The mechanism of protective effect of crocin against liver mitochondrial toxicity caused by arsenic III

Abstract

In this study, we want to understand whether crocin could prevent mitochondrial damage caused by As III. For this purpose, we determined different mitochondrial toxicity endpoints caused by As III. We evaluated mitochondrial ROS formation, lipid peroxidation, mitochondrial membrane potential (MMP) collapse, mitochondrial outer membrane integrity and cytochrome c release. Our results showed that pretreatment with crocin at a concentration of 25 µg/ml significantly (p < 0.001) reduced As III-induced mitochondrial ROS formation, lipid peroxidation, MMP collapse and mitochondrial swelling. Crocin also protected the mitochondria by decreasing the mitochondrial outer membrane damage that leads to reduce the amount of cytochrome c release. These results demonstrated that crocin is a promising antidotal candidate by ameliorating As III-induced oxidative stress through mitochondrial targeting.

Keywords:

• Arsenic (As III)
• crocin
• hepatoprotection
• oxidative stress
• mitochondrial targeting
• antioxidant

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Corrigendum

Disclosure statement

The authors declare that they have no conflicts of interest.

Additional information

Funding

This work was supported by the Pharmaceutical Research Center and the Vice Chancellor of Research, Mashhad University of Medical Sciences and Shahid Beheshti University of Medical Sciences was a part of the PhD thesis.