Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The toxic effects of bis (tributyltin) oxide (TBTO) on the rat liver were studied with an electron microscope and the accumulation sites of tin were determined with an X-ray microanalyzer. The activities of serum enzymes and the concentration of serum bilirubin were also analyzed. Male Wistar rats received an intramuscular injection of 0.5 ml/kg of TBTO. Marked swelling of the mitochondria appeared in the hepatocytes 4 h after injection of TBTO. Cytoplasmic vacuoles, which contained degenerated mitochondria, gradually increased in number in these hepatocytes. This in turn may have caused a decrease in the volume of hepatic cell cords and an enlargement of sinusoids in the entire hepatic lobule. However, fine structures of intrahepatic bile ducts were not altered. By X-ray microanalysis, tin peaks were preferentially obtained from swollen mitochondria of the hepatocytes. By polarographic analysis of the respiratory responses of mitochondria, it was demonstrated that rates of state 4 respiration and respiratory control ratio were significantly disturbed in TBTO-treated rats in comparison with those of controls. The activities of AST (aspartate aminotransferase) and ALT (alanine aminotransferase) were significantly increased after TBTO treatment, but those of ALP (alkaline phosphatase), LAP (leucine aminopeptidase) and total bilirubin were not changed. These results indicated that parenterally administered TBTO accumulated in the liver cell mitochondria and disturbed oxidative phosphorylation. Mitochondrial dysfunction might induce severe damage of the hepatocytes. Four days after injection of TBTO, hepatic structures and chemical indices were almost restored by the regeneration of hepatocytes.
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PMID:Studies on the hepatotoxicity induced by bis (tributyltin) oxide. 149 81

Tin is usually present in foods at levels of less than 4 micrograms/g. Higher levels may be found in some processed foods due to the addition of tin-based preservatives and stabilizers or to corrosion and leaching of the metal from unlacquered cans or from tin foils used in packaging. Estimates of dietary intake range from about 0.2 to greater than 5 mg Sn/day. Diets including a high proportion of canned vegetables and fish could supply greater than 30 mg Sn/day. Although intakes from dietary sources are generally considered to be harmless, a variety of adverse effects of tin have been reported, including effects on serum and bone alkaline phosphatase, lactic dehydrogenase, heme oxygenase, and 5-aminolevulinic acid dehydratase. Perturbations in glutathione metabolism have been reported, as have adverse effects on metabolism of essential trace minerals such as copper, zinc, and iron. Specific effects on calcium content of bone, serum, and kidney have also been described. Reported effects vary with the chemical form, dose of tin, and route and frequency of administration. Effects of tin in animal systems and on essential trace mineral absorption and excretion in human volunteers are reviewed. A summary of recent investigations on dietary tin-copper interactions and effects of tin on rat hepatocellular antioxidant protection are also presented.
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PMID:Anti-nutritive effects of dietary tin. 189 7

Metalorganic and quarternary ammonium compounds when added to culture medium inhibited growth of Aspergillus niger mycelium and activity of neutral and alkaline phosphatase. A quarternary ammonium compound, ethonium, and a tin-organic compound, tributyl oxide, exerted an inhibiting effect on activity of acid phosphatase which amounted to 54% of the total phosphatase activity in mycelium and 94% in the culture liquid. The rest of biocides induced lysis of intracellular membranes, phosphatase release from lysosomas, which made acid phosphatase activity higher. Being introduced into the mycelium homogenate the above compounds inhibited activity of the acid phosphatase. The same biocides inhibited extracellular acid phosphatase in the culture liquid. Recommendations are given on the use of a number of substances as means for protection of industrial materials from biolesions.
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PMID:[The action of different biocides on the phosphatase activity of Aspergillus niger]. 196 49

