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PubMed2005

Origins and mobility of phosphorus forms in the sediments of Lakes Taihu and Chaohu, China.

Phosphorus release from the sediment is generally an important factor for lake eutrophication. We have investigated phosphorus forms in surface sediments from Lake Taihu and Lake Chaohu by a chemical extraction method. The results showed that the concentrations of Fe/Al-bound phosphorus (Fe/Al-P) and organic phosphorus (Org-P) had significant correlations with those of amorphous Fe/Al oxides and organic matter in the sediments. Furthermore, Ca-bound phosphorus (Ca-P) concentrations were well related to total organic carbon (TOC) concentrations. The results also indicated that higher pH weakened the association of phosphates with the Fe/Al hydroxides and then resulted in Fe/Al-P release. The increase of pH was companied with autogenetic progresses of calcium carbonate and then elevated Ca-P concentrations in the sediments. In conclusion, external P loadings determine spatial distribution of P fractions, especially Fe/Al-P and Org-P, and partially contribute to additional Ca-P fractions in these highly human-disturbed lakes. The pH-induced phosphorus mobility in the sediments is very important for these lakes.

Aluminum↗
PubMed1984

Calcium and phosphorus intakes, balances, and blood levels of adults consuming self-selected diets.

Metabolic calcium and phosphorus balances, blood calcium and phosphorus levels, and alkaline phosphatase activity of 34 men and women, 20 to 53 yr of age, were determined each season during 1 yr while consuming customary diets. Dietary records were maintained 365 days. Analysis of variance indicated that serum Ca, P, and alkaline phosphatase levels were affected by season (p less than 0.0001), whereas calcium or phosphorus intakes were not. Calcium and phosphorus intakes of the men (1075 and 1533 mg, respectively) were higher (p less than 0.01) than of the women (695 and 1095 mg, respectively), but balances were not statistically different between them. Daily calcium balances for the men and women for the year were -81 and -85 mg, respectively; daily phosphorus balances were -239 and -130 mg, respectively. Stepwise regression analysis indicated that dietary calcium and protein were significantly associated with calcium and phosphorus balances, but in opposite directions, and only in women over 35 yr of age.

Adult↗
PubMed1986

The effect of phosphorus on endogenous fecal calcium excretion in man.

The effect of phosphorus on the endogenous fecal calcium excretion was investigated in man by administering tracer doses of 47Ca intravenously in control studies and during phosphorus supplementation. The phosphorus intake was approximately 800 mg/day in control studies and 2000 mg during phosphorus supplementation of the constant diet. The studies were carried out during different calcium intake levels of approximately 200, 800, 1300, 2000, and 2600 mg/day. Following the dose of 47CaCl2, the values of the plasma levels, urinary, and fecal excretions of 47Ca were used to calculate the endogenous fecal calcium. None of these values differed significantly during phosphorus supplementation from those in corresponding control studies, irrespective of the calcium intake. During addition of phosphorus to the different calcium intakes, a consistent finding was a significant decrease of the urinary calcium and a slight, but not significant increase of the fecal calcium except during the 800 mg calcium intake.

Aged↗
PubMed1982

Effect of dietary calcium and phosphorus levels on the utilization of iron, copper, and zinc by adult males.

Iron, copper, and zinc utilization were examined in nine adult males fed a moderate calcium-moderate phosphorus diet (MCaMP), a moderate calcium-high phosphorus diet (MCaHP), and a high calcium-high phosphorus diet (HCaHP) during a 39-day balance study. The moderate and high calcium diets contained 780 mg and 2382 mg calcium daily, respectively. The moderate and high phosphorus diets contained 843 and 2442 mg phosphorus daily, respectively. The calcium supplements were fed as calcium gluconate, while the phosphorus supplements were fed as glycerol phosphate. Subjects lost more iron and copper in their feces and apparently retained less iron and copper when fed the HCaHP diet than when fed the other two diets, but these effects were not statistically significant. Urinary iron and copper excretion were significantly affected by the dietary treatments. Dietary treatments had no effect on subjects' fecal and urinary losses of zinc nor on their apparent retention of zinc. Plasma iron, zinc, copper, and transferrin levels and serum ferritin levels were not affected by the dietary treatments.

Adult↗
PubMed1983

Long-term effects of excess protein and phosphorus on bone homeostasis in adult mice.

