Significant changes were not observed in the percentages of NF-kB positive liver haemopoietic cells of the different experimental groups. In the present work we evaluated the effects of postnatal hyperoxia exposure on rat liver with reference to both hepatocytes and hepatic haemopoietic cells, reporting differential effects on the two components. Markers of apoptosis and proliferation were considered, together with a series of factors previously found in other tissues to be involved in hyperoxic response. There are papers in the literature reporting increased apoptotic cell index due to hyperoxia exposure in different tissues, such as lungs, brain and heart. In the present work, statistically significant increase of apoptotic Rapamycin cost hepatocyte percentage was found in the livers of rats exposed to severe hyperoxia compared to unexposed ones. This finding indicates that hyperoxia may exert a noxious effect in the liver tissue of newborn rats, although only as a consequence of exposure to severe hyperoxia. Preceding works of our group involving analogous experimental conditions have also reported increased apoptosis in the heart and dentate gyrus in response to severe, but not moderate, hyperoxia. As it regards haemopoietic foci, instead, a significant increase in the percentage of apoptotic cells was not found. Conversely, we observed a paradoxical response of liver hemopoiesis to hyperoxia, foci of liver haemopoiesis being larger and more numerous in rats exposed to severe hyperoxia with respect to controls. This finding may be interpreted in different ways. For instance, it could be a response to hyperoxia-induced haemolytic reactions, as exposure of rats to 80% hyperoxia for 11 days has been reported to increase haemolysis and decrease haemoglobin concentration. Otherwise, it could be intriguing to hypothesize a direct effect of hyperoxia on haemopoietic stem cells. We have previously found, for instance, that both moderate and severe hyperoxia may induce a proliferative response in the main sites of postnatal neurogenesis, the subventricular zone and dentate gyrus. Some mechanisms involved in hypoxia-induced increase in haemopoiesis could be paradoxically in common with hyperoxia-induced changes. In the present paper, we also evaluated the extracellular matrix in order to find possible signs/mechanisms of liver damage and consider a possible role of its remodeling in the haemopoietic response. A decrease in the reticular fiber content was found in the liver of rats exposed both to moderate and severe hyperoxia.