Abstract
Cadmium (Cd) is a heavy metal that has received considerable concern environmentally and occupationally. Cd has a long biological half-life mainly due to its low rate of excretion from the body. Thus, prolonged exposure to Cd will cause toxic effect due to its accumulation over time in a variety of tissues, including kidneys, liver, central nervous system (CNS), and peripheral neuronal systems. Cd can be uptaken from the nasal mucosa or olfactory pathways into the peripheral and central neurons; for the latter, Cd can increase the blood brain barrier (BBB) permeability. However, mechanisms underlying Cd neurotoxicity remain not completely understood. Effect of Cd neurotransmitter, oxidative damage, interaction with other metals such as cobalt and zinc, estrogen-like, effect and epigenetic modification may all be the underlying mechanisms. Here, we review the in vitro and in vivo evidence of neurotoxic effects of Cd. The available finding indicates the neurotoxic effects of Cd that was associated with both biochemical changes of the cell and functional changes of central nervous system, suggesting that neurotoxic effects may play a role in the systemic toxic effects of the exposure to Cd, particularly the long-term exposure.
Highlights
Cadmium (Cd) is a toxic, nonessential transition metal and classified as a human carcinogen by the National Toxicology Program [1]
The results demonstrate that Cd-induced apoptosis is mediated by calcium signaling pathway, and calcium-mediated apoptosis occurs through the mitochondria-caspase signaling pathway [53]
Cd plays a critical role in neurobiology; a growing number of clinical investigations have pointed to Cd intoxication as a possible etiological factor of neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease, and Huntington’s disease [50, 122, 123]
Summary
Cadmium (Cd) is a toxic, nonessential transition metal and classified as a human carcinogen by the National Toxicology Program [1]. There are several sources of human exposure to Cd, including employment in primary metal industries, production of certain batteries, some electroplating processes (about 29% of year production), and consumption of tobacco products [2]. It is of interest since the natural biogeochemical cycle of Cd has been overwhelmed. Other investigators [18] reported associations between hair Cd concentrations and children’s performance on visual-motor tasks These studies clearly indicate the association of increased total Cd concentration with mental retardation and reduced visual motor abilities. We focus on recent evidence from experimental and epidemiological studies, showing that Cd exposure can induce its neurotoxin effects
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