[摘要]：The continuous recycling of haem iron following phagocytosis and catabolism of senescent and damaged red blood cells by macrophages is a crucial process in the maintenance of systemic iron homoeostosis. However, little is known about macrophage iron handling in haemolytic states resulting from a deficiency in antioxidant defences. Our observations indicate that the recently described chronic, but moderate regenerative, haemolytic anaemia of aged SOD1 (superoxide dismutase 1)-knockout Mice is associated with red blood cell modifications and sensitivity to both intra- and extra-vascular haemolysis. In the present study. we have characterized the molecular pathways of iron turnover in file liver of Sod1-deficient mice. Despite iron accumulation in liver macrophages, namely Kupffer cells, we did not measure any significant change in non-haem liver iron. Interestingly, in Kupffer cells, expression of the rate-limiting enzyme in haem degradation, haem oxygenase-1, and expression of the iron exporter ferroportin were both up-regulated. whereas the hepcidin mRNA level in the liver was decreased in Sod1(-/-) mice. These results suggest that concerted changes in the hepatic expression of iron- and haem-related genes in response to haemolytic anaemia in Sod1(-/-) mice act to reduce toxic iron accumulation in the liver and respond to the needs of erythropoiesis.