In adult human subjects, an interaction between dietary protein and phosphorus has been reported, in which the hypercalciuric effect of excess protein is counteracted by the hypocalciuric effect of phosphorus, with restoration of calcium balance. In adult rodents, bone homeostasis is maintained over a wide range of protein intakes, whereas high phosphorus diets cause bone loss, despite their hypocalciuric effect, as the result of an overriding increase in the excretion of endogenous fecal calcium. The present study was designed to determine whether there is an interaction between dietary protein and phosphorus with respect to bone homeostasis in adult mice. Four-month-old 45Ca-labeled B6D2F1 female mice were fed for 52 weeks the following diets (in percent): control, Ca, 0.6; P, 0.3; protein, 15; high P, Ca. 0.6; P, 1.2; protein, 15; high protein, Ca, 0.6; P, 0.3; protein, 30; and high P + high protein, Ca, 0.6; P, 1.2; protein, 30. Urinary calcium was persistently increased in the high protein group, depressed in the high P group and transiently depressed in the high P + high protein group. Excess dietary protein prevented phosphorus-induced kidney calcinosis. 45Ca loss was increased in the high P groups, but not in the high protein group. There were significant decreases in the mass of the femurs and tibias in both high P groups, whereas there was no effect of high protein intake. These results show that bone homeostasis in adult mice is sensitive to excess dietary phosphorus but not to excess protein, and that there is no interaction between these nutrients with respect to their effects on bone.

Animals↗
PubMed1985

Influence of dietary calcium, phosphorus, zinc and sodium phytate level on cataract incidence, growth and histopathology in juvenile chinook salmon (Oncorhynchus tshawytscha).

To determine the influence of wide variations in dietary levels of calcium, zinc and phytic acid (as sodium phytate) on growth and cataract incidence, juvenile chinook salmon held at 10-11 degrees C were fed daily to satiation for 105 d one of nine purified diets containing one of three levels (grams/kilogram) of calcium (averaged 4.8, 17.7, 50.2), zinc (averaged 0.05, 0.15, 0.39) and phytic acid (1.62, 6.46, 25.8). Diets were formulated to have a calcium-phosphorus ratio of close to unity when considering phosphorus sources other than sodium phytate. High dietary phytic acid concentration (25.8 g/kg) depressed chinook salmon growth, food and protein conversion [protein efficiency ratio (PER)] and thyroid function, increased mortality, promoted cataract formation (zinc at 0.05 g/kg) and induced anomalies in pyloric cecal structure. Calcium at 51 g/kg (or phosphorus) exacerbated the effects of high dietary phytate and low dietary zinc on cataract incidence. Moreover, high dietary levels of calcium (48-51 g/kg) coupled with phosphorus significantly impaired the growth and appetite of low phytic acid (1.62 g/kg) groups and led to nephrocalcinosis in low and high phytic acid groups. Plasma zinc levels were directly related to dietary zinc concentration and inversely related to dietary phytic acid level. Calcium (51 g/kg) and/or phosphorus reduced zinc bioavailability when the diet concurrently contained 0.05 g zinc and 25.8 g of phytic acid per kilogram. It is concluded that zinc is essential for normal eye development in juvenile chinook salmon. Further, zinc deficiency could not be induced in chinook salmon fed diets with high ratios of calcium (or phosphorus) to zinc alone. This required the simultaneous presence of a strong mineral (zinc)-binding agent.

Animal Nutritional Physiological Phenomena↗
PubMed1993

Dietary phosphorus, calcium metabolism and bone.

Many American women consume diets high in phosphorus and low in calcium. Concern about this dietary pattern stems from studies that show high phosphorus, low calcium intake causes secondary hyperparathyroidism and bone loss in several animal models. Recent studies in young adults have shown that a high phosphorus, moderately low calcium intake results in mild secondary hyperparathyroidism that persisted over 4 wk. However, plasma concentrations of the active form of vitamin D did not change in these subjects, despite stimulatory changes in parathyroid hormone and serum ionized calcium. Studies in normal adult men have shown that dietary phosphorus at levels within the observed normal range of intake can finely regulate the renal production and serum concentration of 1,25-dihydroxycholecalciferol. Thus, prolonged high phosphorus intake may impair the usual homeostatic mechanisms that are evoked when dietary calcium is limited. The current dietary patterns of high phosphorus, low calcium consumption result in persistent changes in the calcium regulating hormones that are not conductive to optimizing peak bone mass or slowing the rate of bone loss.

