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

In a replicated 2-yr study, 32 Holstein cows in midlactation were fed diets containing tall fescue hay that was free of or infected with endophyte and with or without added vitamin E in a 7-wk trial to examine the effect of vitamin E supplementation on symptoms associated with fescue toxicosis. Treatments were 1) uninfected tall fescue, 2) tall fescue infected with endophyte, 3) infected tall fescue plus 1000 IU of vitamin E/d, and 4) infected tall fescue plus 2000 IU of vitamin E/d. Feed intake, milk yield, rectal temperature, and body weight change were not significantly altered by dietary treatment. Concentration of prolactin in plasma was lower for cows fed the infected tall fescue than for those fed the uninfected tall fescue. No differences in alkaline phosphatase content of plasma were detected because of tall fescue or vitamin E treatment. Vitamin E supplementation had no effect on symptoms that were associated with fescue toxicosis in lactating dairy cows fed tall fescue hay that was infected with endophyte.
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PMID:Effect of dietary supplementation with vitamin E for lactating dairy cows fed tall fescue hay infected with endophyte. 909 8

Incubation of primary cultures of rat hepatocytes with K2CR2O7 and deferoxamine (DFO), an iron chelator, resulted in a marked decrease in cellular levels of DNA single-strand breaks caused by K2Cr2O7. Cellular treatment with DFO also suppressed both dichromate-induced cytotoxicity--evaluated by the leakage of lactate dehydrogenase, and lipid peroxidation--as monitored by malondialdehyde formation. In addition, treatment with DFO attenuated the suppression of the levels of vitamin E and C as well as the inhibition of alkaline phosphatase and glutathione peroxidase activity attributed to K2Cr2O7. However, DFO had no influence on the cellular level of glutathione or the activity of glutathione reductase and superoxide dismutase suppressed by dichromate. Under the same experimental conditions, cellular uptake and distribution of chromium were not affected by DFO. These results indicate that DFO protects cells from chromium (VI)-induced DNA strand breaks, cytotoxicity, lipid peroxidation, vitamin E and C depression, and glutathione peroxidase inhibition The role of antioxidants in chromium (VI)-induced cytotoxicity, DNA breaks, and lipid peroxidation is discussed.
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PMID:Protective effect of deferoxamine on chromium (VI)-induced DNA single-strand breaks, cytotoxicity, and lipid peroxidation in primary cultures of rat hepatocytes. 919 15

Dietary zinc deficiency in rats causes increased osmotic fragility of their erythrocytes. In this study, the influence of supplementary antioxidants (vitamin C, vitamin E or beta-carotene) on osmotic fragility, oxidative damage and components of the primary defense system of erythrocytes of zinc-deficient rats was investigated. Indicators of hemolysis in vivo were also examined. Five groups of 12 male rats were force-fed a zinc-adequate diet (control rats), a zinc-deficient diet or a zinc-deficient diet enriched with vitamin C, vitamin E or beta-carotene. Compared with the control rats, the rats fed the zinc-deficient diet without supplementary antioxidants had greater red blood cell osmotic fragility, higher concentrations of thiobarbituric acid-reactive substances and alanine, higher glutathione S-transferase activity, lower concentration of glutathione and activity of glutathione peroxidase as well as lower activity of superoxide dismutase in plasma (P < 0.05). Supplementation with antioxidants generally improved osmotic fragility in zinc-deficient rats without influencing zinc concentration or alkaline phosphatase activity in plasma, indicators of zinc status. At some of the hypotonic saline concentrations tested, vitamin C and beta-carotene significantly affected osmotic fragility. The zinc-deficient rats fed a diet without supplementary antioxidants had significantly higher concentrations of alanine in erythrocytes than the zinc-deficient rats supplemented with vitamin C, vitamin E or beta-carotene and had significantly higher levels of thiobarbituric acid-reactive substances in erythrocytes than the rats supplemented with beta-carotene. There was no indication of hemolysis in vivo in rats fed zinc-deficient diets. The results show that supplementary antioxidants decrease osmotic fragility and oxidative damage of erythrocytes in zinc-deficient rats.
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PMID:Supplementation with vitamin C, vitamin E or beta-carotene influences osmotic fragility and oxidative damage of erythrocytes of zinc-deficient rats. 920 82

The present study was designed to investigate the effect of antioxidant supplementation on the in vitro osmotic fragility of erythrocytes from zinc-deficient rats. Rats were fed either a zinc-adequate diet, zinc-deficient diet or a zinc-deficient diet enriched either with vitamin C or vitamin E or beta-carotene. Components of the primary antioxidant system of erythrocytes, parameters of hemolysis in vivo and indicators of liver injuries were also examined. In order to ensure adequate and identical food intake rats were force-fed by intragastric tube. The supplementation with antioxidants led to a marked improvement of the osmotic fragility without having influenced zinc status of the animals and components of the antioxidant system. The strongest effect was exerted by vitamin E. The rats fed the zinc-adequate diet (control group) showed unusually high values of erythrocytes osmotic fragility. Therefore there was no difference between control group and zinc-deficient group. A possible reason for this is discussed. Zinc deficiency led to a reduction of serum zinc concentration and alkaline phosphatase activity as well as to changes in the antioxidant system of erythrocytes characterized by a decrease of glutathione and an increase of glutathione S-transferase activity. Superoxide dismutase activity in serum decreased. There was no indication for hemolysis in vivo and for liver injuries.
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PMID:Influence of vitamin C, vitamin E and beta-carotene on the osmotic fragility and the primary antioxidant system of erythrocytes in zinc-deficient rats. 927 23

