Mechanisms of cell death and neuroprotection II

• Publisher: John Wiley and Sons
• Year: 1994
• Tongue: English
• Weight: 167 KB
• Volume: 9
• Category: Article
• ISSN: 0885-3185
• DOI: 10.1002/mds.870090703

✦ Synopsis

F r e e r a d i c a l 9 such as n i t r i c oxide, superoxide (02'-) and hydroxyl (OH ) as w e l l as non-radicals such as H202 and p e r o x y n i t r i t e (ONOO-) are probably formed continuously i n t h e CNS. They a r e opposed by a n t i o x i d a n t defences, which are inadequate t o prevent o x i d a t i v e damage completely and so s t e a d y -s t a t e l e v e l s of damage t o p r o t e i n s (both oxidati v e damage and n i t r a t i o n ) , l i p i d s and DNA can be measured i n vivo. During o x i d a t i v e stress, t h i s damage may be increa6ed:examples of o x i d a t i v e stress r e l e v a n t t o t h e CNS, caused by metal i o n release and drug exposure, w i l l b e presented. e f f e c t s on o x i d a t i v e stress systems i n v i t r o . Their most s t r i k i n g pro-oxidant e f f e c t i s t o a c -o x i d a t i v e DNA damage i n t h e presence of even traces of copper ions.