Adolescent↗
PubMed2003

Transcriptional activation of phosphoenolpyruvate carboxylase by phosphorus deficiency in tobacco.

Phosphoenolpyruvate carboxylase (PEPC), which catalyses the carboxylation of phosphoenolpyruvate using HCO(3)(-) to generate oxaloacetic acid, is an important enzyme in the primary metabolism of plants. Although the PEPC genes (ppc) comprise only a small gene family, the function of each gene is not clear, except for roles in C(4) photosynthesis and CAM. Three PEPC genes (Nsppc1-3) from the C(3) plant Nicotiana sylvestris were used to investigate their roles and regulation in a C(3) plant, and their regulation by phosphorus depletion in particular. First, the induction of PEPC by phosphorus depletion was confirmed. Next, Nsppc1 was determined to be mainly responsive to phosphorus deficiency at the transcriptional level. Further studies using transgenic tobacco harbouring a chimeric gene consisting of the 2.0 kb promoter region of Nsppc1 and the beta-glucuronidase (GUS) reporter showed that PEPC is transcriptionally induced. It was also found that sucrose had a synergistic effect on the induction of PEPC by phosphorus deficiency. A series of transgenic tobacco containing 5'-deletion mutants of Nsppc1 promoter::GUS fusion revealed that the -539 to -442 bp Nsppc1 promoter region, relative to the translation start site, was necessary for the response to phosphorus deficiency. Gain-of-function analysis using a construct containing three tandem repeats of the -539 to -442 bp region confirmed that this region was sufficient to induce the phosphorus-deficiency response in tobacco.

Base Sequence↗
PubMed1998

The effect of a high phosphorus diet on the parathyroid cell cycle.

High extracellular phosphorus directly increases parathyroid hormone (PTH) secretion and gene transcription. The present study evaluates the effect of high phosphorus diet on the parathyroid cell cycle in rats with normal renal function. Rats were divided into two groups, receiving either a high phosphorus diet (HPD, P=1.2%) or a normal phosphorus diet (NPD, P=0.6%). The dietary calcium content was 0.6% in both diets. Rats were pair fed and sacrificed on days 0, 1, 5, 10 and 15 after initiation of the diet. The parathyroid glands were removed and parathyroid cells dispersed for evaluation of cell cycle and apoptosis by flow cytometry. Serum calcium, phosphorus, PTH and calcitriol were measured. As compared with NPD, the ingestion of a HPD resulted in an increased number of cells in the S phase of the cell cycle from day 1 to 10 (1.2+/-0.09% vs 0.6+/-0.04% for day 1, 1.2+/-0.11% vs 0.6+/-0.06% for day 5 and 1.0+/-0.09% vs 0.5+/-0.04% for day 10, P<0.01). By day 15, the percentage of cells in the S phase in NPD and HPD were not different. In the rats fed the HPD, serum PTH increased significantly from day 5 through 15 (P<0.01). Parathyroid cell apoptosis was minimal and unaffected by the diet. At day 15, the parathyroid gland size in HPD was increased by 27% as compared with NPD (P<0.05). This increase should be attributed to cell proliferation since parathyroid cell size remained unchanged. Serum calcitriol and calcium were not significantly different in the two groups. In HPD, an increase in serum phosphorus was observed only on day 1. The results show that an HPD results in the stimulation of the parathyroid cell cycle independently of changes in calcium and calcitriol.

Animals↗
PubMed2004

Effect of ammonium chloride and dietary phosphorus in the azotaemic rat. Part II--Kidney hypertrophy and calcium deposition.

