Abstract
One of the proinflammatory agents in the human body is lead (Pb), which can enter the blood through the skin, respiratory tract and digestive tract, causing poisoning. Its most significant target is the central nervous system (CNS). Although studies on Pb neurotoxicity have been conducted for many years, the proinflammatory effect of Pb on the brain is rarely reported in contrast to other human tissues and organs. Lead neurotoxicity has been defined as a significant paediatric health problem as the foetal stage is a very susceptible period for Pb exposure at whole blood levels below 10 µg/dL (Pb neurotoxicity threshold in children). However, the mechanisms of the neurotoxic action of Pb in causing brain defects remain unclear. In this review we discuss the role of the blood-brain barrier in the neurotoxicity of Pb, and the role of cytokines as inflammatory mediators (specially interleukin-1 and interleukin-6, nuclear transcription factor κB, cyclooxygenase-1 and cyclooxygenase-2, prostaglandin E2, transforming growth factor β. We also discuss the influence of pre- and neonatal exposure to Pb on inflammatory reactions in the brain.