Mechanisms of mitochondrial dysfunction-mediated cell death generated by neurotoxins: Paraquat crosses the blood brain barrier (BBB) by an as yet unclear mechanism, possibly via an amino acid transporter (AAT)/polyamine transporter (PAT), where it enters the cell and is spontaneously reduced to the paraquat radical or reduced by Complex I or II (CI or II) and can then form reactive oxygen species (ROS). Rotenone and TaClo enter neurons and can cause CI inhibition which leads to the production of ROS. MPTP enters the brain, where it is converted to MPP+ in glial cells by monoamine oxidase-B (MAO-B) which is transported into neurons by the dopamine transporter (DAT). Once in the cell, MPP+ also causes CI inhibition and generation of ROS. ROS formed by these environmental toxins can then exacerbate the CI inhibition as well as causing lipid and protein peroxidation, DNA damage, and, ultimately, cell death.