Few reference values for use in metabolic profile tests for the maintenance of high productivity and the prevention of production diseases have been reported in Japanese Black beef cattle. To obtain basic data, 101 healthy steers at farms with high productivity and low frequencies of disease and death in Miyazaki Prefecture, Japan, were examined for the values of their serum components in this preliminary study. At the later fattening stage (5 to 20 months after introduction), statistically significant increases were observed in the mean serum activities of lactic dehydrogenase, glutamic-oxalacetic transaminase, gamma-glutamyl transpeptidase, and creatine phosphokinase, the mean serum contents of triglyceride, total cholesterol, albumin (Alb), total protein, blood urea nitrogen, magnesium, and vitamin E, and the mean serum calcium (Ca)/inorganic phosphorus (IP) ratio, and statistically significant decreases were seen in the mean serum alkaline phosphatase activity and the mean serum contents of glucose, IP, and vitamin A. The mean serum Alb/globulin ratio and the mean serum Ca and nonesterified fatty acids contents demonstrated no statistically significant changes.
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PMID:Values of the serum components in Japanese black beef steers at farms with high productivity and low frequencies of disease and death in Miyazaki Prefecture. 936 34

Pretreatment of primary cultures of rat hepatocytes with sodium diethyldithiocarbamate (DDTC) for 15 min prior to exposure to K2Cr2O7 resulted in a marked decrease in dichromate-induced cytotoxicity, as evaluated by the leakage of lactate dehydrogenase, and in lipid peroxidation, as monitored by malondialdehyde formation. In addition, pretreatment with DDTC attenuated the suppression of the level of vitamin E attributed to K2Cr2O7. However, DDTC pretreatment had no effect on the cellular levels of glutathione or vitamin C or on the activity of the glutathione reductase, glutathione peroxidase, superoxide dismutase or alkaline phosphatase suppressed by dichromate. Under the same experimental conditions, cellular uptake or distribution of chromium was not affected by DDTC. These results indicate that the protective effect of DDTC on chromium (VI)-induced cytotoxicity as well as lipid peroxidation may be associated with the level of nonenzymatic antioxidants such as vitamin E.
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PMID:Protective effect of diethyldithiocarbamate pretreatment on chromium (VI)-induced cytotoxicity and lipid peroxidation in primary cultures of rat hepatocytes. 949 63

Cisplatin [cis-dichlorodiammineplatinum (II)] is a widely used chemotherapeutic drug that is toxic to the kidney. Concurrent administration of cysteine together with vitamin E, Crocus sativus and Nigella sativa reduced the toxicity of cisplatin in rats. When administered i.p. for 5 alternate days with 3 mg/kg cisplatin, cysteine (20 mg/kg) together with vitamin E (2 mg/rat) an extract of Crocus sativus stigmas (50 mg/kg) and Nigella sativa seed (50 mg/kg) significantly reduced blood urea nitrogen (BUN) and serum creatinine levels as well as cisplatin-induced serum total lipids increases. In contrast, the protective agents given together with cisplatin led to an even greater decrease in blood glucose than that seen with cisplatin alone. The serum activities of alkaline phosphatase, lactate dehydrogenase, malate dehydrogenase, aspartate aminotransferase and alanine aminotransferase of cisplatin-treated rats were significantly decreased, whereas the activities of glutathione reductase and isocitrate dehydrogenase were significantly increased. Addition of cysteine and vitamin E, Crocus sativus and Nigella sativa in combination with cisplatin partially prevented many changes in the activities of serum enzymes. In cisplatin-treated rats, the liver activities of isocitrate dehydrogenase and aspartate aminotransferase were significantly increased, whereas much greater changes were found in the kidneys, with increased activity of glucose-6-phosphate dehydrogenase and decreased activities of alkaline phosphatase, isocitrate dehydrogenase, malate dehydrogenase, aspartate aminotransferase, alanine aminotransferase, sorbitol dehydrogenase and gamma-glutamyl transferase, as well as a decreased phosphorylation to oxidation ratio in the mitochondria, indicating reduced adenosine triphosphate production. Also, administration of cysteine and vitamin E, Crocus sativus and Nigella sativa together with cisplatin partially reversed many of the kidney enzymes changes induced by cisplatin. Cysteine together with vitamin E, Crocus sativus and Nigella sativa tended to protect from cisplatin-induced falls in leucocyte counts, haemoglobin levels and mean osmotic fragility of erythrocytes and also prevented the increase in haematocrit. The results of this study indicate a basis for the toxic effects of cisplatin, and suggest a possible way of counteracting the toxicity by introducing protective agents such sulphydryl compounds, other antioxidants and extracts of natural products. It also appears that cells adapt to the effects of cisplatin through the induction of systems that produce NADPH, which in turn compensates the decrease of free sulphydryl groups. We conclude that cysteine and vitamin E, Crocus sativus and Nigella Sativa may be a promising compound for reducing cisplatin-toxic side effects including nephrotoxicity.
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PMID:Protective effect of cysteine and vitamin E, Crocus sativus and Nigella sativa extracts on cisplatin-induced toxicity in rats. 960 69

