Effects of radiation and alpha-tocopherol on saliva flow rate, amylase activity, total protein and electrolyte levels in oral cavity cancer.

OBJECTIVE: The objective of the present study was to evaluate early and late effects of radiation and a-tocopherol on the secretion rate of saliva and on selected saliva salivary parameters in oral cavity cancer patients. PATIENTS & METHODS: Eighty-nine histologically confirmed oral cavity cancer patients (OCC) were enrolled in the study. Resting whole saliva was collected before, during and at the end of the radiation therapy (RT) and simultaneous supplementation with alpha - tocopherol to the radiation treated patients (RT + AT). RESULTS: Salivary flow rate, pH, amylase activity, total protein, sodium and potassium were analyzed. Increased pH, potassium and decreased flow rate, amylase activity, protein content and sodium were observed in 6 weeks of radiation treated patients when compared to OCC patients. A significant improvement of those parameters was observed on alpha - tocopherol supplementation in RT + AT patients. CONCLUSION: Supplementation with alpha - tocopherol improves the salivary flow rate thereby, maintains salivary parameters.

Effect of alpha-tocopherol on pro-oxidant and antioxidant enzyme status in radiation-treated oral squamous cell carcinoma.

Objectives: The relationships between alpha-tocopherol, pro-oxidant and antioxidant enzyme status, and radiation toxicity were studied in stage II, III, and IVA oral squamous cell carcinoma patients. The low levels of malondialdehyde and increased activities of antioxidant enzymes were correlated with decreased oxidative stress by alpha-tocopherol in oral cancer patients treated with radiotherapy. The objective of the present study was to evaluate the effect of alpha-tocopherol on oxidant-antioxidant enzyme status in oral squamous cell carcinoma patients treated with radiotherapy. Materials and Methods: The study included three groups with histologically confirmed oral squamous cell carcinoma patients (untreated), and they were further divided into two groups, viz., one consisting of patients who underwent radiotherapy alone (radiotherapy was given at the dosage of 6000 cGy in five fractions per week for a period of 6 weeks); and the other group treated with radiotherapy plus alpha-tocopherol supplementation (alpha-tocopherol was supplemented at a dosage of 400 IU/day) for the entire period of radiotherapy. Results: A significant decrease ( P P Conclusion: It was seen that alpha-tocopherol played a role in protecting against the damage caused by irradiation in oral squamous cell carcinoma patients treated with radiotherapy, by enhancing the antioxidant enzyme status and reducing the pro-oxidant status.

Gastroprotective effect of Cissus quadrangularis extract in rats with experimentally induced ulcer.

BACKGROUND & OBJECTIVES: Most of the non-steroidal anti-inflammatory drugs (NSAIDs) including aspirin cause gastric ulcer. In order to study the gastroprotective effect of Cissus quadrangularis extract (CQE), this study was undertaken on aspirin-induced ulcerogenesis in pyloric ligated (ASP-PL) model in rats. METHODS: To assess the possible antiulcer effect of CQE, lesion index, gastric secretions glycoprotein levels, non-protein sulphydryls (NPSH) and adherent mucus content were determined in ASP-PL induced gastric mucosal injury in rats. RESULTS: Pretreatment with CQE significantly prevented the gastric mucosal lesion development and decreased the gastric toxicity produced by ulcerogen. In addition, ulcerated rats showed depletion of gastric wall mucus, glycoproteins and NPSH levels whereas treatment with CQE reverted this decline in ASP-PL induced rats. Histological studies confirmed the results. INTERPRETATION & CONCLUSION: The present finding suggests that CQE promotes ulcer protection by the decrease in ulcer index, gastric secretions and increase in the glycoprotein level, gastric mucin content and NPSH concentration. CQE may protect the gastric mucosa against ulceration by its antisecretory and cytoprotective property.

Effect of Solanum trilobatum against carbon tetrachloride induced hepatic damage in albino rats.

BACKGROUND & OBJECTIVES: Many hepatoprotective herbal preparations have been recommended in alternative systems of medicine for the treatment of hepatic disorders. No systematic study has been done on protective efficacy of Solanum trilobatum to treat hepatic diseases. Protective action of Solanum trilobatum extract (STE) was evaluated by us in an animal model of hepatotoxicity induced by carbon tetrachloride (CCl4). METHODS: Wistar albino rats were divided into five groups. Group I was normal control group; Group II, the hepatotoxic group was given CCl4; Groups III-V received different doses of plant extract with CCl(4). Liver marker enzymes were assayed in serum and antioxidant status was assessed in liver tissue. RESULTS: Levels of marker enzymes such as alanine transminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) were increased significantly in CCl4 treated rats (group II). STE brought about a significant decrease in the activities of all these enzymes. Lipid peroxidation (LP) was increased significant in liver tissue in the CCl4 treated rats (group II) while the activities of glutathione peroxidase (GPx), catalase (CAT) and superoxide dismutase (SOD) were decreased. STE treatment led to the recovery of these levels to near normal. INTERPRETATION & CONCLUSION: The present observations suggested that the treatment with S. trilobatum extract enhance the recovery from CCl4 induced hepatic damage due to its antioxidant and hepatoprotective property.

