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PubMedDate not supplied

Effect of sodium/potassium salt (potash) on the bioavailability of ibuprofen in healthy human volunteers.

The influence of sodium/potassium salt water extract incorporated in a traditional meal on the bioavailability of Ibuprofen tablets 400mg dose was studied in 6 healthy human volunteers. There was a statistically significant decrease in the plasma levels of ibuprofen, and its metabolites, hydroxy-ibuprofen and carboxy-ibuprofen, respectively, when the meal containing sodium/potassium salt extract was administered with the ibuprofen tablets than when taken under fasting state or with the meal without the fruit extract. The Cmax, AUC0-6hr and Ka for ibuprofen decreased from 38.04 +/- 0.70microg/ml to 20.06 +/- 1.21microg/ml (p<0.05); 28.030 +/- 2.40microg/ml.hr to 14.180 +/- 1.12microg/ml.hr (p<0.05) and 1.048 +/- 0.02hr(-1) to 0.602 +/- 0.03hr(-1). Similarly, the Cmax for hydroxy-ibuprofen and carboxy-ibuprofen decreases from 43.04 +/- 0.76microg/ml to 27.21 +/- 0.24microg/ml (p<0.05) and 48 +/- 0.71microg/ml to 31.08 +/- 0.12microg/ml (p<0.05) respectively; while AUC0-6hr for hydroxy-ibuprofen decreased from 34.120 +/- 0.49microg/ml.hr to 16.410 +/- 0.27microg/ml.hr while that of carboxy-ibuprofen decreased from 36.121 +/- 1.97microg/ml.hr to 19.278 +/- 0.92microg/ml.hr respectively. The Kel for hydroxy-ibuprofen increased from 0.71 +/- 0.94 hr(-1) to 0.81 +/- 0.21 hr(-1) (p<0.05) respectively. The study has indicated that sodium/potassium salt extract significantly decreased the bioavailability of ibuprofen.

Adult↗
PubMed1986

Treatment of amiodarone associated thyrotoxicosis by simultaneous administration of potassium perchlorate and methimazole.

Amiodarone iodine induced thyrotoxicosis occurs frequently in patients residing in areas of mild iodine deficiency and in patients with preexisting goiter. Drug therapy of the hyperthyroidism is often unsuccessful. Twenty-three patients with amiodarone induced thyrotoxicosis were either not treated, treated with 40 mg methimazole daily or with methimazole and 1 gm potassium perchlorate daily for up to 40 days and then with methimazole alone. Thyrotoxicosis was more likely to spontaneously remit in patients without goiter. Therapy with methimazole alone was unsuccessful in inducing euthyroidism in 5 patients with goiter. However, combined therapy with methimazole and potassium perchlorate rapidly alleviated hyperthyroidism in almost all patients with goiter. This drug combination is successful because perchlorate inhibits the active transport of iodine into the thyroid and methimazole blocks the intrathyroidal synthesis of thyroid hormones.

Adult↗
PubMed2006

Uptake of amiodarone by thyroidal and non-thyroidal cell lines.

Amiodarone perturbs thyroid function, causing overt hypothyroidism or hyperthyroidism in 15% of patients. Changes in thyroid function are likely due, at least in part, to amiodarone and/or desethylamiodarone (DEA) concentration into the thyroid gland, but mechanisms whereby the drug uptake occurred are not known. Thyroidal (FRTL-5) or non-thyroidal [Chinese hamster ovary wild-type (CHOwt) or CHO stably transfected with NIS (CHO-NIS)] cells were exposed to 10 microM amiodarone or DEA. Cellular content of both drugs was measured by HPLC and normalized by protein concentration. Cellular concentration of the two drugs was higher in FRTL-5 (mean +/- SD 17.2 +/- 1.2 microg/mg protein of amiodarone and 18.9 +/- 0.7 microg/mg protein of DEA) than in CHO-NIS and CHOwt cells (10.8 +/- 0.8 microg/mg protein and 12.8 +/- 0.2 microg/mg protein, respectively, of amiodarone (p < 0.004); 11.9 +/- 0.1 microg/mg protein and 11 +/- 0.2 microg/mg protein, respectively, of DEA (p < 0.0002). DEA concentration was higher than that of amiodarone in all cell lines (p < 0.002). Differences between FRTL-5 and CHO cell lines were not dependent on TSH: in fact, cellular content of either drug did not change in the presence or absence of TSH in the culture medium. NIS did not intervene in amiodarone or DEA entry into thyroid cells, since amiodarone and DEA content was the same in CHOwt and CHO-NIS cells; in addition, KClO4 inhibited NIS function, but had no effect on drug uptake by the cells. At variance, 80 microM DEA reduced 125I uptake by CHO-NIS cells by 40% at 30 min without affecting cell viability. In conclusion, mechanisms whereby amiodarone is taken up by thyroid cells remain largely unknown, but the two main factors involved in thyroid-specific cellular transport, ie, NIS and TSH, seem to be excluded.

