DNA Damage and Repair in the Brain After Cerebral Ischemia

Author: Liu, P.K.

Source: Current Topics in Medicinal Chemistry, Volume 1, Number 6, 1 December 2001 , pp. 483-495(13)

Publisher: Bentham Science Publishers

Buy & download fulltext article:

Price: $63.10 plus tax (Refund Policy)

Abstract:

In experimental models of brain injury of the ischemia-reperfusion type, there is a period of time in which the formation of oxidative damage exceeds its repair. Simultaneously, the expression of immediate early genes is induced to activate the expression of late effector genes. Drugs that reduce the need to repair during this transient period of time also attenuate neuronal death after brain injury. An example discussed in this review is the activator protein-1 (AP-1), the product of the c-fos gene and other imme-diate early genes. What is the effect of a delayed expression of these genes in relationship to the process of cell death? This short period presents a window of opportunity to study the effects of oxidative damage on gene expression in the brain and specific deficiencies in gene repair that have been associated with particular neurological disorders.

Keywords: DNA Damage; Repair; guanosine glycosylase; oxidative; ap endonuclease; flip exonuclease; neuronal nitric oxide synthase; polymerase

Document Type: Review article

DOI: http://dx.doi.org/10.2174/1568026013394688

Publication date: 2001-12-01