Effects of Hepatic Enervation on Glutathione Homeostasis after Lipopolysaccharide Addition in Rats.

The tripeptide glutathione (GSH) is an important nonprotein thiol that plays multiple critical functional roles, and is a scavenger of superoxide in cells. Hepatic transport of glutathione is an essential process in the interorgan homeostasis of GSH. Hepatocellular G~SH is available to other extrahepatic organs. The present study examined the effects of hepatic nerve on GSH homeostasis after lipopolysaccharide (LPS) addition. A systemic depletion of GSH was observed in a denervated liver model compared with normal liver. Of particular interest was the observation that GSH was significantly decreased in the adrenal gland. This result exhibited that hepatic denervation diminished GSH concentration in other organs, resulting in these organs being vulnerable to the effects of active oxygen species. GSH concentration following LPS addition was significantly decreased in the normal liver. In contrast, LPS augmented the GSH concentrations in these organs in the denervated liver. These results were not yet sufficient to conclude whether the effects of hepatic denervation were favorable. However, it can be concluded that hepatic denervation causes the collapse of GSH homeostasis.

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