We showed previously that supplementation for 30 d with 800 IU (727 mg) vitamin E/d did not adversely affect healthy elderly persons. We have now assessed the effects of 4 mo of supplementation with 60, 200, or 800 IU (55, 182, or 727 mg) all-rac-alpha-tocopherol/d on general health, nutrient status, liver enzyme function, thyroid hormone concentrations, creatinine concentrations, serum autoantibodies, killing of Candida albicans by neutrophils, and bleeding time in 88 healthy subjects aged >65 y participating in a double-blind, placebo-controlled trial. No side effects were reported by the subjects. Vitamin E supplementation had no effect on body weight, plasma total proteins, albumin, glucose, plasma lipids or the lipoprotein profile, total bilirubin, alkaline phosphatase, serum aspartate aminotransferase, serum alanine aminotransferase, lactate dehydrogenase, serum urea nitrogen, total red blood cells, white blood cells or white blood cell differential counts, platelet number, bleeding time, hemoglobin, hematocrit, thyroid hormones, or urinary or serum creatinine concentrations. Values from all supplemented groups were within normal ranges for older adults and were not significantly different from values in the placebo group. Vitamin E supplementation had no significant effects on plasma concentrations of other antioxidant vitamins and minerals, glutathione peroxidase, superoxide dismutase, or total homocysteine. There was no significant effect of vitamin E on serum nonspecific immunoglobulin concentrations or anti-DNA and anti-thyroglobulin antibodies. The cytotoxic ability of neutrophils against Candida albicans was not compromised. Thus, 4 mo of supplementation with 60-800 IU vitamin E/d had no adverse effects. These results are relevant for determining risk-to-benefit ratios for vitamin E supplementation.
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PMID:Assessment of the safety of supplementation with different amounts of vitamin E in healthy older adults. 970 Nov 88

Oxidant stress has been implicated as playing a role in the pathogenesis of cholestatic liver injury. The objective of this study was to determine whether the xanthine oxidase/xanthine dehydrogenase enzyme system was involved in this oxidant stress. Adult Sprague-Dawley rats were treated with the xanthine oxidase inhibitor, oxypurinol, and randomized to bile duct ligation or sham surgery; vehicle-treated, sham-operated rats served as controls. After 5 d of bile duct ligation, serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and total and direct bilirubin concentrations were significantly elevated, and increased lipid peroxidation of hepatic mitochondria and microsomes was present. Treatment with oxypurinol reduced the aspartate aminotransferase, alanine aminotransferase, and bilirubin values by 26-47% but did not alter the increased lipid peroxidation of mitochondria and microsomes. Serum vitamin E:total lipids ratio was also reduced in both bile duct-ligated groups, consistent with oxidant injury. These data show that inhibition of xanthine oxidase reduces biochemical evidence of hepatocellular injury during bile duct ligation without affecting oxidant damage to intracellular hepatocyte organelles. Thus, in this model a component of cholestatic injury appears to have been caused by oxidant stress from a source outside of the hepatocyte.
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PMID:Effect of oxypurinol, a xanthine oxidase inhibitor, on hepatic injury in the bile duct-ligated rat. 972 20

DEHP [di-(2 ethyl hexyl) phthalate], a widely used plasticizer in blood storage bags, leaches out in appreciable amounts into blood (about 10 mg/100 ml) resulting in exposure of recipients of blood transfusion to this compound. Various reports indicate the toxicity of DEHP, particularly in liver and reproductive organs but all these studies used large doses (up to 2 g or more/Kg body weight) and oral route of administration which are not relevant to the intravenous administration during blood transfusion or the low amounts present in blood. We have studied changes in the activity of some important enzymes-gamma-GT, ALT, CPK, LDH, alkaline phosphatase, acid phosphatase, beta-glucuronidase and few other parameters like vitamin E, glutathione, serum albumin etc in rats administered low doses of DEHP (corresponding to transfusion of 2, 4, 6 and 10 units of blood). Histopathology of the organs has also been carried out. The results obtained indicate no serious toxic effects for DEHP at the level present in blood stored in DEHP plasticized blood bags as evidenced by the lack of any significant alteration in most of the biochemical parameters studied. Even in those cases where there was alteration (for e.g., decrease in the level of vitamin E) 24 hr after administration of DEHP, it returned to near normal level with in 72 hr to 7 days. No histopathological changes were observed in any of the organs at these levels of DEHP. It is concluded that DEHP did not cause any serious toxic effect even at doses corresponding to transfusion of several units of blood in a recipient.
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PMID:Toxic effect of systemic administration of low doses of the plasticizer di-(2-ethyl hexyl) phthalate [DEHP] in rats. 975 59


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