Abstract  Twelve Florida native wethers were given ammonium metavandate, calcium orthovanadate and calcium pyrovanadate by capsule in a study to examine the toxicity of the compounds. The initial daily dosage of 100 mg elemental vanadium was increased by 50 mg at 2-d intervals for an assessment not only of the toxic effects, but also to determined the amount that caused a decline in feed intake to 25% of that of control animals. The initial decline in feed intake was observed at 400 to 500 mg vanadium/d (9.6 to 12 mg/kg body weight, 310 to 350 ppm); a rapid decline in feed intake was accompanied by diarrhea. One sheep fed 550 mg vanadium as calcium orthovanadate died 3 d after dosing. One animal on each of the other three treatments was killed and necropsied for immediate comparison. Extensive mucosal hemorrhage of the small intestine and diffuse or petechial subcapsular hemorrhages of the kidneys were observed for sheep fed all compounds. The three vanadium compounds appeared to be similar in toxicity, as determined by abrupt declines in feed intake and pathological changes of the intestine and kidney. For a determination of acute toxicosis, three sheep were given 40 mg/kg body weight of vanadium as NH4VO3 in gelatin capsules and two sheep were included as controls. Two of the treated animals died within 80 h after administration and the other three were killed at 96 h. Vanadium content of kidney, liver, bone, spleen, lung and muscle was elevated by treatment.

Abstract  Sodium metavanadate (NaVO3) and vanadyl sulphate pentahydrate (VOSO4 X 5H2O) were administered to rats and mice. The following LD50 (14-day) were determined: NaVO3, 98.0 mg/kg (rats) and 74.6 mg/kg (mice) when given orally, and 18.4 mg/kg (rats) and 35.9 mg/kg (mice) when given i.p.; VOSO4 X 5H2O, 448.0 mg/kg (rats) and 467.2 mg/kg (mice) when given orally, and 74.1 mg/kg (rats) and 113.0 mg/kg (mice) when given i.p. The majority of deaths occurred during the first 24 h. The clinical and physical signs appearing after the intoxication include irregular respiration, diarrhea, ataxia and paralysis of the hind legs. These signs disappeared for the most part after 48 h, which suggests a quick elimination of vanadium.

Abstract  Acute toxicity tests on 113 environmental chemicals were conducted by the order of the Japanese government agencies. The LD50S or LC50S for 23 household chemicals, 11 medical drugs, 10 drug additives, 20 food additives, 13 industrial chemicals, 14 environmental pollutants, 12 agricultural chemicals and 5 organic solvents are presented together with the major toxic signs and symptoms and macroscopic changes in tissues. These toxicity data will be useful as an information source for regulatory purposes and also for prediction of the potential for acute toxicity of a wide variety of new chemicals.

Abstract  Diabetes is characterized by derangements in carbohydrates, protein and fat metabolism caused by the complete or relative insufficiency of insulin secretion. The decreased oxidative stress in diabetes includes the autoxidation of glucose and non enzymaticglycation and also changes in the antioxidants defense systems. As the diabetes is lowered in human the pharmacological effects of a drug becomes toxic. Our aim was to evaluate the invivo effect of the anti diabetic compound Vanadium in non- diabetic rat models. The oral administration of Vanadium peroxide shows significant changes in the Cholesterol and TG with organ morphology and enhancement in clinical and experimental parameters.Vanadium is an important environmental and industrial pollutant. It is a dietary micronutrient and it has been recently considered as a pharmacological agent. Vanadium compounds have a major role in cellular regulation, with profound effects on enzymes of plasma membrane. Vanadium is one of the abundance trace elements widely distributed in the environment. It is used in steel and chemical industries, and is a containment of many ores, coals, and petroleum oils the manufacture of pigments, in photography and in insecticides. It is been used medicinally as anticeptic, spirochetocide, antituberculotic and antianemic agents and general tonic.

Abstract  The protective effect of Eucalyptus tereticornis leaf extract and its potency has been compared with Liv.52 following V(2)O(5) induced hepatotoxicity in albino rats. LD(50) estimated for V(2)O(5) was 69.6 mg/kg b.wt. The administered doses of V (2)O(5) were LD(50)/10(th) for acute and 1/7(th), 1/14(th) and 1/21(th) of sublethal close for subacute (7, 14 and 21 ds) respectively. Body weight, liver weight and hepatosomatic index were assessed. Hepatotoxicity was assessed in terms of hepatic total proteins, total lipids and total cholesterol. V,05 intoxication significantly increased liver weight, hepatosomatic index, total lipids and total cholesterol, while significantly decreased body weight and total proteins. Pretreatment with close of 100 mg/kg b.wt of Eucalyptus tereticornis leaf extract and 0.125 ml/kg b.wt. of Liv.52 syrup restored the increased liver weight, hepatosomatic index, total lipids and total cholesterol and decreased parameters like body weight and total proteins toward normalcy. The results reveal that Eucalyptus terelicornis leaf extract modulates V(2)O(5) toxicity like well known hepatoprotectant, however the modulation is less than Liv.52.