Lycopene Prevents Amyloid [Beta]-Induced Mitochondrial Oxidative Stress and Dysfunctions in Cultured Rat Cortical Neurons.

Brains affected by Alzheimer's disease (AD) show a large spectrum of mitochondrial alterations at both morphological and genetic level. The causal link between β-amyloid (Aβ) and mitochondrial dysfunction has been established in cellular models of AD. We observed previously that lycopene, a member of the carotenoid family of phytochemicals, could counteract neuronal apoptosis and cell damage induced by Aβ and other neurotoxic substances, and that this neuroprotective action somehow involved the mitochondria.

Protective effects of lycopene against methylmercury-induced neurotoxicity in cultured rat cerebellar granule neurons.

Methylmercury (MeHg) is a neurotoxin that induces neuronal degeneration in the central nervous system. Oxidative stress and mitochondrial dysfunction are widely accepted as central pathogenic mechanisms of MeHg-mediated neurotoxicity. Lycopene, a carotenoid compound, is a potent antioxidant with demonstrated neuroprotective properties in several experimental models of oxidative damage.