Author/Authors :
Kalanaky, S Iranian Blood Transfer Organization, ايران , Farsinejad, A kerman university of medical sciences - Cardiovascular Research Center - Department of physiology, ايران , Fakharzade, S Iranian Blood Transfer Organization, ايران , Karbasian, MA Iranian Blood Transfer Organization, ايران , Keshavarz, M Iranian Blood Transfer Organization, ايران , Mehrvar, A MAHAK children Hospital, ايران , Mehrvar, N MAHAK children hospital - Research department, ايران , Rahbar, M semnan university of medical sciences, ايران , Faranoush, M Iranian Blood Transfer Organization, ايران
Abstract :
Background: Iron overload is a clinical consequence of repeated blood transfusions and causes significant organ damage, morbidity, and mortality in the absence of proper treatment. The primary targets of Iron chelators used for treating transfusional Iron overload are the prevention of Iron ingress into tissues and its intracellular scavenging. The present study was aimed at elucidating the capacity of clinically important Iron chelator, deferoxamine to gain access to intracellular Iron pools of key Iron accumulating cells (hepatocytes). Material and methods: The study was conducted as an in vivo investigation. Iron-rich chow fed rats and regular chow fed rats were given deferoxamine and hepatic Iron concentration was measured using atomic absorption spectroscopy. Results: In Iron-loaded rats, the results showed that deferoxamine did not alter hepatocyte Iron levels compared with the control group but increased urinary excretion. Conclusion: We conclude that short term deferoxamine treatment is ineffective in Iron removal from rat hepatocytes.
