In-vivo and In-vitro Antioxidant Activity of Troxerutin on Nickel Induced Toxicity in Experimental Rats.

The aim of the present study was to evaluate the effect of troxerutin (TXN) on Nickel (Ni) toxicity by using rats and in-vitro model. Ni toxicity induced in male albino wistar rats (20 mg/kg body weight (b.w) was administered orally for 20 days). TXN was administered orally (100 mg/kg (b.w) for 20 days with administration of Ni. The toxic effect of Ni and the action of TXN was measure by determining the lipid peroxidation markers and antioxidant levels in plasma and various in-vitro antioxidant systems. TXN exhibited a significant (p < 0.05) antioxidant activity in Ni induced toxicity by reversing the changes observed in TBARS, HP, Vitamin C, E and GSH. The free radical scavenging properties of TXN at different concentrations (10-50ug/mL) were investigated with various in-vitro methods such as 2, 2'-diphenyl-1- picrylhydrazyl radical (DPPH), 2, 2'-azinobis (3-ethylbenzothiazoline-6-sulfonic acid) radical (ABTS•+), hydroxyl radical, superoxide anion scavenging activity and reducing power. Among the different concentrations, 50 µg/mL of TXN was more effective compared to other concentrations in all in-vitro assays. The above study conclude that TXN possesses potent in-vivo and in-vitro antioxidant activity with effective free radical scavenger for potential therapeutic value.

Beneficial Protective Effect of Troxerutin on Nickel-Induced Renal Dysfunction in Wistar Rats.

Nickel (Ni) is an important environmental toxicant that can cause cancer and cardiovascular disease. The aim of this study was to examine the protective effects of troxerutin (Txn) Ni-induced renal dysfunction in rats using biochemical and histopathological approaches. Nickel (20 mg/kg body weight [b.w.]/day) was administered intraperitoneally (i.p.) for 20 days. Renal damage from Ni toxicity was evident from the changed levels of serum and urinary markers in Ni-treated rats. The levels of lipid peroxidation markers also significantly increased, while the levels of nonenzymatic and enzymatic antioxidants significantly decreased in the kidney of Ni-intoxicated rats. Troxerutin was administered orally (100 mg/kg b.w.) for 20 days along with Ni, resulting in a reversal of Ni-induced biochemical changes in kidney accompanied by a significant decrease in lipid peroxidation and an increase in the level of renal antioxidant defense system. Histopathological studies in the kidneys of rats also showed that troxerutin (100 mg/ kg b.w.) markedly reduced the toxicity of Ni and preserved the normal histological architecture of the renal tissue. The present study results suggest the nephroprotective potential of Txn in Ni toxicity, which might be due to its antioxidant and metal-chelating properties.

Protective Role of Tetrahydrocurcumin: an Active Polyphenolic Curcuminoid on Cadmium-InducedOxidative Damage in Rats.

In the present work, protective effect of tetrahydrocurcumin (THC) against oxidative damages in cadmium (Cd)-induced toxicity in rats was evaluated. Cd is an important environmental and industrial toxicant that affects almost all the organs, especially liver. Liver is the major organ responsible for the metabolism and the primary target for many toxic chemicals and drugs. Effect of THC, the curcumin-derived polyphenolic compound on Cd-induced oxidative stress and hepatic damage was evaluated using male albino Wistar rats. In Cd-administered rats (5 mg/kg body weight (b.w.), orally for 4 weeks), activities of aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and gamma glutamyl transferase (GGT) were significantly increased in serum with the elevated level of bilirubin. Red blood cells (RBC), haemoglobin contents and haematocrit values were also significantly decreased in Cd-treated rats. In addition, the levels of lipid peroxidation markers like thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LHP), protein carbonyl contents (PCC) and conjugated dienes (CD) were significantly increased followed by the significant decrease in the levels of reduced glutathione (GSH), total sulphydryl groups (TSH), ascorbic acid (vitamin C) and vitamin E in liver of Cd-administered rats. Oral administration of THC (20, 40 and 80 mg/kg b.w.) followed by Cd for 4 weeks showed a significant restoration of the above changes to near normal. Histopathological changes observed in Cd intoxicated hepatic tissues were minimized on treatment with THC. This study suggests that THC at the dose of 80 mg/kg b.w. effectively subdues the Cd-induced toxicity and controls the free radical-induced liver damage in rats.

Protective Effect of Troxerutin on Nickel-Induced Testicular Toxicity in Wistar Rats.

Nickel (Ni)-induced oxidative damage is a serious problem that leads to reproductive system failure through testicular damage. The present investigation was carried out to determine the effect of troxerutin (Txn) on testicular toxicity induced by Ni in experimental rat testes. The oral administration of Txn (100 mg/kg body weight [bw]) showed a significant (p < 0.01) increase in superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PD), reduced glutathione, ascorbate, total sulphydryl groups, and testis-organ weight. Subsequently, the administration of Txn also significantly reduced the accumulation of Ni, lipid peroxidation products, and protein carbonyl levels in Txn-treated animals. Testicular protection in the experimental animals by Txn is further substantiated by a remarkable reduction of Ni, which was revealed through testicular tissue histopathology. These studies suggest that Txn could prevent oxidative damage and testicular toxicity induced by Ni in experimental animals.