Abstract
In spite of long and extensive use of hexachlorophene (HCP) as an antibacterial and antifungal agent in a wide variety of cosmetics, medical and home care products since 1949 (Gump & Walter 1968), it was only in 1971 that the toxic potential of this compound was recognized; mainly because of the HCP-induced neuropathologic changes observed by kimbrough et al. Since then, several studies concerned with the neurotoxic i ty of HCP have been conducted, however the biochemical mechanism of HCP action remained obscure. HCP is reported to exert toxic effects on non nervous tissues as well. Freeze fracture studies showed that administration of an acute dose of 30 mg HCP/kg causes disorganization in t ight junctions, increase in number of gap junctions and disruption of mitoehondria in the l iver of rats (Robenek et al. 1980). When HCP was given intragastrical ly at doses of 60 mg/kg/day for 1 week, mice exhibited degenerative changes in l iver (Prasad 1986). Since hepatic degeneration is most commonly associated with abnormal ammonia metabolism and brain function, an at tempt has been made in the present study to investigate the cerebral ammonia, glutamate and related metabolite patterns in mice during HCP-induced neurotoxici ty.
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