The mechanisms of mitochondrial neuron dysfunction under the influence of arsenic and aluminium (review)

Abstract

Exposure to neurotropic chemicals (aluminum, arsenic, etc.) as a result of pollution of environmental objects can cause disruption of the bioenergetics of nerve cells. Objectives. To analyze and summarize the literature data on the mechanisms of the effects of arsenic and aluminum on the structure and functions of neuronal mitochondria. Sources of data: literature sources reflecting the mechanisms of the influence of these neurotoxicants on neuronal mitochondria. Methods. The basis of this study was the review of literature on this topic. Results. The influence of arsenic compounds on nerve cells causes mitochondrial dysfunction due to the activation of oxidative stress, an increase in the intracellular level of Ca2+, a decrease in the mitochondrial membrane potential and the level of calpain 1, but aluminum compounds increase the formation of reactive oxygen species (ROS) and disrupt the activity of cytochrome c-oxidase and the energy-producing function of mitochondria in various types of neurons. Mitochondrial dysfunction, caused when exposed to these metals is accompanied by the decrease in ROS resynthesis and the activation of oxidative stress, which in its turn decreases energy generation in mitochondria still to a greater extent according to the mechanism of a vicious circle («CIRCULUS VITIOSUS»). Conclusions. The presented information deepens our knowledge about the mechanisms of neuronal bioenergetics disorders under the influence of arsenic and aluminum compounds, which is the basis for further research in order to develop effective methods of prevention, detoxification and antioxidant therapy for acute and chronic arsenic and aluminum poisoning and to implement the results obtained in practical healthcare.

Keywords

• mitochondria
• neuronal bioenergetics
• nervous system
• arsenic and aluminum neurotoxicity
• electron transport chain