The present study was carried out to evaluate the herbal adaptogens Withania somnifera and Ocimum sanctum on cadmium-induced oxidative toxicity in broiler chicken. Cadmium administration at the rate of 100 ppm orally along with feed up to 28 days produced peroxidative damage, as indicated by increase in TBARS, reduction in glutathione (GSH) concentration in liver and kidney, and increase in catalase (CAT) and superoxide dismutase (SOD) of erythrocytes. Herbal adaptogens Withania somnifera roots and Ocimum sanctum leaf powder administration at the rate of 0.1% through feed reversed the antioxidant enzyme of RBC, i.e., CAT and SOD, nonenzymatic antioxidants GSH and lipid peroxidation marker TBARS of liver and kidney. Liver and kidney tissue repair and normal function was assessed by alanine aminotransaminase for liver and creatinine and blood urea nitrogen for kidney. In conclusion, oral administration of Withania somnifera root and Ocimum sanctum leaf powder prevented cadmium-induced peroxidation of tissues.

In the present study, effect of doxorubicin at 2 mg/kg b.wt. (i/p), alone, once in a wk for 4 wks and in combination with vitamin E at 250 and 500 mg/kg b.wt., orally, daily for 4 wks was evaluated on histological alterations, if any, on heart, liver, kidney, and testes of rats. Doxorubicin alone treated group showed marked congestion and degenerative changes in heart, kidney, liver, and testis. Treatment with vitamin E showed marked improvement in all the degenerative changes, though more protection was observed with the dose of 500 mg/kg.

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Aim:The aim of this study is to evaluate the hepatoprotective effect of rutin (RTN) in comparison to silymarin (SLM) against acetaminophen (APAP)-induced hepatotoxicity in rats.Materials and Methods:Male Wistar albino rats (n=24) of 3 months age were equally divided into four groups. Group 1 served as normal control. Hepatotoxicity was induced in the remaining three groups with administration of 500 mg/kg po APAP from day 1-3. Groups 2, 3, and 4 were subsequently administered orally with distilled water, 25 mg/kg of SLM, and 20 mg/kg of RTN, respectively, for 11 days. The mean body weights and biomarkers of hepatotoxicity were estimated on day 0, 4 (confirmation of toxicity), and 15 (at the end of treatment). Hematological parameters were evaluated on day 4 and 15. Antioxidant profile and adenosine triphosphatases (ATPases) were assessed at the end of the experiment. Liver tissues were subjected to histopathology and transmission electron microscopy after the sacrifice on day 15.Results:Antioxidant profile, ATPases, and hematological and sero-biochemical parameters were significantly altered, and histopathological changes were noticed in the liver of toxic control group. These changes were reversed in groups 3 and 4 that were administered with SLM and RTN, respectively.Conclusion:The results of the present investigation enunciated that SLM has potent hepatoprotective activity though the RTN was found superior in restoring the pathological alterations in paracetamol-induced hepatotoxicity in Wistar albino rats.

Objective:To assess pharmacokinetic interaction of garlic with atorvastatin in dyslipidemic rats.Materials and Methods:Sprague Dawley rats with induced dyslipidemia were divided into five groups of eight rats each. Group 1 was given atorvastatin (10 mg/kg body weight (b.wt) orally), group 2 was given atorvastatin (10 mg/kg b.wt orally)+garlic (1% w/w in feed), group 3 was maintained on atorvastatin (5 mg/kg b.wt orally)+garlic (0.5% w/w in feed), group 4 was maintained on atorvastatin (7.5 mg/kg b.wt orally)+garlic (0.25% w/w in feed), and group 5 was maintained on atorvastatin (2.5 mg/kg b.wt orally)+garlic (0.75% w/w in feed) for 12 weeks. Blood samples were collected at predetermined time intervals for kinetic analysis after the first and last oral dosing of atorvastatin for single and multiple dose studies, respectively. Plasma samples were assayed for atorvastatin concentration by High-Performance Liquid Chromatography (HPLC) and then the concentration-time data were analyzed.Results:Maximum observed plasma concentration (Cmax), half-life, Area Under Plasma Concentration Time Curve (AUC), and Mean Resident Time (MRT) were significantly (P<0.05) increased during multiple dose kinetic study and elimination rate constant was significantly (P<0.05) decreased in comparison with their respective single-dose values, while there was no significant difference in time to achieve maximum concentration (tmax) in all groups during both phases of the study. The highest values for kinetic parameters were observed in group 2 with correspondingly low activity of Cytochrome P450 (CYP450).Conclusion:The study revealed higher values [Cmax, AUC, Area Under The Moment Curve (AUMC), MRT, and half-life] of atorvastatin in garlic-treated groups.

Aim:To avert the health problems induced by many environmental pollutants, available antioxidants have been evaluated. The present study was aimed to investigate whether α-tocopherol could protect the hexavalent chromium (Cr VI)-induced peroxidation in the liver and kidney and to explore the underlying mechanism of the same.Materials and Methods:A total of 24 Wistar adult female rats were equally divided into four groups. Group 1 served as control while Groups 2 and 3 were administered K2Cr2O7(10 mg/kg b.wt. s.c. single dose). In addition to (Cr VI), Group 3 also received α-tocopherol (125 mg/kg, daily) by oral gavage for 14 days. Group 4 was maintained as α-tocopherol control (dose as above). At the end of 14 days, blood samples were drawn for hematology. Subsequently, all the rats were sacrificed to collect liver and kidney samples for assay of tissue peroxidation markers, antioxidant markers and functional markers and histopathology.Results:Administration of chromium (Cr VI) in Group 2 significantly (P < 0.05) reduced the antioxidant markers such as superoxide dismutase and reduced glutathione along with significant (P < 0.05) increase in peroxidation markers such as malondialdehyde and protein carbonyls in the liver and kidney as compared with other groups. The functional markers in serum such as total protein was decreased significantly (P < 0.05), whereas other functional markers viz. alanine transaminase, blood urea nitrogen and creatinine were increased significantly (P < 0.05) in Group 2 as compared with the other groups. Significant (P < 0.05) decrease in hemoglobin, packed cell volume, total erythrocyte count, mean corpuscular volume, mean corpuscular hemoglobin and total leukocyte count were observed in Cr VI treated Group 2 rats. Prominent pathological changes were observed in the liver and kidney of Group 2. Co-treatment with α-tocopherol in Group 3 rats significantly (P < 0.05) reversed the Cr VI induced changes. The parameters in the study in Group 4 did not differ as compared with Group 1.Conclusions:α–tocopherol exhibited protective effect against Cr VI-induced damage to the liver and kidney by inhibition of lipid peroxidation owing its antioxidant activity.

