Methyl Mercury Injury to CNS: Mitochondria at the Core of the Matter?

Maria Rosaria Carratù and Anna Signorile
Additional contact information
Maria Rosaria Carratù: Department of Biomedical Sciences and Human Oncology, University of Bari, Italy
Anna Signorile: Department of Basic Medical Sciences, Neurosciences and Sense Organs, University of Bari, Italy

Open Access Journal of Toxicology, 2015, vol. 1, issue 1, 1-6

Abstract: Methyl-mercury (MeHg) is one of the most hazardous environmental pollutants of great concern to public health and regulatory agencies because of its primary toxicity to the human central nervous system. The major source of MeHg exposure to the general population is through consumption of contaminated fish and other food products. MeHg, absorbed from the gastrointestinal tract, is easily transported across the blood-brain barrier (BBB). Cysteine-facilitated transport of MeHg into the brain has been demonstrated, and in particular a neutral amino acid transport system capable of mediating MeHg-cysteine uptake has been identified in astrocytes where MeHg accumulation induces cell swelling and inhibition of glutamate uptake. Elevation of glutamate levels in the extracellular space may, in turn, trigger or accelerate processes of excitotoxic neuro degeneration. The rising of extracellular glutamate levels is responsible for the sustained activation of glutamate receptors, hence enhancing Na+ influx and Ca2+ release from intracellular organelles that may trigger a biochemical cascade which promotes the reactive oxygen species (ROS) production. In this scenario, mitochondria may play a crucial role, as these organelles act as a buffer against cytosolic calcium and mediate ROS formation in cells. Herein, we summarize studies providing insights into the molecular and cellular mechanisms involved in MeHg-induced neuro degeneration with particular focus on the role of astrocytes and mitochondria. Indeed, mitochondria may be supposed to lie at the crossroads of a network of events (microtubule disorganization, Ca2+ dyshomeostasis, ROS generation) leading to neuro degeneration, although it is difficult to establish the upstream mechanisms and downstream effectors in this cascade of events.

Keywords: juniper publishers:Open Access Journal of Toxicology; Toxicology open access journals; toxicology journal impact factor; toxicology journals list; international journal of toxicology impact factor; toxicology citation; toxicology letters impact factor; toxicology reports impact factor; juniper publishers reivew (search for similar items in EconPapers)
Date: 2015
References: View complete reference list from CitEc
Citations:

Downloads: (external link)
https://juniperpublishers.com/oajt/pdf/OAJT.MS.ID.555551.pdf (application/pdf)
https://juniperpublishers.com/oajt/OAJT.MS.ID.555551.php (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:adp:jpoajt:v:1:y:2015:i:1:p:1-6

DOI: 10.19080/OAJT.2015.01.555551

Access Statistics for this article

Open Access Journal of Toxicology is currently edited by Sophia Mathis

More articles in Open Access Journal of Toxicology from Juniper Publishers Inc.
Bibliographic data for series maintained by Robert Thomas ().