Serum and liver iron concentration in dogs with experimentally induced hepatopathy.

BACKGROUND AND AIM: Iron (Fe) status is altered in human and experimental animal hepatopathies. In dogs limited data are available. The aim of this study was to investigate serum iron (SI), total iron binding capacity (TIBC), percentage transferrin saturation (SAT) and Fe status in the liver of dogs with experimentally induced hepatopathy. METHODS: Fourteen 1-year-old dogs were divided into two equal groups. In order for hepatopathy to be induced, 0.25 mL/kg body weight of carbon tetrachloride (CCl4) solution was administered once daily, orally, for a 10-week period in group B dogs, while group A dogs were used as controls. SI, TIBC and SAT values were measured 3 times before the beginning (baseline value) and 10 times at weekly intervals during the experiment. Liver samples, obtained before the administration of CCl4 and at the end of the experimental period (10 weeks), were subjected to Fe determination, as well as to histopathological and histochemical analysis. RESULTS: At the end of the experiment SI, TIBC and liver iron concentration, as well as liver total iron score were significantly increased in group B dogs. Distribution of granular hemosiderin iron in hepatocytes, Kupffer cells, and portal triads was noticed. Positive correlations were found between SI and liver Fe concentration, as well as histochemically determined Fe. Moreover, positive correlations were evident between liver fibrosis and serum, as well as liver Fe values. CONCLUSIONS: Experimentally induced chronic hepatopathy in dogs causes Fe status disturbances. Increased serum and liver iron concentration produces liver histopathological deterioration and it may be worth attention during laboratory evaluation in canine hepatopathy.