However, HDN restored the elevated levels significantly (P < 0.05) to within normal range in these animals
when compared to their respective control groups. The changes in the levels of serum and tissue lipids in normal and experimental rats are illustrated in Table 3. The levels selleck chemical of serum and tissue (Liver & Kidney) total cholesterol, triglycerides (TGs), free fatty acids (FFAs) and phospholipids (PLs) were highly altered in Fe treated rats when compared with control group. Oral administration of HDN to Fe intoxicated rat changes in the levels of serum and tissue total cholesterol, TGs, FFAs and PLs were near to normal. Table 4 shows the levels of lipid peroxidative markers (measured by the levels of thiobarbituric acid reactive substances and lipid hydroperoxides) were significantly increased in the plasma and tissue (Liver & Kidney) of Fe treated rats. Administration of HDN significantly (p < 0.05) decreased the levels of thiobarbituric acid reactive substances and lipid hydroperoxides on iron intoxicated rats Table 5 illustrates the activities of enzymatic antioxidants namely superoxide dismutase, catalase, glutathione GSK2118436 manufacturer peroxidase, glutathione-S-transferase in tissue (Liver & Kidney) of control and experimental rats. A significant (P < 0.05) depletion in the activities of enzymatic antioxidants in Fe treated rats was observed. Treatment of HDN along with Fe increased the levels of enzymatic antioxidants in
tissue (Liver & Kidney). Table 6 shows the changes in the levels of plasma and tissue (Liver & Kidney) non-enzymatic antioxidants
namely reduced glutathione, vitamin C and vitamin E. A significant (P < 0.05) decrease in the levels of non-enzymatic Calpain antioxidants was noticed in rats treated with Fe when compared to control rats. Treatment with HDN (80 mg/kg body weight) along with Fe restored the levels of non-enzymatic antioxidants to near normal. Histological analysis showed that Fe administration induces the pathological changes in liver. The liver of control rats (Fig. 3A) and HDN (Fig. 3B) treated rats showed a normal architecture. Fe exposure resulted in changes in liver architecture as indicated by focal necrosis, inflammatory cell infiltration and giant cell formation (Fig. 3 C). Fe along with HDN administration (Fig. 3D) showed near normal hepatocytes with mild portal inflammation. Histological studies showed that Fe administration induces the pathological changes in kidney. The focal areas of hemorrhage and inflammation of renal cells (Fig. 4C) were observed in Fe alone intoxicated rats. Rats administered with HDN along with Fe showed near normal appearance of glomerulai and tubules (Fig. 4D). Administration of HDN to normal rats did not produce any pathological changes in kidney (Fig. 4B) when compared with normal control rats (Fig. 4A). The objective of the present work was to investigate the protective effects of hesperidin on iron induced toxicity in rats.