Many experimental and clinical studiessuggest that chronic iron deposition promotes the progression of liver damage and increases the risk of fibrosis, cirrhosis, and hepatocellular carcinomain chronic hepatitis Cpatients. Accumulating evidencesuggests that excess iron catalyzes the formation of highly reactive free radicals and hydroxyl radicals, which can damage lipids, Lithium citrate proteins and DNA. Liver satellite cells are susceptible to oxidative injury, and are easily transformed into collagen producing cells that contribute to the development of fibrosis. Furthermore, some studiessuggest that excess iron in the liver may have an adverse effect on a patient’s response to antiviral therapy. Many hypotheseshave been put forward to explain the accumulation of iron in the liver of patients with CHC, including hemochromatosis mutations, loss of iron from damaged hepatocytes, and HCV-induced disturbance of iron homeostasis. The mechanism underlying iron accumulation in HCV-infected livers is unclear; however, the recent discovery of hepcidin, a peptide hormone that regulates iron hemostasis, may provide some clues. Alterations in iron distribution are common in infectious diseases and many of these alterations may be attributable to actions of the iron-regulatory hormone hepcidin. Hepcidin degrades the sole cellular iron exporter ferroportin leading to reduced iron absorption in the intestine and iron retention in monocytes, macrophages and spleen.Several studiesreport increased or decreased iron levels in the serum of HIV patients. The liver is the main organ responsible for iron homeostasis, and the status of the liver is closely related to the distribution of iron within the body. Some iron-associated proteins, such as 
hepcidin and transferrin, are primarily synthesized by hepatocytes. Oxysophocarpine Pathological iron overload is observed in.50% of chronically-infected HCV patients. This is important because increased hepatic iron storage is an independent risk factor for the development of HCC. Here, we found that serum iron and ferritin levels were higher in HCV-monoinfected patients than in healthy controls. Iron is stored in the liver in the form of ferritin. When the liver is damaged by viral infection, ferritin is released from the damaged hepatic cells and actively secreted by macrophages during inflammation as well. This leads to higher serum ferritin concentrations in HCV-infected patients. We also found that HCV-infected patients had lower serum concentrations of hepcidin and transferrin. Hepcidin is a 25-amino acid peptide hormone primarily synthesized by hepatocytes, which regulates iron homeostasis by controlling iron absorption in the gut, iron release from macrophages, and the recycling of iron through erythrophagocytosis. In agreement with the results presented herein, several studies report low hepcidin levels in HCV-infected patients. Hepcidin binds to ferroportin, a membrane iron exporter expressed at high levels on enterocytes and macrophages. This results in ferroportin internalization and degradation, and a subsequently reduction in iron levels in the plasma. Recent studies suggest that reduced serum hepcidin levels in patients with chronic hepatitis C are associated with higher Tfs and increased serum iron accumulation. HCV infection may directly modulate hepcidin expression, and that higher Tfs and increased iron accumulation result in resistance to hepcidin.