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Korean J Occup Environ Med. 1997 Feb;9(1):40-48. Korean. Original Article. https://doi.org/10.35371/kjoem.1997.9.1.40
Jung DE , Ryu SH , Cho JA , Song JC , Park HB .
Seong-ae Hopital, Korea.
Department of Preventive Medicine, Hanyang University College of Medicine, Korea.
Abstract

The effects of NMDA-receptor antagonist (MK-801) were assessed for the oxygen free radical mediated brain (hippocampus) injury with eighty rats which were exposed to carbon monoxide (CO) followed by hyperbaric oxygen (HBO) treatment. Superoxide dismutase (SOD) and malondialdehyde (MDA) were used as parameters of the oxygen free radical reaction. Experimental groups consisted of (1) control group (=breathing with air), (2) CO group (=exposed to CO after air breath), (3) CO-air group(exposed to CO after air breath followed by air breath), and (4) CO-HBO group (=exposed to CO after air breath followed by 3 ATA HBO). Each group was divided two subgroup according to the pretreatment (normal saline or MK-801). CO, CO-air and HBO groups increased in SOD activity as compared with control group. And CO-air and HBO groups increased in MDA as compared with control and CO group. Pretreatment of MK-801 decreased SOD activities significantly (p-value<.05) , but MDA amount not significantly (p-value=.107). These results suggest a useful protective effect of NMDA-receptor antagonist (MK-801) in CO induced hippocampal injury mediated by oxygen free radicals.

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