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Objectives: To assess the protective effect of quercetin, a plant bioflavonoid, on cisplatin (CisDDP) induced nephrotoxicity in rats. Methods: Effect of the simultaneous treatment of quercetin (20 mg/kg, i.p., once a week x5) on cisplatin (3mg/kg, i.p., once a week x 5 ) induced renal epitheleal damage and lipid peroxidation was studied in the kidney of rats. Levels of markers indicative of nephrotoxicity such as urea, uric acid and creatinine were assessed in the serum. Changes in body weight were noted every week. The total protein content, levels of lipid peroxides and the activities of Na+ K + ATPase, Ca 2+ ATPase and Mg2+ ATPase were also assayed in the kidney. The glutathione content and the activities of antioxidant enzymes such as super oxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-s-transferase were estimated in the kidney. Results: Cisplatin administration caused a significant increase in the levels of all serum biochemical indices. The levels of lipid peroxides (in terms of TBA reactants) were increased significantly in serum and kidney. The activities of Na+ K+ ATPase, Ca2+ ATPase and Mg2+ ATPase were decreased significantly in the kidney. The glutathione content and activities of antioxidant enzymes were decreased considerably in the kidney of cisplatin treated rats when compared to normal control. Quercetin administration per se did not cause any change compared to the controls. However concomitant treatment of quercetin with cisplatin showed considerable decrease in levels of markers for nephrotoxicity and lipid peroxides and increased ATPase activities compared to CisDDP treated group. Glutathione content and antioxidant enzyme activities were significantly increased . Conclusion: Quercetin has significant cytoprotective effect in cisplatin-induced renal tubular damage in vivo in rats.

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Objective: To find out the suitability of horizontal strips of rat fundus for bioassay of acetylcholine (ACh). Methods: Dose response curves to ACh were obtained using a horizontal strip of rat fundus suspended in Tyrode solution. The effects of histamine (H) and 5-hydroxytryptamine (5-HT) were also studied. Results: Horizontal strips of rat fundus were stable over a long period of time (more than 6 hrs) showing reproducible responses to Ach with good discrimination between doses. It did not respond to H and 5-HT. Thus it was specific to ACh, the sensitivity being 10 -8 g/ml. Conclusion: The modified preparation of rat fundus described by us is simple and satisfies the prerequisites for the bioassay of ACh.

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Objective: To evaluate the hepatoprotective potential of jigrine pre-treatment on thioacetamide induced liver damage in rats. Methods: Albino rats (Wistar strain) were prophylactically treated with jigrine at two dose levels (0.5 ml and 1.0 ml/kg/day p.o.) for seven days. On days 6, rats were also given a single dose of thioacetamide (100 mg/ kg s.c.). Activity of jigrine against thioacetamide induced hepatotoxicity was also compared with silymarin (25 mg/kg/day p.o.). Biochemical parameters like serum AST, ALT, Na+ , K+ , tissue glutathione, tissue TBARS were estimated to assess the liver function. Biochemical observations were supplemented with histopathological examination of liver sections. Results: Thioacetamide administration increased the AST, ALT, Na+ and K+ levels in serum and TBARS in liver. Pre-treatment of the rats with jigrine or silymarin reduced the thioacetamide induced elevated levels of the above indices. Thioacetamide administration decreased the concentration of GSH in rat liver. Jigrine pre-treatment at both the doses and silymarin restored the GSH levels to near normal values in the liver of rats treated with thioacetamide. Similarly the elevation in liver TBARS levels due to thiocetamide was prevented by silymarin and jigrine pretreaments. Thioacetamide administration induced centrilobular necrosis. Pre-treatment of the rats with jigrine at both the doses showed mild protection while silymarin showed marked protection on pre-treatment. Conclusions: Jigrine pretreatment exhibited hepatoprotective action against thioacetamide induced toxicity. The effects of jigrine was comparable with that of silymarin.

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Objective: To study the possible protective effects of melatonin against sodium valproate induced hepatotoxicity in mice. Methods: Mice were treated with melatonin (15 mg/kg, i.p.), valproate (30 mg/kg, p.o.), or a combination of both in an acute and a chronic study schedule. After testing the effectiveness of the combination in the Increasing Current Electroshock Seizure (ICES) model of epilepsy, liver glutathione (GSH) and lipid peroxidation, and the serum aspartate transaminase (AST) & alanine transaminase (ALT) activities were estimated for studying the protection against valproate hepatotoxicity by melatonin. Results: Valproate produced significant depletion of GSH and increase in lipid peroxidation products in liver and AST-ALT activities in serum. These changes were effectively reversed by melatonin. Conclusion: Melatonin can effectively counter valproate hepatotoxicity on account of its strong antioxidant properties.

