A Comprehensive Review on Lead Acetate Neurotoxicity

Abstract

Lead acetate, a widely utilized industrial compound, poses significant neurotoxic risks. It easily crosses the blood-brain barrier, leading to accumulation in the brain and subsequent disruption of critical neuronal and glial functions. Key findings indicate that lead acetate interferes with calcium homeostasis, induces oxidative stress, and impairs mitochondrial function, which collectively contribute to neuronal damage and apoptosis. Experimental approaches, including in vitro and in vivo studies, have elucidated these mechanisms. In vitro studies using neuronal cell cultures have demonstrated cytotoxic effects such as reduced cell viability and altered gene expression. Animal models have shown cognitive and motor impairments, correlating with biochemical changes in the brain. Epidemiological studies in humans link lead acetate exposure to cognitive deficits, especially in children, and neurodegenerative disorders in adults. Current therapeutic interventions focus on chelation therapy and antioxidant treatments, while emerging research explores neuroprotective agents and gene therapy. These results highlight the pressing need for strict laws and public health initiatives to reduce exposure to lead acetate. For lead-induced neurotoxicity to be completely understood over the lifelong and for effective treatments to be developed, more research is necessary.