فهرست مطالب monika bhadauria

Vanadium is an important environmental and industrial pollutant. It has a status of reproductive toxicant and is reported to cross placental barrier. The current study was performed to assess the therapeutic efficacy of Tiron and its combination with selenium against vanadium induced toxicity in lactating and suckling rats. Rats were exposed to vanadium at a dose of 7.5 mg/kg/day (p.o.) for 20 days from 0 day of post partom (p.p.). Tiron (606 mg/kg/day, i.p.) and selenium (0.5 mg/kg/day, p.o.) were administered for 5 days on 21-25 day PP. Vanadium exposure decreased blood sugar level while serum transaminases and serum alkaline phosphatase showed increased values significantly (p<0.01). Elevation in glycogen content of liver and kidney of suckling and kidney of lactating rats was found after toxicant administration. Toxicant intoxication increased the enzymatic activity of acid phosphatase in liver of suckling and lactating and kidney of suckling rats. On the contrary alkaline phosphatase and adenosine triphosphatase activities were inhibited significantly (p<0.01) in all the organs. Lipid peroxidation was enhanced whereas glutathione was reduced significantly in liver of suckling and lactating rats (p<0.01). Vanadium also caused histopathological lesions. Therapies of Tiron per se and Tiron along with selenium maintained almost all blood and tissue biochemical parameters towards normal. Tiron along with selenium reduced vanadium induced lesions in lactating and sucklings rats. Tiron along with selenium is more effective than Tiron alone against vanadium induced toxic effect on lactating and suckling rats.

Hepatoprotective efficacy of propolis extract (honeybee hive product, 200 mg/kg, p.o.) was studied against carbon-tetrachloride-(CCl4, 0.15 ml/kg, i.p.) induced biochemical and histopathological changes. Silymarin, a known hepatoprotective drug was used as a positive control. Subchronic exposure to CCl4 for 3 weeks (5 days a week) caused sharp elevation in the activity of liver enzymes i.e., serum transaminases, alkaline phosphatase and lactate dehydrogenase. CCl4 administration significantly decreased blood glucose level and increased serum proteins. Tissue biochemistry revealed significant reduction in total protein and glycogen contents, alkaline phosphates activity and adenosine triphosphatase along with significant increase in acid phosphatase activity both in liver and kidney. CCl4-induced oxidative stress was measured by estimating reduced glutathione level and amount of TBARS formed as an index of lipid peroxidation. Hepatorenal glutathione level showed marked depletion whereas lipid peroxidation was enhanced significantly. Posttreatment of propolis extract after toxicant administration reversed for five days alterations in blood and tissue biochemical variables including liver function test and markers of oxidative stress, which was similar to silymarin-treated positive control. Histopathological studies of liver and kidney showed improved cellular architecture after propolis therapy and confirmed its hepatoprotective efficacy. In conclusion, propolis extract is a natural product with hepatoprotective properties.