Establishment of Hepatic Iron Overload Model and Its Effect on Serum Hepcidin Levels in Male Sprague Rats

Iron toxicity is caused by the accumulation of iron in different organs, especially the liver, heart and endocrine glands. This disorder causes side effects such as growth retardation, hypogonadism, diabetes, cirrhosis of the liver and heart failure. This study paves the way for identifying the ways of overcoming this disorder through iron overload model.

In this study, 12 adult male Sprague rats weighing 280-300 g were used. 12 Sprague rats were divided into two groups: control and iron overload groups. To create iron overload, iron dextran was injected. Hematoxylin and Eosin (H&E) staining was used for the examination of iron deposits in the liver tissue. Serum hepcidin levels were measured by ELISA method. Serum iron levels were measured using the photometric method.

The results showed a considerable iron accumulation in liver tissue of the Sprague rats in intervention group compared to the control group. Serum hepcidin (0.22±0.02 versus 0.12±0.01 pg/dl) and iron (258±6.18 versus 186±3.34 mg/dl) levels in the iron overload group were more than that of the control group and both groups had a significant relationship under iron overload conditions (P<0.05).

Intraperitoneal injection of 75 mg/kg iron dextran creates iron overload model and increases serum Hepcidin levels in Sprague rats. This model is used for the investigation of iron metabolism pathways and its disorders.