Physiological Changes in Cellular and Systemic Activity Due to Aluminum Toxicity

Abstract

The toxic effects of aluminum (Al) are variable and can lead to multifaceted systemic toxicity, which can induce cellular damage that leads to apoptosis and disrupt cellular homeostasis. These negative alterations are leading to systemic toxicity associated with functional and structural cellular and systemic disturbances. Cytotoxic activity of Al is attributed mainly due to oxidative stress, free radical scavenging and prooxidant action on the lipids and proteins of the cells. Inflammatory effects have confirmed in different tissues such as pulmonary, hepatic, renal and cardiovascular tissues. This appears due to the oxidative stress of Al and formation of free radicals due to Al, which increases pro-inflammatory cytokines. There is an increase in levels of IL-1β and TNF-α in addition to MIP-1α as a result of increases of gene expression. Chronic Al exposure accumulates in the nervous system and causes severe damage to cellular structures in the hippocampus resulting in thickening and discoloration with edema and severe changes in tissue appearance. Tau phosphorylation is often thought to enhance tau accumulation due to increased hyperphosphorylation and aggregation. Neurobehavioral data are of great significance in risk estimation because behavior could appear as a net consequence of many functions occurred in nervous system. As well as, neurotoxicity of Al could be coincided by motor and speech disorders.