Background: The present study was designed to examine the ant hyperglycemic and antihyperlipidemic effect of Epigallocatechin gallate (EGCG) on fluoride induced oxidative changes in the metabolisms of rats. Methods: The control group received the vehicles only. EGCG alone treated group received the EGCG orally at a dose of 40mg/kg in 10% tween 80 for 4 weeks. The Fl treated group received NaF (25 mg/kg) orally in saline for 4weeks. EGCG + Fl treated group received the EGCG at a dose of 40mg/kg/bw along with NaF. Results: The levels of serum SGOT, SGPT, ALP, ACP and plasma glucose, G6PD, cholesterol, triglycerides, free fatty acids, phospholipids, low density lipoprotein, very low density lipoprotein were significantly increased in fluoride intoxicated rats. Furthermore, a significant increase HMG CoA with decreased glycogen, hexokinase, total protein, albumins, high density lipoprotein, lipoprotein lipase, and lecithin cholesterol acyl transferase was observed in fluoride treated rats with altered histological changes. Pre-oral administration of EGCG at a dose of 40 mg/kg bw to fluoride intoxicated rats for a period of 28 days resulted in a significant reduction in the cholesterol, triglycerides, free fatty acids, phospholipids, low density lipoprotein, very low density lipoprotein, and elevation of high density lipoprotein with hexokinase. Moreover, lipoprotein lipase, lecithin cholesterol acyl transferase, total protein, and albumins were also increased with decreased serum markers and HMG CoA after EGCG treatment. The histological findings of liver also significantly improved with EGCG pretreatment. Conclusions: These results indicate that the natural dietary antioxidant EGCG showed significant protective effect against Fl-induced oxidative stress mediated metabolic alternations in rats. This may be due to its antihyperlipidemic and ant hyperglycemic property; it will provide an accessible and cheap traditional medicine source for treatment of Fl mediated environmental and occupational ailments.

Arsenic (As) is an environmental toxic metalloid that is present in everywhere such as air, water and soil. Generally, inorganic arsenic has a tendency to be more toxic than organic arsenic. The present study was designed to determine whether oral administration of silibinin (SB), which has been shown to have substantial antioxidant properties, when pre-administered (75 mg/kg body weight) once daily for 4 weeks along with arsenic (5 mg/kg) would prevent arsenic-induced changes in antioxidant defense system, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX),glutathione-S-transferase (GST),glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PD), reduced glutathione (GSH), total sulfhydryl groups (TSH) and vitamin C in rat brain regions such as cortex, striatum, cerebellum, hippocampus and brain stem. Our study also examined the effect of SB over arsenic-induced reactive oxygen species (ROS) production and lipid peroxidation level (LPO) and protein carbonyl content (PC) in distinct brain regions of rats. Moreover, As also alters the lipid profiles such as total lipids, phospholipids, cholesterol, cerebrosides and gangliosides in various regions of the brain. Pre-administration of SB restores the altered enzymatic and non-enzymatic antioxidants, lipid profiles and also markedly reduced the ROS, LPO, PC and accumulation of As in various regions of the brain. These results suggested that arsenic-induced deficits in antioxidant enzyme activities and increase in ROS production and lipid peroxidation levels in brain regions can be remarkably prevented by pre-administration of SB.

Objective: To study the ameliorative effects of grape seed proanthocyanidins (GSP) against cadmium (Cd) induced hyperglycemia, hypercholesterolemia and hyperlipidemia in rats. Methods: Wistar rats, body weight 180-200g, were randomly divided into four groups, six rats in each group. First group (control) represented the control animal, the second group (Cd) was fed orally with Cd in the form of CdCl 2 (5mg/kg bw), the third group (GSP) was fed with GSP (200 mg/kg bw) and to the fourth group (Cd+GSP), CdCl 2 was administered orally at a dose of (5 mg/kg bw) and pretreated with GSP (200 mg/kg bw) 90 min before Cd intoxication for 4 weeks. At the end of experiment, rats were sacrificed; blood and liver samples were collected and used for analysis of various metabolic parameters. Results: The result of the present study revealed that Cd exposure caused significant reduction in food intake and body weight gain, but increased the liver weight. GSP administration significantly revert all these changes to normal level. Cd intoxication induced hyperglycemia, elevate plasma glucose and lipid profiles and decline in high density lipoprotein (HDL) -cholesterol respectively. The GSP pretreatment regimen was beneficial in the restoration of the increased serum levels of TC, TG and lipid profiles and of the suppressed insulin and total antioxidants on Cd exposure. Conclusion: From the present investigation, it may be concluded that Cd intoxication caused deleterious effects on the metabolism of rats which were successfully restored by GSP. Therefore, the present work suggests that GSP is a feasible therapeutic agent to improve and treat patients with hyperlipidemia, obesity, hyperglycemia in addition to its anti-oxidant properties and can be used as a component in food to promote the health of people.

Background:The aim of this study was to investigate the possible protective role of the Mentha piperita leaf extract (MPE) on cadmium (Cd)-induced nephrotoxicity using biochemical and histopathological approaches. Methods:The control group received the vehicles only. The Cd treated group received Cdcl 2 (5 mg/kg) orally in isotonic saline for 4weeks. Cd + MPE treated group received the MPE at a dose of (100mg/kg in 5% tween 80) along with Cd. MPE alone treated group received the MPE alone orally at a dose of 100mg/kg in 5% tween 80 for 4 weeks. Results:In experimental rats oral administration of CdCl 2 (5 mg/kg) for 4weeks significantly induced renal damage which was evident from the increased levels of serum urea, uric acid and creatinine with a significant (p<0.05) decrease in creatinine clearance. Cd also significantly (p<0.05) decreased the levels of urea, uric acid and creatinine in urine. Cdinduced oxidative stress in kidney tissue was indicated by the increased levels of renal lipid peroxidation markers (thiobarbituric acid reactive substances and lipid hydro peroxides) and protein carbonyl content with a significant (p<0.05) decrease in non-enzymatic (total sulfhydryl group, reduced glutathione, vitamin C and E) and enzymatic antioxidants (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST), glutathione reductase (GR). Moreover the kidneys of Cd-treated rats also exhibit significantly (p<0.05) increased levels of tumor necrosis factor (TNF-α) and nitric oxide (NO). The histopathology of Cd treated rats showed tubular necrosis, degeneration, dilation, desquamation, thickening of basement membrane and luminal cast formation. MPE (100mg/kg/day) treatment markedly attenuated the Cd-induced biochemical alterations in serum, urine and renal tissue, and brings the TNF-α and NO in to normal levels. MPE also ameliorated the Cd-induced pathological changes when compared with Cd-alone-treated group. Conclusions:These results indicate that the natural dietary antioxidant MPE might have significant protective effect against Cdinduced oxidative stress mediated in rats. Due to its antioxidant and anti-inflammatory effects, it will provide an accessible and cheap traditional medicine source for treatment of Cd mediated environmental and occupational ailments.