BACKGROUND: Kidney hypertrophy is stimulated by both partial nephrectomy and NH(4)Cl administration. Also, parathyroidectomy (PTX) has been reported to prevent kidney hypertrophy induced by a high protein diet. Our goal was to determine in the azotaemic rat: (i) the combined effects of NH(4)Cl administration and dietary phosphorus on the development of kidney hypertrophy and calcium deposition in the kidney and (ii) whether the absence of parathyroid hormone (PTH) affected the development of kidney hypertrophy and calcium deposition. METHODS: High (HPD, 1.2%), normal (NPD, 0.6%) or low (LPD, <0.05%) phosphorus diets were given to 5/6 nephrectomized rats for 30 days. In each dietary group, one-half of the rats were given NH(4)Cl in the drinking water. The six groups of rats were: (i) HPD + NH(4)Cl; (ii) HPD; (iii) NPD + NH(4)Cl; (iv) NPD; (v) LPD + NH(4)Cl and (vi) LPD. In a separate study, PTX was performed to determine whether PTH affected renal hypertrophy in 5/6 nephrectomized rats given NH(4)Cl. RESULTS: Both with and without NH(4)Cl (+/-NH(4)Cl), kidney weight was greatest (P<0.05) in the HPD groups. In each dietary phosphorus group, kidney weight was greater (P<0.05) in the NH(4)Cl group. In both the +/-NH(4)Cl groups, kidney calcium content was greatest (P<0.05) in the HPD group, but was less (P<0.05) in the NPD and HPD groups given NH(4)Cl. An inverse correlation was present between creatinine clearance and kidney calcium content (r = -0.51, P<0.001). When factored for kidney weight, creatinine clearance was less (P<0.05) in the HPD group in both the +/-NH(4)Cl groups, but was greater in the HPD + NH(4)Cl than in the HPD group. In PTX rats, kidney weight was greater (P<0.05) and kidney calcium deposition was less (P<0.05) in rats given NH(4)Cl. CONCLUSIONS: In azotaemic rats studied for 30 days, NH(4)Cl administration induced kidney hypertrophy. A HPD also induced kidney hypertrophy. The effects on kidney calcium deposition were divergent for which NH(4)Cl administration decreased and a HPD increased calcium deposition. The inverse correlation between kidney calcium content and creatinine clearance suggests that kidney calcium deposition is harmful to renal function. When factored for kidney weight, the lower creatinine clearance in the high phosphorus group suggests that kidney hypertrophy does not completely compensate for the harmful effects of a HPD. This result also suggests that a longer study would probably result in more rapid deterioration in the high phosphorus group. In PTX rats, the absence of PTH did not prevent NH(4)Cl from inducing kidney hypertrophy and reducing kidney calcium deposition. In conclusion, NH(4)Cl and dietary phosphorus each independently affect kidney growth and calcium deposition in the growing rat with renal failure.

Ammonium Chloride↗
PubMed1994

The effect of thrombocytosis on serum potassium and phosphorus concentrations.

Thrombocytosis is a cause of falsely elevated serum potassium concentrations, and phosphorus concentrations may be similarly distorted. Because plasma concentrations are not affected, the difference between the serum and plasma concentrations detects spurious elevations. The authors, in this study, sought to determine the degree of correlation between thrombocytosis and false elevations in serum potassium and phosphorus concentrations. Ninety-one general, medical/surgical patients with elevated platelet counts were identified by laboratory reports. Subjects were stratified into blocks by platelet count. Samples were obtained simultaneously for serum and plasma potassium and phosphorus concentrations and complete blood counts. The serum minus plasma concentrations for potassium (Kdiff) and phosphorus (Pdiff) were calculated and analyzed against each other and the platelet count by linear regression. A control group of 20 subjects with normal platelet counts was used to verify laboratory results with literature values. The Kdiff and Pdiff values in the control group very closely approximated literature values of 0.4 mmol/L and 0.08 mmol/L, respectively. Platelet count was a moderate predictor of Kdiff, r2 = 0.55 (p = 0.00001). Kdiff exceeded the upper limit of control at a platelet count of approximately 600 x 10(9)/L. Platelet count also correlated with Pdiff, r2 = 0.31 (p = 0.00001). Additionally, Kdiff correlated with Pdiff, r2 = 0.39 (p = 0.00001). Thrombocytosis is associated with false elevations in measured serum potassium and phosphorus concentrations. Additionally, the magnitude of elevations in potassium and phosphorus concentrations appear to be related.

Adult↗
PubMed1989

Effect of high calcium and phosphorus intake on mineral retention in very low birth weight infants chronically treated with furosemide.

