Cadmium neurotoxicity and its role in brain disorders

Abstract

Cadmium (Cd) is a ubiquitous industrial and environmental pollutant that accumulates in humans and animals. The sources of human exposure to Cd include primary metal industries, production of certain batteries, intake of contaminated food or water, and inhalation of tobacco smoke or polluted air. Cd accumulates and is toxic for many organs, including kidneys, lungs, and testis. Cd also reaches the central nervous system (CNS) causing neurological alterations in humans and animals, leading to lower attention, olfactory dysfunction, and memory deficits. Moreover, Cd exposure in critical developmental periods, at doses much lower than those which affect adults, can cause damage to the CNS. The cellular and molecular bases of behavioral and neuropsychological impairment or damage to brain development by Cd are essentially unknown. However, a diversity of models of neural cells (astrocytes, microglia, and neurons) exposed to Cd point to reactive oxygen species (ROS) production, cell death, and disturbance of cell signaling pathways as a foremost mechanism of Cd neurotoxicity. Therefore, a careful review regarding Cd neurotoxicity points out Cd exposure as a concern in clinical and subclinical brain disorders.