Format

Send to

Choose Destination
Iran J Pharm Res. 2016 Fall;15(4):834-841.

Repeated Administration of Mercury Intensifies Brain Damage in Multiple Sclerosis through Mitochondrial Dysfunction.

Author information

1
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
2
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran. ; Department of Pharmacology and Toxicology, School of Pharmacy, Ardabil University of Medical Science, Ardabil, Iran.; Students research committee, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
3
Department of Immunology, Faculty of medicine, Tehran University of Medical Sciences, Tehran, Iran.
4
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran. ; Students research committee, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Abstract

In this study we investigated the additive effect of mercury on the brain mitochondrial dysfunction in experimental autoimmune encephalomyelitis (EAE) model. Experimental animals (female C57BL/6 mice) are divided into four groups (n = 8); control, Hg, EAE, EAE with Hg. EAE model of MS induced by injecting myelin oligodendrocyte glycoprotein (MOG). Neurobehavioral alterations are recorded and then mice were sacrificed at day 28 and brain mitochondria were isolated and mitochondrial toxicity parameters including mitochondrial swelling, reactive oxygen species (ROS) formation, collapse of mitochondrial membrane potential (MMP) and cytochrome c release were measured. Our results showed that repeated treatment of mercury following induction of EAE in mice significantly increased the neurobehavioral scores, as well as mitochondrial toxicity through ROS formation, mitochondrial swelling, collapse of MMP and cytochrome c release. Our findings proved that repeated exposure with mercury accelerates progression of MS through mitochondrial damage related to oxidative stress and finally apoptosis.

KEYWORDS:

Apoptosis; Brain mitochondria; EAE model; Mercury; Oxidative stress

PMID:
28243280
PMCID:
PMC5316262

Supplemental Content

Full text links

Icon for PubMed Central
Loading ...
Support Center