The treatment of premature infants with the diuretic furosemide appears to be a contributory factor in the development of metabolic bone disease presumably because of furosemide-induced hypercalciuria. In this study, we measured calcium and phosphorus balance in furosemide-treated very low birth weight infants (VLBW) infants with bronchopulmonary dysplasia (BPD) who were fed a specialized premature formula containing increased amounts of calcium and phosphorus. Furosemide-treated infants received 166 +/- 37 mg/kg/day and retained 80 +/- 34 mg/kg/day of calcium, and 87 +/- 19 mg/kg/day and retained 52 +/- 14 mg/kg/day of phosphorus. The amounts retained were approximately 65% of the calcium and 72% of the phosphorus requirements for in utero mineral accretion. Compared to a group of similarly fed VLBW infants without BPD and not treated with the diuretic, the furosemide-treated infants excreted a larger percent of the calcium intake in the urine but had similar total urinary calcium and phosphorus losses (mg/kg/day) and serum calcium, phosphorus, alkaline phosphatase, and parathyroid hormone (PTH) levels. From the latter two findings, we suggest that the extra mineral content of the formula may have promoted bone mineralization and prevented the occurrence of secondary hyperparathyroidism.

Calcium↗
PubMedDate not supplied

The 2002 Moyer Award. Metabolic effects of vitamin D on serum calcium, magnesium, and phosphorus in pediatric burn patients.

Severe burn injury results in profound metabolic derangements. Recently, we have shown that vitamin D metabolism is disturbed after burn injury. Vitamin D is essential for calcium and phosphorus homeostasis and skeletal bone integrity. The role of vitamin D on magnesium homeostasis is not well understood. The purpose of this study was to assess the effects of vitamin D deficiency on serum electrolytes. Forty-one pediatric burn patients with a mean (+/- SEM) total body surface area burn of 53.1 +/- 2.9% and full-thickness injury of 44.2 +/- 4.1% were studied from July 1996 to December 2000. The mean age of the patients was 6.5 +/- 0.8 years. Patients were studied for 6 weeks after admission to the hospital. Blood samples were obtained weekly for serum 25-hydroxycholecalciferol (25D), 1,25-dihydroxycholecalciferol (1,25D), and daily for calcium, magnesium, and phosphorus. Total intravenous (IV) replacement of calcium, magnesium, and phosphorus was also quantitated retrospectively. Bivariate and multivariate correlational analysis was used for statistical comparison. For the study duration, multivariate analysis demonstrated a positive correlation between 25D and serum calcium (r =.47, P <.05) and 1,25D and calcium (r =.27, P <.05). Overall, calcium had a positive correlation with phosphorus and a negative correlation with IV calcium replacement (ie, patients with lower calcium received more IV replacement). During the initial week of hospitalization (week 0), decreased 25D (mean 11.6 ng/ml; normal range 15-57 ng/ml) and 1,25D (mean 13.9 pg/ml; normal range 15-75 pg/ml) did not correlate with any other measured variable. In week 1, 1,25D (mean 15.2 ng/ml) had a positive correlation (r =.410, P <.05) with calcium (mean 7.70 mg/dl). Hypovitaminosis D observed in burn injury correlates with serum calcium and phosphorus abnormalities. Early after injury (<1 week) there was no observed correlation between vitamin D and other variables possibly because of the effects of burn shock. After 1 week, vitamin D appears to significantly effect phosphorus homeostasis. The relationship between vitamin D and magnesium is not well established. These results may indicate a role for vitamin D replacement therapy during the initial phase of burn resuscitation.

Burns↗
PubMed2005

The LPB1 gene is important for acclimation of Chlamydomonas reinhardtii to phosphorus and sulfur deprivation.