Background and Aim: Cyclophosphamide therapy is known to be associated with the risk of female infertility as a result of ovarian toxicity. Alpha-lipoic acid (LA) and omega-3 fatty acids are known for their antioxidant and anti-inflammatory activities. The present study investigated the potential protective effect of alpha-LA, omega-3 fatty acids, and its combination against cyclophosphamide-induced ovarian toxicity in rats. Materials and Methods: Thirty rats were equally divided into Groups I, II, III, IV, and V. Group I was normal control, wherein the rats were fed with normal feed and water ad libitum. Group II served as cyclophosphamide-induced group, wherein the rats were injected with cyclophosphamide at 75 mg/kg through intraperitoneal route once a week to induce ovarian toxicity. Groups III and IV were treated with alpha-LA at the rate of 25 mg/kg and omega-3 fatty acids at the rate of 400 mg/kg, respectively, in parallel to cyclophosphamide induction as in Group II. Group V animals were coadministered with alpha-LA (25 mg/kg) and omega-3 fatty acids (400 mg/kg) along with cyclophosphamide induction as in Group II. The respective treatments were administered daily through oral route for a period of 30 days. Regularity of estrous cycle was evaluated by vaginal cytology. Post-treatment period, the animals were humanely sacrificed, and the blood samples were subjected to the estimation of follicle-stimulating hormone (FSH) and estrogen. The ovarian tissue was weighed and subjected to histopathology, transmission electron microscopy, estimation of decreased glutathione (GSH), and tumor necrosis factor (TNF)-alpha. Results: Rats treated with cyclophosphamide alone manifested irregularity in estrous cycle, increased FSH, and reduced estrogen levels. The ovaries showed decreased GSH and increased TNF-alpha concentrations. Histopathological and transmission electron microscopic analysis of the ovarian follicles revealed degenerative changes. Administration of alpha-LA and omega-3 fatty acids as well as the combination of both the treatments demonstrated significant normalization of the estrous cycle and antioxidant defense mechanism as well as ameliorated the hormonal profile and histological architecture of the ovarian follicles. However, appreciable synergistic efficacy of the combination therapy (alpha-LA+omega-3 fatty acids) with respect to the monotherapies was not observed in the present study. Conclusion: The efficacy of alpha-LA and omega-3 fatty acids against cyclophosphamide-induced ovarian toxicity could be attributed to its antioxidant and anti-inflammatory activities that prevented the oxidative damage to the ovaries caused by cyclophosphamide. Hence, our findings suggest that dietary supplementation of alpha-LA and omega-3 fatty acids in women receiving cyclophosphamide therapy could carry potential benefits in preventing cyclophosphamide-induced infertility in childbearing women.

Objectives:To evaluate the effect of various herbal adaptogens such as shade-dried powders of Withania somnifera, Ocimum sanctum, Asperagus recemosus, Andrographis paniculata, Asphaltum panjabinum (Shilajith), Gymnema sylvestre, Spirulina platensis, and Panex ginseng on cadmium (Cd)-induced oxidative stress and its accumulation in broiler chicken.Materials and Methods:A total of 80 male broiler chicks of day old age were randomly assigned to 10 equal groups. Group 1 birds were fed with basal diet throughout the experiment (1–42 days). Group 2–10 chicks were fed with basal diet containing cadmium at 100 ppm from day 1 to day 28 (4 weeks). From 29th to 42nd day (2 weeks), basal diet alone was fed to group 2 chicks which acted as toxic control and group 3–10 birds were fed with feed containing 0.1% powder of W. somnifera, O. sanctum, Aspe. recemosus, An. paniculata, Asph. panjabinum (Shilajith), G. sylvestre, S. platensis, and P. ginseng, respectively. Body weight gain, levels of non-enzymatic antioxidants such as reduced glutathione (GSH), lipid peroxidation markers such as thiobarbituric acid reacting substances (TBARS), liver functional markers such as serum alanine transaminase (ALT), kidney functional markers such as blood urea nitrogen (BUN) and serum creatinine and concentration of cadmium in liver and kidney were investigated.Results:Body weight gains were significantly decreased in birds of groups 2–10 compared to group 1 at the end of 4th week. Supplementation of various medicinal herbs in feed after 4th week significantly improved the body weight gain compared to that in group 2 chicks. The increase in TBARS and decrease in GSH concentrations of liver and kidney tissues in cadmium intoxicated birds were significantly reversed by the above-said herbs. The liver and kidney functional markers were also restored to normal levels. Highest concentration of cadmium was found accumulated in kidney, followed by liver in birds of group 2. Herbal supplementation in groups 3–10 prevented Cd bioaccumulation which was most evident in liver, followed by kidney.Conclusions:Administration of herbal adaptogens at the rate of 0.1% in feed significantly prevented the bioaccumulation of Cd and reversed the Cd-induced oxidative tissue damage.