Amiodarone↗
PubMed2004

Ki-ras mutational analysis in rat follicular-cell proliferative lesions of the thyroid gland induced by radioactive iodine and potassium perchlorate.

Although in both human and experimental pathology ras mutations have been related to the origin and progression of follicular-cell tumours, reports differ considerably with respect to the frequency of such mutations. The present paper reports, using direct sequencing, the incidence of Ki-ras mutations (codons 12 and 13) in follicular-cell carcinomas of the thyroid gland in Wistar rats induced by administration of radioactive iodine and potassium perchlorate. Direct sequencing revealed no mutations in the amplified gene segment of any of the 72 carcinoma samples studied. This absence of mutations agrees with some and is in sharp contrast with other previous reports in the literature, both for experimental animals and in studies of human thyroid follicular-cell carcinoma. Our results suggest that Ki-ras activation via mutations at codons 12 and 13 is neither a constant event nor an early event in the development of rat thyroid follicular-cell carcinoma.

Adenocarcinoma, Follicular↗
PubMed1998

Iodine supplementation of laying hen feed: a supplementary measure to eliminate iodine deficiency in humans?

Iodine deficiency still exists in many countries worldwide, to a certain degree this is also true for Germany. Food of animal origin can be a good source for iodine depending on the feed. To investigate the possible use of laying hen feed enriched with iodine, we conducted a feeding experiment with 40 laying hens receiving feed with different amounts of iodine either as KIO3 or in the form of seaweed. Iodine concentration in eggs increased significantly depending on iodine intake after a 2 week period. Seaweed could also be used as an iodine source by the hens. A subsequent consumption study with 24 volunteers showed that eggs enriched with iodine can increase human's iodine excretion and therefore improve human's iodine supply. This new strategy is thought to accompany salt iodization programs, not to replace them.

Animals↗
PubMed2003

Intravenous phosphate in the intensive care unit: more aggressive repletion regimens for moderate and severe hypophosphatemia.

OBJECTIVE: To evaluate efficacy and safety of aggressive correction of hypophosphatemia with intravenous potassium phosphate in the ICU. DESIGN AND SETTING: Randomized interventional prospective study in the medical and surgical ICU of a tertiary university hospital. PATIENTS: Critically ill patients with hypophosphatemia between June and November 1998. MEASUREMENTS AND RESULTS: Patients with moderate hypophosphatemia (<0.65 and >0.40 mmol/l; n=37) were randomized into two groups: group 1 received 30 mmol potassium phosphate intravenously in 50 ml saline over 2 h, and group 2 received 30 mmol potassium phosphate in 100 ml saline over 4 h. Patients with severe hypophosphatemia (<0.40 mmol/l; n=10) were also randomized into two groups: group 3 received 45 mmol potassium phosphate intravenously in 100 ml saline over 3 h, and group 4 received 45 mmol potassium phosphate in 100 ml saline over 6 h. Electrolytes, blood gas, renal function were monitored until day 3; urine was collected during and until 6 h after infusions. The overall efficacy of the protocols was 98% by the end of the infusion. There was no statistical difference in phosphate values between groups at the end of infusion or at 24 h. No adverse events were noted; one patient had an increase in serum potassium to 6.1 mmol/l. Phosphaturia in all groups was elevated as evidenced by fractional excretion above 20%. CONCLUSIONS: More rapid administration of large potassium phosphate boluses is effective and safe for correcting hypophosphatemia in ICU patients with preserved renal function if baseline serum potassium is below 4 mmol/l.

Aged↗
PubMed2004

Phosphate addition to hemodiafiltration solutions during continuous renal replacement therapy.

