Abstract：
:CNS inflammation is a sequela of a variety of neuropathological conditions resulting in extensive tissue loss. Inflammation is mediated primarily by phagocytic cells, but the mechanisms of CNS tissue destruction are not fully understood. Hypochlorous acid (HOCl) is by far the most abundant agent generated by phagocytic cells and may be the major mediator of inflammatory tissue damage. However, the effects of HOCl on nervous tissue have not been examined. In this study we used an in vitro model system of rat brain slices to determine neurotoxicity of HOCl. The slices were exposed to HOCl at pathologically relevant doses, and the incorporation of [3H]leucine into proteins and lipids was analyzed in total homogenate, and in particulate fractions obtained by density gradient centrifugation. The results demonstrated that a brief HOCl exposure profoundly suppressed protein biosynthesis in the slices. Also, lipid synthesis was suppressed in nonmyelin particulate fraction. However, lipid synthesis in myelin was significantly stimulated in HOCl-exposed slices indicating that oligodendrocyte response to the oxidant differs from that of other CNS cells. The effects of HOCl could be blocked by coadministration of antioxidants, i.e., N-acetylcystein (NAC), uric acid (UA) and ascorbic acid (AA). The protective potency of the antioxidants was NAC>UA>AA. In conclusion, our study demonstrated that HOCl generated by phagocytic cells during inflammatory episodes has a potential to damage surrounding CNS tissue, and that tissue damage can be prevented by HOCl scavenging with clinically applicable antioxidants.
journal_name
Brain Resjournal_title
Brain researchauthors
Krasowska A,Konat GWdoi
10.1016/j.brainres.2003.09.080subject
Has Abstractpub_date
2004-02-06 00:00:00pages
176-84issue
2eissn
0006-8993issn
1872-6240pii
S0006899303039635journal_volume
997pub_type
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