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 1 publication

(1 citation statement)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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.

View full text Add to dashboard Cite

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.

show abstract

Section: Introductionmentioning

confidence: 99%