Open AccessLycopene antagonizes lead toxicity by reducing mitochondrial oxidative damage and mitochondria‐mediated apoptosis in cultured hippocampal neurons
Author(s) -
Qu Mingyue,
Ni Yanli,
Guo Baoshi,
Feng Xin,
Jiang Zheng
Publication year - 2020
Publication title -
medcomm
Language(s) - English
Resource type - Journals
ISSN - 2688-2663
DOI - 10.1002/mco2.17
Subject(s) - oxidative stress , neurotoxicity , reactive oxygen species , mitochondrial permeability transition pore , lycopene , mitochondrion , apoptosis , cytochrome c , mitochondrial ros , mitochondrial respiratory chain , antioxidant , microbiology and biotechnology , chemistry , biology , pharmacology , programmed cell death , biochemistry , toxicity , organic chemistry
Lead (Pb) exhibits serious adverse effects on the central nervous system, and the major pathogenic mechanism of Pb toxicity is oxidative stress. As one of the carotenoid family members with potent antioxidant properties, lycopene has shown its protections by inhibiting oxidative stress damage in numerous models of neurotoxicity. The current study was designed to explore the possible protective property in primary cultured rat hippocampal neurons challenged with Pb. We observed that 5 μM lycopene pretreatment for 4 h efficiently ameliorated Pb‐caused damage in cell viability, accumulation of reactive oxygen species (ROS), and apoptosis in a dose‐dependent manner. Moreover, lycopene (5 μM) attenuated the 50 μM Pb‐induced mitochondrial ROS production, improved the activities of mitochondrial respiratory chain enzymes and ATP production, and ameliorated the 50 μM Pb‐induced depolarization of mitochondrial membrane potential as well as opening of mitochondrial permeability transition pores. In addition, 5 μM lycopene restored the imbalance of Bax/Bcl‐2, inhibited translocation of cytochrome c, and reduced caspase‐3 activation. Taken together, these findings indicate that lycopene antagonizes against Pb‐induced neurotoxicity and the underlying mechanism probably involves reduction of mitochondrial oxidative damage and mitochondria‐mediated apoptosis.