Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of two new chelating agents-Tiron (4,5-dihydroxy-1,3-benzene disulphonic acid disodium salt) and succinic acid--on the mobilization of beryllium was studied. Animals were exposed to beryllium nitrate (1 mg kg(-1) i.p.) daily for 21 days. Administration of beryllium nitrate showed a marked decrease in haemoglobin percentage, blood sugar, serum alkaline phosphatase and serum protein and a significant increase in the activity of transaminases. Tissue protein and glycogen contents and the activity of alkaline phosphatase, adenosine triphosphatase and succinic dehydrogenase showed significantly decreased values, but beryllium nitrate provoked a considerable increase in the activity of acid phosphatase and glucose-6-phosphatase in the vital and reproductive organs. Significant improvement in the haematological and biochemical parameters was observed with Tiron but no therapeutic effect was seen with succinic acid. Atomic absorption spectrophotometry (AAS) also showed a decreased level of beryllium concentration in the liver and kidney after Tiron therapy.
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PMID:Influence of chelating agents on the toxicity and distribution of beryllium in rats. 980 33

The efficacy of Tiron (4,5-dihydroxybenzene 1,3-disulfonic acid disodium salt) was examined in the treatment of beryllium-induced maternal and developmental toxicity in rats. Single administration of beryllium nitrate at a dose of 50 mg/kg (i.m.) on day 13 of gestation caused reductions in fetal and placental weights, the number of implantation sites and number of corpora lutea, as well as causing post-implantation loss, stunted growth, increase in the number of resorptions, and also a disturbed sex ratio. Maternal toxicity was demonstrated by reduction in body weight gain. Administration of beryllium also showed significant alteration in the hematological and biochemical indices of the mother as well as the fetus. Marked decreases were recorded in hemoglobin percentage, blood sugar levels, serum protein contents and serum alkaline phosphatase activity. By contrast, significant elevation was found in the activity of transaminases (aspartate aminotransferase and alanine aminotransferase). Tissue protein contents, glycogen contents, activities of alkaline phosphatase, adenosine triphosphatase and succinic dehydrogenase of kidney, lungs and uterus, and maternal and fetal liver all showed significantly decreased values after beryllium exposure, and remarkable elevation was observed in acid phosphatase, glucose-6-phosphatase and hepatic lipid peroxidation. These parameters were restored considerably with administration of 471 mg/kg i.m. Tiron from days 14 to 18 of gestation. Atomic absorption spectrophotometry also revealed a high concentration of beryllium in different organs of pregnant rats. Interestingly, a small amount of metal ion was also detected in the fetus and reduced accumulation of beryllium was noticed after Tiron treatment.
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PMID:Protective effect of Tiron (4,5-dihydroxybenzene-1,3-disulfonic acid disodium salt) against beryllium-induced maternal and fetal toxicity in rats. 1218 11

Influence of adjuvants i.e., alpha-tocopherol (25 mg/kg, p.o.) and piperine (10 mg/kg, p.o.) on therapeutic potential of chelator tiferron (300 mg/kg, i.p.) was evaluated to encounter toxicogenic events of beryllium exposure. Albino rats were exposed to beryllium nitrate (1 mg/kg, i.p.) daily for 28 days followed by treatment of aforesaid therapeutic agents for 5 consecutive days. Results were considered to be significant at p < or =0.01 and p < or =0.05. Exposure to beryllium increased its concentration in liver, kidney and serum causing significant alterations in the activity of CYP-450 2E1 system, microsomal lipid peroxidation and protein; alkaline phosphtase, lactate dehydrogenase, gamma-glutamyl transpeptidase, bilirubin, creatinine and urea in serum; activity of acid phosphatase, alkaline phosphatase, adenosine triphosphatase, glucose-6-phosphatase and succinic dehydrogenase in liver and kidney. Beryllium exposure also induced severe alterations in histopathology and ultramorphology of liver and kidney proving its toxic consequences at cellular level. Tiferron along with adjuvants dramatically reversed alterations of all variables more towards control rather than individual treatment. Study concluded that tiferron in combination with alpha-tocopherol and piperine respectively was beneficial in diluting beryllium induced systemic toxicity; however, combination of tiferron and piperine presented more pronounced therapeutic potential.
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PMID:Amelioration of beryllium induced alterations in hepatorenal biochemistry and ultramorphology by co-administration of tiferron and adjuvants. 1727 10

In the present study an attempt has been made to evaluate the effect of Tiron along with Zinc, Selenium and Vitamin E against vanadium intoxication in female albino rats. Toxicant caused significant increase in the activities of serum transaminases, serum alkaline phosphatase and lactate dehydrogenase. Significant decrease was observed in blood sugar, serum albumin and triglyceride levels whereas serum proteins, cholesterol and urea levels increased significantly during toxicity (p </= 0.001). Hepatic lipid peroxidation increased significantly, whereas significant depletion was observed in reduced glutathione after vanadium administration. The activity of glucose-6-phosphatase in the liver was also inhibited significantly after vanadium administration. A significant rise was observed in glycogen content of liver and kidney after toxicant exposure. Activities of alkaline phosphatase, adenosine triphosphatase and succinic dehydrogenase were inhibited significantly on the contrary activity of acid phosphatase elevated in kidney. Histopathological examination of the liver and kidney using light and ultramicroscopic study also substantiated the above findings. It was found that therapy with Tiron was effective but significant recovery in all the parameters was found with Tiron + Se followed by Tiron+ VitE and Tiron +Zn.
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PMID:Effect of tiron and its combination with nutritional supplements against vanadium intoxication in female albino rats. 1753 42

Intervention of chelating agent tiferron (sodium-4,5-dihydroxy-1,3-benzene disulfonate; 300 mg/kg, intraperitoneal) with propolis (honey beehive product; 200 mg/kg, p.o.) was evaluated to encounter the characteristic biochemical and ultra-morphological alterations following subchronic exposure to beryllium. Female albino rats were challenged with beryllium nitrate (1 mg/kg, i.p.) daily for 28 days followed by treatment of the above-mentioned therapeutic agents either individually or in combination for five consecutive days. Exposure to beryllium increased its concentration in the serum, liver and kidney, and caused significant alterations in cytochrome P450 activity, microsomal lipid peroxidation and proteins. Activities of alkaline phosphatase, lactate dehydrogenase, gamma-glutamyl transpeptidase, bilirubin, creatinine and urea in the serum and activity of acid phosphatase, alkaline phosphatase, adenosine triphosphatase, glucose-6-phophatase and succinic dehydrogenase in the liver and kidney were significantly altered after beryllium administration. Beryllium exposure also induced severe hepatorenal alterations at histopathological and ultra-morphological level. Tiferron along with propolis dramatically reversed the alterations in all the variables more towards control rather than their individual treatment. The study concludes that pharmacological intervention of tiferron and propolis is beneficial in attenuating beryllium-induced systemic toxicity.
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PMID:Pharmacological intervention of tiferron and propolis to alleviate beryllium-induced hepatorenal toxicity. 1870 51