Protective effects of nanomicelle curcumin on the phosphine-induced oxidative stress and apoptosis in human liver HepG2 cells

Document Type : Research Paper

Authors

1 Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran

2 Department of Drug Control, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran

3 Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran

4 Medical Toxicology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran

5 Department of Clinical Toxicology, Imam Reza Hospital, Mashhad University of Medical Sciences, Mashhad, Iran

6 Nanotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran

7 Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran

Abstract

Objective(s): Aluminium phosphide is used worldwide as a rodenticide and fumigant against sorted grain. Accidental or intentional exposure to aluminium phosphide (determined as PH3) results in extreme toxic effects on human. Due to the lack of a specific antidote, management of PH3 poisoning remains supportive and symptomatic. Curcumin, the main compounds of turmeric, has been reported to possess strong antioxidant and anti-apoptotic properties. This study was conducted to evaluate the effect of nanocurcumin on PH3 toxicity in HepG2 cell line. 
Materials and Methods: For this study, the cells pretreated with nanocurcumin (nCUR) and then exposed to PH3 for 6 hr. The cytotoxic and apoptotic effects of PH3 and nCUR were evaluated by MTT and propidium iodide flow cytometry. Indeed, the level of reactive oxygen species and glutathione were determined by fluorometric and colorimetric method. The oxidative DNA damage (8-OHdG) marker was also measured by ELISA kit. 
Results: Pretreatment with nCUR elevated the cell viability in PH3-treated cells and antagonized the PH3-induced glutathione depletion at high doses. Indeed, a significant decrease in the level of ROS and 8-OHdG as well as apoptotic activities were observed following exposure to nCUR.
Conclusion: These results indicated that nCUR could protect HepG2 cells against PH3 induced cell injury by attenuation of ROS and increasing GSH level. The nCUR efficiently suppressed increased apoptosis activity and formation of 8-OHdG and ultimately improved cell viability. Therefore, nCUR can be considered as promising therapeutic agents in treatment of aluminium phosphide poisoning.

Keywords


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