Protective effect of Terminalia chebula against experimental myocardial injury induced by isoproterenol.

Cardioprotective effect of ethanolic extract of Terminalia chebula fruits (500 mg/kg body wt) was examined in isoproterenol (200 mg/kg body wt) induced myocardial damage in rats. In isoproterenol administered rats, the level of lipid peroxides increased significantly in the serum and heart. A significant decrease was observed in the activity of the myocardial marker enzymes with a concomitant increase in their activity in serum. Histopathological examination was carried out to confirm the myocardial necrosis. T. chebula extract pretreatment was found to ameliorate the effect of isoproterenol on lipid peroxide formation and retained the activities of the diagnostic marker enzymes.

Role of Arogh, a polyherbal formulation to mitigate oxidative stress in experimental myocardial infarction.

Antioxidant role of Arogh in isoproterenol induced myocardial infarction in rats has been studied. The activity of heart tissue antioxidants like glutathione, superoxide dismutase, catalase, glutathione peroxidase and glutathione-s-transferase were significantly decreased in isoproterenol administered group. The activity of ceruloplasmin and levels of glutathione, vitamins E and C were also found to be substantially decreased in serum with a concomitant rise in lipid peroxide levels after isoproterenol exposure to rats. The synergistic effect of Arogh pretreatment, significantly suppressed the alterations induced by isoproterenol alone in rats.

Modulatory effect of quercetin on azathioprine induced membrane changes in the mouse spleen.

Modulatory effect of quercetin on azathioprine induced toxic changes was studied in spleen of experimental animals. Azathioprine treatment caused an increase in serum albumin/globin ratio and a decrease in total protein in spleen tissue. An increase in a membrane bound ATPases was also noted. Supplementation of quercetin with azathioprine increased the protein content and lowered the activities of membrane ATPase in spleen. There was a decrease in serum albumin globulin ratio. It was concluded that quercetin modulated the protein and membrane bound ATPase activities and protected the spleen from azathioprine induced membrane damage.

Vitamin E protects intestinal basolateral membrane from CMF-induced damages in rat.

CMF is a combination of anticancer chemotherapeutic agents Cyclophosphamide, Methotrexate and 5-Fluorouracil. Vitamin E protects the basolateral membrane (BSM) from CMF induced lipid peroxidative damages. Rats were treated intravenously with cyclophosphamide-10 mg, methotrexate-1.0 mg and 5-fluorouracil-10 mg per kg body weight for six cycles. Vitamin E (600 mg/kg body weight) was administered orally, daily. Intestinal basolateral membrane bound ATPases (3.6.1.3), Alkalinephosphatase (3.1.1) and 5'-Nucleotidase (3.1.3.5) were protected by co-administration of vitamin E with CMF. In CMF treated rats the lipid peroxidation levels were found to be elevated with a significant depletion in membrane sulfhydryl groups. In vitamin E co-administered animals, the enzyme activities were found to be restored with concomitant reduction in malondialdehyde levels and an increase in the sulfhydryl groups. The membrane cholesterol and phospholipid levels which were altered in CMF treated rats were bought back to the normal in co-administration of vitamin E.

Effect of alpha-tocopherol on the microsomal lipid peroxidation induced by doxorubicin: influence of ascorbic acid.

alpha-Tocopherol (40 mg/rat/day) was administered, orally, to doxorubicin treated rats (2 mg/kg, twice weekly, for 4 weeks) singly and also in combination with ascorbic acid (1 g/100 ml/day) in drinking water. The vitamin therapy was carried out for a period of 1 month. The microsomal lipid peroxide levels in liver and heart were found to be increased in doxorubicin treated rats. alpha-tocopherol and ascorbic acid treatment decreased the lipid peroxide level and also NADPH-dependent lipid peroxidation. A significant depletion of glutathione in liver and heart of doxorubicin treated animals was found to be ameliorated by vitamin therapy. Ascorbic acid was found to maintain the level of microsomal alpha-tocopherol. The activities of the detoxifying enzymes like catalase, superoxide dismutase and glutathione peroxidase were suppressed in doxorubicin treated rats and vitamins coadministration maintained the levels of these enzymes. Ascorbic acid was found to potentiate the antioxidant nature of alpha-tocopherol.