Premium
Ellagic acid mitigates arsenic‐trioxide‐induced mitochondrial dysfunction and cytotoxicity in SH‐SY5Y cells
Author(s) -
Firdaus Fakiha,
Zafeer Mohd. Faraz,
Waseem Mohammad,
Anis Ehraz,
Hossain M. Mobarak,
Afzal Mohammad
Publication year - 2018
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22024
Subject(s) - arsenic trioxide , sh sy5y , viability assay , cytotoxicity , ellagic acid , reactive oxygen species , chemistry , apoptosis , mitochondrion , toxicity , biochemistry , pharmacology , glutathione , dna damage , antioxidant , microbiology and biotechnology , in vitro , cell culture , biology , neuroblastoma , dna , enzyme , polyphenol , organic chemistry , genetics
In the current study, neuroprotective significance of ellagic acid (EA, a polyohenol) was explored by primarily studying its antioxidant and antiapoptotic potential against arsenic trioxide (As 2 O 3 )‐induced toxicity in SH‐SY5Y human neuroblastoma cell lines. The mitigatory effects of EA with particular reference to cell viability and cytotoxicity, the generation of reactive oxygen species, DNA damage, and mitochondrial dynamics were studied. Pretreatment of SH‐SY5Y cells with EA (10 and 20 μM) for 60 min followed by exposure to 2 μM As 2 O 3 protected the SH‐SY5Y cells against the harmful effects of the second. Also, EA pre‐treated groups expressed improved viability, repaired DNA, reduced free radical generation, and maintained altered mitochondrial membrane potential than those exposed to As 2 O 3 alone. EA supplementation also inhibited As 2 O 3 ‐induced cytochrome c expression that is an important hallmark for determining mitochondrial dynamics. Thus, the current investigations are more convinced for EA as a promising candidate in modulating As 2 O 3 ‐induced mitochondria‐mediated neuronal toxicity under in vitro system.