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Abstract Title:

Lycopene prevents DEHP-induced hepatic oxidative stress damage by crosstalk between AHR-Nrf2 pathway.

Abstract Source:

Environ Pollut. 2021 Sep 15 ;285:117080. Epub 2021 Apr 7. PMID: 33965855

Abstract Author(s):

Yi Zhao, Rong-Kun Bao, Shi-Yong Zhu, Milton Talukder, Jia-Gen Cui, Hao Zhang, Xue-Nan Li, Jin-Long Li

Article Affiliation:

Yi Zhao

Abstract:

Di (2-ethylhexyl) phthalate (DEHP) is a widespread plasticizer that persists in the environment and can significantly contribute to serious health hazards of liver especially oxidative stress injury. Lycopene (LYC) as a carotenoid has recently gained widespread attention because of antioxidant activity. However, the potential mechanism of DEHP-induced hepatotoxicity and antagonism effect of LYC on it are still unclear. To explore the underlying mechanisms of this hypothesis, the mice were given by gavage with LYC (5 mg/kg) and DEHP (500 or 1000 mg/kg). The data suggested that DEHP caused liver enlargement, reduction of antioxidant activity markers, increase of oxidative stress indicators and disorder of cytochrome P450 enzymes system (CYP450s) homeostasis. DEHP-induced reactive oxygen species (ROS) activatedthe NF-E2-relatedfactor2 (Nrf2) and nuclear xenobiotic receptors (NXRs) system including Aryl hydrocarbon receptor (AHR), Pregnane X receptor (PXR) and Constitutive androstane receptor (CAR). Interestingly, these disorders and injuries were prevented after LYC treatment. Taken together, DEHP administration resulted in hepatotoxicity including oxidative stress injury and disordered CYP450 system, but these alterations might be ameliorated by LYC via crosstalk between AHR-Nrf2 pathway.

Study Type : In Vitro Study

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Sayer Ji
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