ABSTRACT
The novice effects of most neurotoxins and neurotoxicants are dependent on their direct interaction or the structural modification of cellular macromolecules (e.g., lipids, proteins, or nucleic acids). A unique property of the central nervous system (CNS) is its composition of both actively dividing and differentiated cells, e.g., astrocytes and neurons, respectively. Both astrocytes and neurons are capable of de novo synthesis of proteins and lipids; however, unlike astrocytes, neurons do not replicate their genomic DNA and are more susceptible to toxicological outcomes following chemical exposures because of diminished levels of antioxidants, antioxidant enzymes, and DNA repair enzymes (Nouspikel and Hanawalt, 2000; Nouspikel and Hanawalt, 2002; Wang and Shum, 2002). Furthermore, the DNA in CNS is predisposed to a higher burden of damage from reactive oxygen species (ROS) because of CNS high rate of oxygen consumption and high metabolic requirements (Harman, 1993). Thus, an understanding of DNA damage and DNA repair in the context of the CNS is essential for elucidating processes of neurodegeneration
associated with idiopathic neurological deficits or those conditions resulting from exposure to neurotoxins or neurotoxicants.
