Blood Brain Barrier Inhibitors: Mercury
Introduction to Mercury
Mercury is a type of heavy metal that has been proven its significant role in affecting the function of the nervous system, the stomach, the kidneys, as well as intestines. Up to now, it has been classified into several types, such as inorganic mercury, elemental mercury, organic mercury, and organic or inorganic mercury according to the different oxidation forms. In general, all types of mercury are toxic even at trace doses. Moreover, pilot studies have shown that the high level of some organic mercury molecules can be treated as neurotoxins that induce abnormalities in the function of the nerve center. The common symptoms of toxicities caused by mercury include but are not limited to, nausea, dizziness, difficulty walking, or loss of nerve function.
Fig.1 Interrelated association among MeHg-induced oxidative stress, Ca2+ and glutamate dyshomeostasis. (Farina, 2011)
Mercury-Induced Neurotoxicity
Organic mercury is typically combined with the sulfhydryl group in the L-cysteine, which is then demethylated to form inorganic mercury. Studies have shown that inorganic mercury can not pass through the blood-brain barrier, so it accumulates in large quantities in the brain and eventually causes neurological damage. Furthermore, a large number of data have also indicated that mercury can affect the process of cell differentiation, cell growth, and tissue apoptosis. In addition, recent reports have revealed that mercury-induced neurotoxicity is associated with changes in reactive oxygen species (ROS) levels. The combination of mercury and sulfhydryl groups consumes large amounts of glutathione, which are ultimately converted into compounds. The formation of these compounds inhibits the activity of glutathione reductase, mitochondrial, and glutathione peroxidase, promoting the production of neurotoxins in humans.
Besides, organic mercury can increase the expression level of NMDA receptors, thus promoting the expression of calcium ions. Increased levels of calcium not only help mitochondria to produce ROS but also activate nNOS to produce large amounts of NO. Also, in recent studies, a battery of animal models has been generated for analyzing the role of methylmercury (MeHg) in the blood-brain barrier (BBB). The results have suggested that exposure to MeHg can lead to the increased expression level of vascular endothelial growth factor (VEGF) and the BBB damage in mice. Further studies are still needed to determine whether treatment with VEGF can improve mercury-induced toxicity.
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Reference
- Farina, M.; et al. Mechanisms of methylmercury-induced neurotoxicity: evidence from experimental studies. Life sciences. 2011, 89(15-16): 555-563.
