Studies on DNA Damage and Repair in the Mammalian Brain

Abstract

Methods for studying breaks in DNA strands and their repair, originally developed for prokaryotes and cultured cell lines, have been applied to preparations from rat brain. The relative sensitivities of these methods, which include alkaline sucrose density gradient sedimentation, nucleoid sedimentation, and ADP-ribosyltransferase assay, are compared.

Subchronic exposure of rats to sublethal dose of microcystin-YR induces DNA damage in multiple organs

“…The low antioxidant and DNA repair capacity of the brain could be the explanation for the highest level of DNA damage in the brain. 36 MCYR induced DNA damage also in lung, however, little is known about the effects of MCs on lung. The only report we are aware of is by Gupta et al 37 who found that in mice after the acute exposure to MCLR, MCRR and MCYR induced pulmonary inflammation, congestion and haemorrhage.…”

Loss of the Xeroderma Pigmentosum Group A Gene (XPA) Enhances Apoptosis of Cultured Cerebellar Neurons Induced by UV but Not by Low‐K+ Medium

“…y irradiation (Inoue and Kameyama, 1983;Harmon and Allan, 1988;Wood and Youle, 1995;Enokido et al, l996b), and UV irradiation (Caelles et al, 1994) induce apoptotic neuronal death. In addition, some genes such as those encoding DNA-repair enzymes (Waser et al, 1979;Kuenzle, 1985;Walker and Bachelard, 1988;Mazzarello et al, 1992;Rao, 1993;Weng and Sirover, 1993;Brooks et al, 1996) and the tumor suppressor p 53 gene (Chopp et al, 1992;Freeman et al, 1994;Sakhi et al, 1994;Wood and Youle, 1995), which is a critical regulator of the cell cycle and of apoptosis after exposure of normal cells to DNA damage, are expressed in the nervous system. Furthermore, we have shown that p53 is involved in DNA strand break-induced apoptosis of postmitotic cerebellar neurons (Enokido et al, 1996b).…”