inhibitor GSK'872, or RIPK3 gene silencing alleviated 1,3-DCP-induced cell necroptosis. The data indicated that 1,3-DCP induced necroptosis through the ROS/RIPK3/MLKL pathway in NRK-52E cells. In further mechanistic studies, we explored how 1,3-DCP induced ROS production. We found that 1,3-DCP inhibited the expressions of nuclear and cytoplasmic Nrf2. But pretreatment with an Nrf2 activator dimethyl fumarate (DMF) up-regulated the expressions of nuclear and cytoplasmic Nrf2 and down-regulated ROS levels and RIPK3 and MLKL expressions. We also examined the effects of mitophagy on 1,3-DCP-induced ROS. The data manifested that 1,3-DCP suppressed mitophagy in NRK-52E cells by decreasing LC3-II, Pink1, and Parkin levels, increasing p62 levels, and decreasing colocalization of LC3 and Mito-Tracker Red. Pretreatment with an autophagy activator rapamycin (Rapa) decreased 1,3-DCP-induced ROS. Taken together, our data identified that 1,3-DCP caused renal necroptosis through the ROS/RIPK3/MLKL pathway.

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Section: Introductionmentioning

confidence: 99%

1,3-Dichloro-2-propanol-Induced Renal Tubular Cell Necroptosis through the ROS/RIPK3/MLKL Pathway

Fan

Lü

et al. 2022

J. Agric. Food Chem.

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1,3-Dichloro-2-propanol Induced Renal Cell Ferroptosis via the Circadian Clock Protein BMAL1 Targeting GPX4

Chen,

Guan,

Liu

et al. 2024

J. Agric. Food Chem.

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1,3-Dichloro-2-propanol (1,3-DCP), a representative chloropropyl alcohol contaminant in food, has shown toxic effects on the kidney. Ferroptosis is a newly identified cell death driven by iron-dependent lipid peroxidation that is associated with renal injury. However, the role of 1,3-DCP in ferroptosis in renal cells remains unclear. In this study, we found that ferroptosis was involved in a 1,3-DCP-induced renal injury. Mechanistically, we revealed that 1,3-DCP triggered ferroptosis by inhibiting GPX4 activity and disturbing iron homeostasis in NRK-52E cells. The circadian clock is crucial in modulating physiological cellular functions through the regulation of various downstream proteins. Furthermore, our findings also showed that 1,3-DCP triggered ferroptosis through interference with the circadian clock. The data showed that the expression of GPX4 was regulated by clock core protein BMAL1. 1,3-DCP interfered with GPX4 rhythmic expression through disordering BMAL1 and led to lipid peroxidation, ultimately inducing ferroptosis. In conclusion, our study uncovered that BMAL1 was responsible for controlling GPX4 to mediate 1,3-DCP-induced ferroptosis. The BMAL1/GPX4 axis may be a potentially novel pathway for ferroptosis. Our work may offer a fresh perspective for toxicological research examining the interactions between food pollutants, circadian clock, and ferroptosis.

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Characterization of Electron Ionization Mass Spectral (EIMS) Fragmentation Patterns of Chloropropanol Esters of Palmitic Acid Using Isotope Labeling Technique

Cited by 2 publications

References 11 publications

1,3-Dichloro-2-propanol-Induced Renal Tubular Cell Necroptosis through the ROS/RIPK3/MLKL Pathway

1,3-Dichloro-2-propanol-Induced Renal Tubular Cell Necroptosis through the ROS/RIPK3/MLKL Pathway

1,3-Dichloro-2-propanol Induced Renal Cell Ferroptosis via the Circadian Clock Protein BMAL1 Targeting GPX4

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