DNA Damage, Poly(ADP-Ribose) Polymerase Activation, and Phosphorylated Histone H2AX Expression During Postnatal Retina Development in C57BL/6 Mouse

Abstract

Oxidative DNA damage in postnatal retina increases during development. It is low during the first postnatal week when PARP-1 activity is high but increases thereafter. The rise in DSBs when PARP activity is downregulated may be attributable to accumulated oxidative damage and SSBs. At P7 and P14, γ-H2AX-positive cells are repairing naturally occurring DNA damage, but some are dying (mostly at P7), probably due to an accumulation of irreparable DNA damage.