It has been reported that hepatocyte metabolism and function can be modulated by the activated Kuper cell through the release of dierent biomolecules like cytokines, eicosanoids, oxygen free radicals and enzymes. In relation to these paracrine factors involved in circuits of intercellular communication, the existence of a hepatic oxygen sensor located in the Kuper cell has been postulated. According to this postulate the oxygen metabolism of the liver parenchymal cells could be under the control of the Kuper cells.
In order to study the role of the Kuper cell in the reperfusion syndrome of the liver, a lobular ischaemia± reperfusion model was performed in rats with or without previous treatment with gadolinium chloride to block Kuper cell function. Spontaneous chemiluminescence of the liver surface, oxygen uptake by tissue slices and tertbutyl hydroperoxide-initiated chemiluminescence determinations were performed to evaluate the oxygen metabolism and the oxy-radical generation by the liver. The lower basal photoemission, in parallel with a lower basal oxygen uptake registered in the hepatic lobes from the animals pretreated with gadolinium chloride clearly indicates that the gadolinium chloride-dependent functional inhibition of Kuper cell leads to a downregulation of oxygen metabolism by the liver. Moreover, the intensity of oxidative stress exhibited by the postischaemic lobes appears to be closely linked with the Kuper cell activity. On the basis of the data obtained we propose that a paracrine circuit between activated Kuper cell and hepatocytes is an early key event in the induction of postischaemic oxidative stress in the liver. Furthermore the interference with the mitochondrial electron ¯ow by some biomolecules released from the activated Kuper cell, such as tumour necrosis factor, interleukins, eicosanoids, etc., would increase the rate of generation of reactive oxygen species by the inhibited mitochondrial respiratory chain.