ABSTRACT
Similarities in clinical picture between manganese toxicity and chronic hepatic encephalopathy suggest that this metal may have a role in the pathogenesis of chronic hepatic encephalopathy. As, dietary manganese is normally cleared by liver, we hypothesized that hepatic dysfunction could lead to manganese overload with its abnormal deposition in brain tissues that account for magnetic resonance imaging [MRI] signal hyperintenisity seen in these patients. To examine the phenomenon of manganese overload in an experimental model of cirrhotic rats and to determine the importance of a normal liver function as a natural barrier agairst the development of manganese overload with its hazardous neuropsychatric sequels in chronic hepatic disease We induced liver cirrhosis in a group of rats to examine the phenomenon of manganese overload in experimental models of cirrhotic rats. We made use also of a healthy group of rats that was fed a manganese enriched food for 4 weeks. The !eve of manganese in blood and brain tissues was assayed by atomic absorption spectrometry. There was a significant increase in both blood and brain manganese level in cirrhotic rats when compared to normal control group. The blood and brain level of manganese did not change significantly in healthy rats that fed high manganese enriched food when compared to control rats. These findings support the hypothesis that normal liver function is of utmost importance as a barrier against the development of manganese overload. Chronic hepatobiliary dysfunction might lead to manganese overload. Further studies in cirrhotic rats could be useful because the use of chelating agent and! or treatment of dopaminergic deficit could prove to be a new therapeutic option to prevent or reverse this neuropsychatric syndrome in chronic liver disease