Restoration and stabilization of acrylamide-induced DNA, mitochondrial damages and oxidative stress by chrysin in human lymphocyte

ABSTRACT

Background

Acrylamide (AA) is a water-soluble toxic chemical that is considered one of the most important food contaminants. Furthermore, AA is considered a major public health risk.

Methods

This study was designed to evaluate the effects of AA on cytotoxicity, oxidative damage and genotoxicity in human lymphocytes and also to evaluate the protective effects of the chrysin (CH). Lymphocytes after isolation from the blood were treated with AA (50 µM), AA (50 µM) plus CH (10, 25, 50 µM) and CH (50 µM), and parameters such as cell viability, mitochondrial and lysosomal damage, as well as oxidative damage to DNA were examined.

Results

The results showed that CH was able to reduce cytotoxicity, reactive oxygen species (ROS) levels, lipid peroxidation (LPO) level, collapse in mitochondrial membrane potential (MMP) and oxidative damage of DNA caused by AA in human lymphocytes. Also, co-treatment of the AA-exposed human lymphocytes with CH increases the glutathione (GSH) levels.

Conclusion

Results suggest that CH (10, 25, 50 µM) shows a protective role in AA-induced cytotoxicity, oxidative stress, mitochondrial damage and DNA oxidative damage.

KEYWORDS:

• Acrylamide
• chrysin
• oxidative stress
• mitochondria
• cytotoxicity

Acknowledgments

The data provided in this article was extracted from the Pharm D. thesis of Dr. Niloufar Hashemidanesh. The thesis was conducted under supervision of Dr. Ahmad Salimi at Department of Pharmacology and Toxicology, School of Pharmacy, Ardabil University of Medical Sciences, Ardabil, Iran.

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Author contributions

Ahmad Saimi, Enayatollah Seydi, Hassan Ghobadi and Niloufar Hashemidanesh designed the study. Niloufar Hashemidanesh, Elahe Baghal, Farzad Khodaparast, and Ahmad Salimi performed all the cells experiments. Ahmad salami and Enayatollah Seydi processed the data and performed statistical analysis. Ahmad salami, Enayatollah Seydi and Hassan Ghobadi wrote the original draft preparation. Ahmad Salami and Enayatollah Seydi revised the manuscript.

Additional information

Funding

This study was supported by Ardabil University of Medical Sciences, Deputy of Research with ethics code IR.ARUMS.REC.1398.497.