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Objective: To investigate the effect of nicotine on monoamine mediated behaviour in laboratory animals. Methods: The effect of intraperitoneal administration of nicotine was studied on the monoamine mediated behaviour in rats or mice. The effect of nicotine on dopamine mediated behaviour was studied by observing the effect on amphetamine-induced stereotyped behaviour, sensitivity of alcohol withdrawn mice to pentylenetetrazol, and haloperidol-induced catalepsy. The effect on serotonin mediated behaviour was studied by observing the effect on lithium induced head twitches in rats and the effect on noradrenaline mediated behaviour was studied by observing the effect on clonidine induced hypothermia in rats. The effect on behavioural despair induced by forced swimming was also studied to explore its antidepressant potential. Results: Nicotine potentiated amphetamine-induced stereotyped behaviour, both after acute and chronic administration. It delayed haloperidol-induced catalepsy and aggravated symptoms of alcohol withdrawal. It decreased lithium-induced head twitches and diminished the noradrenaline mediated behaviour. Nicotine potentiated the antidepressant activity of amitriptyline. Conclusion: Nicotine modified the behavioural effects mediated via monoamine neurotransmitters and potentiated antidepressant activity of amitriptyline.

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Obesity threatens to become the 21st century's leading health problem. Its prevalence is on the rise in all age groups and in all developed countries of the world. The exact aetiology of obesity still remains obscure. It is mainly caused by a combination of genetic factors, inappropriate eating and reduced activity. Besides, dysregulation of various hypothalamic mechanisms controlling energy intake and energy expenditure have also been implicated in its development and progression. In the last few years, steady advances made in the understanding of the body's weight regulating mechanisms has helped to define novel sites for targeting and intervention in order to reduce intake and enhance expenditure. Based on this, many new antiobesity drugs have been developed. Some of them are in the early stages of development and some of compounds acting on these sites are already available.

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Objective: To investigate the interaction between haloperidol and bicuculline in seizure and catalepsy models of mice. Methods: The effect of different doses of bicuculline (0.7-2.1 mg/kg, i.p.) was studied on severity of haloperidol (1 mg/kg, i.p.)-induced catalepsy using that Bar test and the effect of varying doses of haloperidol (1-3 mg/kg, i.p.) was studied on the onset of myoclonic spasm and clonic convulsions induced by bicuculline in mice. Results: Haloperidol-induced catalepsy was potentiated by bicuculline and bicuculline-induced seizures were inhibited by haloperidol. Conclusion: Haloperidol inhibited bicuculline-induced seizures probably by reducing the excitatory input to the cerebral cortex and bicuculline potentiated haloperidol-induced catalepsy by reducing dopaminergic transmission in substantia nigra.

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Objective: To evaluate whether pre-treatment with alpha tocopherol (Vitamin - E) can minimise gastric ulceration induced by pyloric ligation in rats and to delineate the probable mechanism of action. Methods: Alpha tocopherol was administered orally in two different doses for 2 weeks to two groups of 10 rats each, followed by pyloric ligation. After 18 hours, the pH, volume and mucopolysaccharide content of gastric juice and ulcer index were estimated. The results were compared with the control group which did not receive the vitamin, but was subjected to pyloric ligation. Results: Alpha tocopherol administration, in a dose dependent manner, decreased the ulcer index and volume of gastric secretion and increased the mucopolysaccharide content and pH of the juice. Conclusion: Vitamin E protects the gastric mucosa by decreasing gastric acid secretion and increasing the mucus secretion. Its effects may be mediated through its anti-oxidant effect.

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Objectives: To study the disposition of (-)-norepinephrine (NE) and (-)-epinephrine (E) in ileum of WLH chicken. Method: Disposition study was conducted using oil-immersion technique of Kalsner and Nickerson. The segments of ileum were mounted in isolated organ bath using standard methods. The relaxant response of carbachol contracted ileum to NE and E alone and in presence of different combinations of inhibitors of different routes of disposition, such as at any given time only one route of disposition of CAs was left uninhibited, was recorded. Then PSS was replaced by mineral oil and recovery of relaxation was recorded. The t50 values of control experiments were compared with t50 values in presence of inhibitors. Results: The relative rate of different routes of disposition of catecholamines was in the following order: for (-)-NE, uptake 2 > COMT > uptake 1 > MAO; for (-)-E, COMT > uptake 2 > MAO = uptake 1 . The role of enzymatic degradation is almost equal to that of uptake processes for both (-)-NE and (-)-E. Conclusion: In chicken ileum reuptake is still an important route of inactivation of catecholamines but its role is almost equal to that of enzymatic degradation.

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