The present study was undertaken with a view to evaluate the efficacy of spinach against arsenic (As) induced toxicity in rats during the period between July to October 2008. Thirty six female Long Evans rats (age about 120days; average body weight at day 0 = 154.5g) were randomly divided into three equal groups (n=12) and marked as T 0, T 1 and T 2 groups. Rats of T 0 group were given normal feed and water and kept as control. Rats of T 1 and T 2 groups were given 5mg Sodium arsenite/kg body weight (BW) and 5mg Sodium arsenite/kg (BW) plus spinach extract 100 mg/kg body weight respectively daily for 30 days orally. Four rats from each group were sacrificed at 10 days interval in order to quantitatively determine the As content in liver, lungs and kidney by using Hydride Generation Atomic Absorption Spectrophotometer. Serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT) and serum creatinine were determined by Autoanalyser. No visible clinical sign were observed in any group of experimental rats except loss of body weight in the spinach treated group. Tissue (lung, liver and kidney) concentration of As was significantly (p<0.01) higher in T 1 group rats compared to that of T 0 and T 2 groups and the highest concentration of As was found in kidney followed by lung and liver in T 1 group rats. After 30 days of feeding, spinach significantly (p<0.01) decreased As from lung, liver and kidney. As intoxication significantly (p<0.01) increased SGOT values but insignificantly decrease SGPT values and spinach treatment improve these condition. There was no significant effect found in serum creatinine level. It can be concluded that feeding of spinach could reduce body burden of As in rats.

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Indian J Case Reports 120 Ghosh et al. Two cases of neonatal dengue

The experiment was performed on 75 long Evans male rats (Rattus norvegicus), weighing about 145 -170 gm, maintained under standard laboratory condition on pellet diet and drinking water ad libitum. All the rats were randomly divided into five equal groups. Each group comprised of fifteen (15) rats and were marked as group A, B, C, D and E. Group A without treatment, group B lead acetate alone @ 20 mg/kg b.wt., group C lead acetate @ 20 mg/kg b.wt. plus sodium selenite 5 ml (from a stock solution 1.5 mg diluted in 1 litre distilled water), group D lead acetate @ 20 mg/kg b.wt. plus vitamin B6 45 mg/kg b.wt., group E lead acetate @ 20 mg/kg. b.wt. plus sodium selenite 5 ml (from a stock solution 1.5 mg diluted in 1 litre distilled water) plus vitamin B6 45 mg/kg b.wt. All treatments were given once daily for 28 consecutive days. In the present study, the effect of sodium selenite and vitamin B6 in lead induced toxicities in rats were observed. Toxic signs and body weight change, haematological parameters like Total Erythrocyte Count (TEC), Total Leukocyte Count (TLC), hemoglobin content (Hb%) and Packed Cell Volume (PCV), biochemical parameters such as Serum Glutamate Pyruvate Transaminase SGPT/ALT, Serum Glutamate Oxaloacetate Transaminase (SGOT/AST) and postmortem changes in rats were investigated. Rats treated with lead acetate showed severe toxic signs and significantly (p< 0.01) reduced TEC, TLC, Hb% and PCV. Significant (p< 0.01) elevation of SGPT and SGOT were also found. But rats treated with lead acetate along with sodium selenite and vitamin B6 showed almost normal levels of haematological and biochemical parameters. Lead acetate produces congestion and necrosis in liver, spleen and kidney, whereas simultaneous use of lead acetate, sodium selenite and vitamin B6 recovered the condition. From this experiment it is revealed that combine use of sodium selenite and vitamin B6 is highly protective against lead toxicity. DOI = 10.3329/bjvm.v8i1.8352 Bangl. J. Vet. Med. (2010). 8(1): 63-73