In a 106-wk toxicity and carcinogenicity study, groups of 60 male and 60 female weanling Wistar rats were fed 0, 0.5, or 50 mg bis(tri-n-butyltin)oxide (TBTO)/kg diet. In males, feed consumption was increased in all treated groups and increased water consumption occurred at 5 and 50 mg/kg. During the second year, body weight decreased in the 50-mg/kg males, while the females in that group showed no weight gain. Excess mortality was confined to the 50-mg/kg group towards the end of the study. Haematological changes, comprising anaemia, lymphocytopenia and thrombocytosis were noted mainly at the high-dose level. Also, signs of decreased kidney function and increased plasma enzyme activities (alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase) were noted. No effects on serum hormone concentrations (thyrotropin, follicle stimulating hormone, luteinizing hormone or insulin) were observed, except for a decrease in the free thyroxin:thyroxin ratio in both sexes at the high-dose level. Higher serum IgM and IgA levels were present at 50 mg/kg, while, in females, IgG was decreased. At 50 mg/kg, the ovaries, adrenals, spleen (females), heart (males), pituitary, liver and kidneys were increased in weight, but the thyroid weight was decreased in females. The total tin concentrations in liver and kidneys showed a dose relationship and, in general, the concentrations were similar after 1 and 2 yr. Non-neoplastic histological alterations after 1 yr consisted of a decrease in the cell height of the thyroid follicles in all dose groups, with a reduced number of psammoma bodies at 50 mg/kg, a decrease in splenic iron content at 5 (females only) and 50 mg/kg, and a slight bile-duct activation. After 2 yr, only the thyroid changes were still present. In addition, at 2 yr, vacuolation and pigmentation of the proximal tubular epithelium and nephrosis were enhanced at 50 mg/kg. The incidence of benign tumours of the pituitary was significantly elevated and enhanced at 0.5 and 50 mg/kg. At 50 mg/kg increases in pheochromocytomas in the adrenal medulla and in parathyroid adenomas (males) were noted, while adrenal cortical tumours were decreased (males). There was a low, non-dose-related incidence of pancreatic carcinoma. Other tumour rates were in line with control data. It is concluded that lifetime feeding of 50 mg TBTO/kg diet induces toxicity in various organ systems. An increase in some common tumours was found at the high dose, probably due to hormonal or immunological changes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Chronic toxicity and carcinogenicity of bis(tri-n-butyltin)oxide (TBTO) in the rat. 234 92

4 organotin derivatives (tributyltin acid, dibutyltin chloride, triphenyltin chloride, and triphenyltinbis (diethyl) dithiophosphate) were tested through subchronic treatment in 19 days old chickens. Their effects upon mineral metabolism were studied through biochemical investigations in kidney, bone, and blood. Bone mineral disturbances (depletion of Ca/P ratio) induced Ca elimination in blood, immobilised as calcium urates in kidney, and also increased values for alkaline phosphatase, following tin accumulation in bone. Butyl and phenyltin chloride were more toxic than dithiophosphate, and the intensity of effects was proportionate to the dose.
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PMID:Metabolic disturbances induced by organotins through subchronic treatment in chickens. Second communication: mineral metabolism. 277 39

After application of SnCl2 and tin incorporated into baker's yeast, the effects on carbonic anhydrase (CA), glutathione peroxidase (GPx), lactate dehydrogenase (LDH), alkaline phosphatase (AP) and leucine aminopeptidase (LAP) were measured. The tin contents of liver and kidneys were determined. CA and GPx are not affected. AP and LAP are inhibited by high concentrations of tin (as SnCl2). Tin incorporated into yeast exerts no effect. Inorganic tin produces increases in liver and kidneys.
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PMID:[Effects of tin on rats. II. Comparison of the effects of tin (II) chloride and yeast-incorporated tin]. 677 55

