Lycopene prevents Di-(2-ethylhexyl) phthalate-induced mitophagy and oxidative stress in mice heart via modulating mitochondrial homeostasis

Di-(2-ethylhexyl) phthalate (DEHP) is a plasticizer that is easily found in the environment. Excessive daily exposure of it may lead to an increased risk of cardiovascular disease (CVD). Lycopene (LYC), as a natural carotenoid, has been shown to have the potential to prevent CVD. However, the mechanism of LYC on cardiotoxicity caused by DEHP exposure is unknown. The research was aimed to investigate the chemoprotection of LYC on the cardiotoxicity caused by DEHP exposure. Mice were treated with DEHP (50 0 mg/kg or 1,0 0 0 mg/kg) and/or LYC (5 mg/kg) for 28 d by intragastric administration, and the heart was subjected to histopathology and biochemistry analysis. The results indicated that DEHP caused cardiac histological alterations and enhanced the activity of cardiac injury indicators, and interfered with mitochondrial function and activating mitophagy. Notably, LYC supplementation could inhibit DEHP-induced oxidative stress. The mitochondrial dysfunction and emotional disorder caused by DEHP exposure were significantly improved through the protective effect of LYC. We concluded that LYC enhances mitochondrial function by regulating mitochondrial biogenesis and dynamics to antagonize DEHP-induced cardiac mitophagy and oxidative stress.(c) 2023 Elsevier Inc. All rights reserved.

Automated summary

This study investigated the chemoprotective effect of lycopene (LYC) on the cardiotoxicity caused by di-(2-ethylhexyl) phthalate (DEHP). The results showed that DEHP caused cardiac histological alterations, enhanced cardiac injury indicators, and interfered with mitochondrial function and mitophagy. LYC supplementation inhibited DEHP-induced oxidative stress and improved mitochondrial dysfunction and emotional disorder caused by DEHP exposure. The study concluded that LYC enhances mitochondrial function to counteract DEHP-induced cardiac mitophagy and oxidative stress.