Lycopene Attenuates Di(2-ethylhexyl) Phthalate-Induced Mitochondrial Damage and Inflammation in Kidney via cGAS–STING Signaling

Di­(2-ethylhexyl) phthalate (DEHP) is a highly harmful and persistent environmental pollutant. Due to its unique chemical composition, it frequently dissolves and enters the environment to endanger human and animal health. Lycopene is a natural bioactive component that can potentially reduce the ris...

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Bibliographic Details
Published in:Journal of agricultural and food chemistry 2023-01, Vol.71 (1), p.569-579
Main Authors: Li, Mu-Zi, Dai, Xue-Yan, Zhao, Ying-Xin, Li, Xiao-Wei, Zhao, Yi, Li, Jin-Long
Format: Article
Language:English
Subjects:
Animals
Bioactive Constituents, Metabolites, and Functions
Diethylhexyl Phthalate - toxicity
DNA, Mitochondrial - metabolism
Inflammation - genetics
Interferons
Kidney - metabolism
Lycopene
Mice
Nucleotidyltransferases - metabolism
Protein Kinases - metabolism
Signal Transduction
Ubiquitin-Protein Ligases - genetics
Ubiquitin-Protein Ligases - metabolism
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Summary:Di­(2-ethylhexyl) phthalate (DEHP) is a highly harmful and persistent environmental pollutant. Due to its unique chemical composition, it frequently dissolves and enters the environment to endanger human and animal health. Lycopene is a natural bioactive component that can potentially reduce the risk of environmental factor-induced chronic diseases. The present study sought to explore the role and underlying mechanism of lycopene (LYC) on DEHP-induced renal inflammatory response and apoptosis. In this study, mice were orally treated with LYC (5 mg/kg BW/day) and/or DEHP (500 or 1000 mg/kg BW/day) for 28 days. Our results indicated that LYC prevented DEHP-induced histopathological alterations and ultrastructural injuries, including decreased mitochondrial membrane potential (ΔΨm), PINK1/Parkin pathway-mediated mitophagy, and mitochondrial energetic deficit. When damaged mitochondria release mitochondrial DNA (mtDNA) into cytosol, LYC can alleviate inflammation and apoptosis caused by DEHP exposure by activating the cyclic GMP-AMP synthase-stimulator of interferon gene (cGAS–STING) signal pathway. Collectively, our data demonstrate that LYC can reduce mitophagy caused by DEHP exposure by activating the PINK1/Parkin pathway and then reduce renal inflammation and apoptosis through the cGAS–STING pathway.
ISSN:0021-8561
1520-5118
DOI:10.1021/acs.jafc.2c08351