The effect of stannous chloride on bone metabolism was examined in weanling male rats given oral dose of 1.0 mg Sn/kg at 12-h intervals for 28 days. Tin administration produced progressive increase in tin content of the femoral diaphysis and epiphysis. Calcium content in the femoral epiphysis but not diaphysis was significantly decreased by tin administration for 28 days, while inorganic phosphorus contents in the femoral diaphysis and epiphysis were not changed significantly. Acid and alkaline phosphatase activities in the femoral diaphysis and epiphysis were markedly reduced by tin administration for 3 days, and significant decreases in the femoral epiphysis were also observed at 28 days. Meanwhile, ATPase and pyrophosphatase activities in the femoral diaphysis and epiphysis were not altered significantly by tin administration. From the present study, of mineral composition and its related enzyme activity, the decreases of acid and alkaline phosphatase activities in the femoral epiphysis were regarded as the biochemical manifestation of the toxic action of inorganic tin.
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PMID:Changes in mineral composition and its related enzyme activity in the femur of rats orally administered stannous chloride. 732 88

The dose-effect of stannous chloride on biochemical indices was examined in weanling male rats given oral doses of 0.3, 1.0 and 2.0 mg/kg at 12-h intervals for 90 days. The 3.0 mg/kg dose caused significant decreases of the relative weights of the femur, calcium concentration, lactic dehydrogenase and alkaline phosphatase activities in the serum, succinate dehydrogenase activity in the liver, and calcium content and acid phosphatase activity in the femoral diaphysis and epiphysis. Of the above indices, the 1.0 mg/kg dose produced significant reduction of succinate dehydrogenase activity in the liver, and calcium content and acid phosphatase activity in the femoral epiphysis. Those significant decreases were not observed with the 0.3 mg/kg dose, although a slight but not significant decrease of calcium content in the femoral epiphysis was observed. These results suggest that the no-effect level of inorganic tin orally administered would be lower than 0.6 mg/kg/day.
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PMID:Dose-effect of inorganic tin on biochemical indices in rats. 742 35

The dose-effect of inorganic tin (Sn) was examined in rats given 6 oral doses of stannous chloride at 12-h intervals. Of the biochemical indices for the toxicity of Sn reported previously, i.e. gastric acid secretion, duodenal alkaline phosphatase and hepatic phosphorylase activities, serum calcium (Ca) concentration, and femoral calcium content, significant decreases were found, except in gastric acid secretion (6X10 mg/kg). Sn, 6X3 mg/kg, decreased significantly the calcium content in the epiphysis of the femur but the decrease was not significant at 6X1 mg/kg. These results suggest that the critical organ in inorganic Sn toxicity is bone and that the oral no-effect dose level is 6X3 mg/kg.
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PMID:The oral administration of stannous chloride to rats. 746 57

Dibutyltin dichloride (DBTC; 6 mg/kg body weight, i.v.) induced acute interstitial pancreatitis in rats. The course of the pancreatitis was examined within 28 days by light and electron microscopy as well as by pathobiochemistry (amylase, lipase, alkaline phosphatase, and bilirubin in serum; tin concentration in biliopancreatic juice, tissue, and concretions). The pathogenesis of the DBTC-induced pancreatitis in rats was studied by different experimental designs (in intact animals, after bile duct ligation, after surgical bypass of the bile duct). DBTC caused toxic necrosis of the biliopancreatic duct epithelium, which is then shed into the duct and forms obstructing plugs in the distal common bile duct. Interstitial pancreatitis occurred during the first 4 days, accompanied by significantly increased activities of serum alpha-amylase and lipase. After 7 days extensive infiltration of the pancreatic interstitium with mononuclear cells was observed. Twenty-eight days after administration of DBTC one-third of the rats showed periductal and interstitial fibrosis as well as an active inflammatory process in the pancreas. The findings suggest a twofold pathogenesis of the DBTC-induced pancreatitis: first, the cytotoxic effects on the biliopancreatic duct epithelium lead to epithelial necrosis with obstruction of the duct, subsequent cholestasis, and interstitial pancreatitis; and second, the hematogenic DBTC effects cause direct injury of pancreatic cells (mitochondrial damage, autophagy, cell necrosis) followed by interstitial edema and inflammation. Both processes lead to this special type of DBTC-induced acute pancreatitis with a tendency to a chronic course, when the obstruction of the duct and cholestasis persist.
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PMID:Acute interstitial pancreatitis in rats induced by dibutyltin dichloride (DBTC): pathogenesis and natural course of lesions. 936 Oct 94


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