OBJECTIVE: Hypophosphatemia often occurs during continuous renal replacement therapy (CRRT). The addition of phosphate to dialysate and replacement solutions facilitates phosphate handling, but the risk of precipitation with calcium within these solutions has not been addressed. DESIGN AND SETTING: Experimental study with a retrospective observational study in a medico-surgical intensive care unit. METHODS AND PATIENTS: We tested the addition of phosphate to calcium-rich lactate- and bicarbonate-based solutions (Hemosol LG2 and Hemosol B0) used in CRRT to see whether precipitation occurs. Two milliliters of potassium phosphate added to 5-l bags gives a physiological phosphate concentration of 1.2 mmol/l. In addition, calcium and phosphate homeostasis was retrospectively evaluated in 20 consecutive CRRT patients where potassium phosphate had been added to these solutions. MEASUREMENTS AND RESULTS: Total and ionized calcium, phosphate, pH, PCO(2) and bicarbonate remained essentially unchanged 5 h after the addition of 2 ml of potassium phosphate to 5-l Hemosol solutions. Visual inspection did not reveal any precipitate. Of the 20 patients studied, 14 received more than 24 h of phosphate supplementation to dialysate and replacement solutions. Phosphate remained stable throughout CRRT despite phosphate intake from nutrition in 11 cases. No adverse event was noted on potassium, calcium, pH and bicarbonate homeostasis. CONCLUSIONS: The addition of phosphate to Hemosol solutions does not precipitate with the calcium within these solutions. This practical method effectively prevents hypophosphatemia in CRRT patients.

Aged↗
PubMed2004

Purification and characterization of 2,6-dihydroxybenzoate decarboxylase reversibly catalyzing nonoxidative decarboxylation.

A nonoxidative decarboxylase, 2,6-dihydroxybenzoate decarboxylase, was found in Agrobacterium tumefaciens IAM12048. The enzyme activity was induced specifically by 2,6-dihydroxybenzoate. The purified enzyme was a homotetramer of identical 38 kDa subunits. The purified decarboxylase catalyzed the nonoxidative decarboxylation of 2,6-dihydroxybenzoate and 2,3-dihydroxybenzoate without requiring any cofactors. In the presence of KHCO(3), the enzyme also catalyzed the regioselective carboxylation of 1,3-dihydroxybenzene into 2,6-dihydroxybenzoate at a molar conversion ratio of 30%.

Agrobacterium tumefaciens↗
PubMed1997

Properties and primary structure of a thermostable L-malate dehydrogenase from Archaeoglobus fulgidus.

A thermostable l-malate dehydrogenase from the hyperthermophilic sulfate-reducing archaeon Archaeoglobus fulgidus was isolated and characterized, and its gene was cloned and sequenced. The enzyme is a homodimer with a molecular mass of 70 kDa and catalyzes preferentially the reduction of oxaloacetic acid with NADH. A. fulgidus L-malate dehydrogenase was stable for 5 h at 90 degrees C, and the half-life at 101 degrees C was 80 min. Thus, A. fulgidus L-malate dehydrogenase is the most thermostable L-malate dehydrogenase characterized to date. Addition of K2HPO4 (1 M) increased the thermal stability by 40%. The primary structure shows a high similarity to L-lactate dehydrogenase from Thermotoga maritima and gram-positive bacteria, and to L-malate dehydrogenase from the archaeon Haloarcula marismortui and other L-lactate-dehydrogenase-like L-malate dehydrogenases.

Amino Acid Sequence↗
PubMed1996

Protective effect of vitamin E on chromium (VI)-induced cytotoxicity and lipid peroxidation in primary cultures of rat hepatocytes.

Pretreatment of primary cultures of rat hepatocytes with alpha-tocopherol succinate (vitamin E) for 20 h prior to exposure to K2Cr2O7 resulted in a marked decrease of chromium (VI)-induced cytotoxicity, as evaluated by the leakage of lactate dehydrogenase, without affecting cellular uptake and the subcellular distribution of chromium. The levels of chromium (VI)-induced lipid peroxidation, as monitored by malondialdehyde formation, were also inhibited by pretreatment with the vitamin. Pretreatment with vitamin E normalized the levels of nonenzymatic antioxidants such as glutathione and vitamin C suppressed by dichromate, and caused a distinct accumulation of vitamin E in hepatocytes. However, vitamin E pretreatment did not affect the activities of enzymatic antioxidants including glutathione reductase, superoxide dismutase, and catalase suppressed by dichromate. These results indicate that the protective effect of vitamin E against chromium (VI)-induced cytotoxicity as well as lipid peroxidation, may be associated more with the level of nonenzymatic antioxidants than the activity of enzymatic antioxidants.

Animals↗