Antioxidant activity of calcitriol reduces direct methamphetamine-induced mitochondrial dysfunction in isolated rat heart mitochondria

Abstract

We investigated this hypothesis that methamphetamine could directly cause mitochondrial dysfunction and calcitriol could reduce its adverse effects in rat heart isolated mitochondria. Results indicated that 250 µM methamphetamine caused a deleterious alteration in mitochondrial functions, reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP) collapse, mitochondrial swelling, oxidative stress and lipid peroxidation. While our results indicated that calcitriol (5 µM) can reduce methamphetamine-induced toxicity in isolated cardiac mitochondria. Altogether, the results of the current study showed that methamphetamine directly induce mitochondrial dysfunction through oxidative stress in isolated cardiac mitochondria, which were ameliorated by calcitriol with its antioxidant potential.

Keywords:

• Vitamin D
• oxidative stress
• cardiotoxicity
• cardiomyopathy
• illicit drugs

Acknowledgement

The results presented in current article was extracted from the Pharm D. thesis of Dr. Morteza Minouei. This thesis was performed under supervision of Dr. Ahmad Salimi Assistance Professor of Toxicology and Pharmacology at Department of Pharmacology and Toxicology, School of Pharmacy, Ardabil University of Medical Sciences, Ardabil, Iran.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This study was supported by Ardabil of Medical Sciences, Deputy of Research with ethics code IR.ARUMS.REC.1398.604.