Organisms exhibit a diverse set of responses when exposed to low-phosphate conditions. Some of these responses are specific for phosphorus limitation, including responses that enable cells to efficiently scavenge phosphate from internal and external stores via the production of high-affinity phosphate transporters and the synthesis of intracellular and extracellular phosphatases. Other responses are general and occur under a number of different environmental stresses, helping coordinate cellular metabolism and cell division with the growth potential of the cell. In this article, we describe the isolation and characterization of a mutant of Chlamydomonas reinhardtii, low-phosphate bleaching (lpb1), which dies more rapidly than wild-type cells during phosphorus limitation. The responses of this mutant to nitrogen limitation appear normal, although the strain is also somewhat more sensitive than wild-type cells to sulfur deprivation. Interestingly, depriving the cells of both nutrients simultaneously allows for sustained survival that is similar to that observed with wild-type cells. Furthermore, upon phosphorus deprivation, the lpb1 mutant, like wild-type cells, exhibits increased levels of mRNA encoding the PHOX alkaline phosphatase, the PTB2 phosphate transporter, and the regulatory element PSR1. The mutant strain is also able to synthesize the extracellular alkaline phosphatase activity upon phosphorus deprivation and the arylsulfatase upon sulfur deprivation, suggesting that the specific responses to phosphorus and sulfur deprivation are normal. The LPB1 gene was tagged by insertion of the ARG7 gene, which facilitated its isolation and characterization. This gene encodes a protein with strong similarity to expressed proteins in Arabidopsis (Arabidopsis thaliana) and predicted proteins in Oryza sativa and Parachlamydia. A domain in the protein contains some similarity to the superfamily of nucleotide-diphospho-sugar transferases, and it is likely to be localized to the chloroplast or mitochondrion based on programs that predict subcellular localization. While the precise catalytic role and physiological function of the putative protein is not known, it may function in some aspect of polysaccharide metabolism and/or influence phosphorus metabolism (either structural or regulatory) in a way that is critical for allowing the cells to acclimate to nutrient limitation conditions.

Acclimatization↗
PubMed2004

The role of abnormal phosphorus metabolism in the progression of chronic kidney disease and metastatic calcification.

The role of abnormal phosphorus metabolism in the progression of renal disease and metastatic calcification. Hyperphosphatemia is a common biochemical abnormality in advanced renal failure. The resulting increase serum calcium x phosphorus product results in the deposition of hydroxyapatite crystals. The crystalline properties of these deposits incite an inflammatory response manifested by encapsulated tumoral deposits around joints, acute inflammatory arthritis, and irritative conjunctivitis. These deposits occur in association with marked elevation of serum phosphorus levels, and are prevented and eradicated by normalizing serum phosphorus levels. The calcium-phosphate deposits which occur in heart and lungs are nonapatitic. These deposits were never clearly related to hyperphosphatemia. They are mainly of historic interest because currently they are rarely seen. Their eradication appears to be more of a result of improved dialytic techniques than correction of serum phosphorus levels. The presence, persistence, and progression of vascular calcification are more closely related to patient age and duration of dialysis than hyperphosphatemia. This suggests that these deposits are a result of dystrophic calcification occurring de novo in a diseased or damaged vessel wall. Phosphorous restriction has also been shown to be protective of renal functional deterioration in experimental renal disease. It is unclear whether the protective effect is mediated through phosphate restriction or phosphate depletion. In conclusion, control of serum phosphorus levels in dialyzed uremic patients has clearly decreased morbidity associated with periarticular, articular, and conjunctiva hydroxyapatite deposits. In contrast, phosphorous control has had little effect on the presence or severity of vascular calcification.

Calcinosis↗
PubMed1998

Interactions among iron, calcium, phosphorus and magnesium in the nutritionally iron-deficient rat.

We studied the development of nutritional iron deficiency 0, 10, 20, 30 and 40 days after the intake of a semisynthetic diet lacking iron (diet 0) and the possible interactions with calcium, phosphorus and magnesium in both control rats and rats after 40 days of iron deficiency. During this period, iron deficiency was found to produce stress in the rats, as evidenced by high levels of cortisol in the serum. High levels of parathyroid hormone (PTH) were also found. There was a considerable increase in the absorption of calcium, phosphorus and magnesium, but the phosphorus and magnesium balance decreased and that of calcium remained practically unchanged, although there was an increase in calcium urinary elimination. Despite the noticeable degree of bone demineralization, which was evident in the femur, serum levels of calcium, phosphorus and magnesium remained constant. The present study shows that severe nutritional ferropenic anaemia provokes significant alterations in the metabolism of calcium, phosphorus and magnesium. We conclude that these alterations should be taken into account in the treatment of this pathology, given its prevalence and the fact that it may exacerbate other pathologies, particularly those related to the metabolism of calcium and phosphorus.

Anemia, Iron-Deficiency↗
PubMed2004

Growth of Escherichia coli coexpressing phosphotriesterase and glycerophosphodiester phosphodiesterase, using paraoxon as the sole phosphorus source.

Phosphotriesterases catalyze the hydrolytic detoxification of phosphotriester pesticides and chemical warfare nerve agents with various efficiencies. The directed evolution of phosphotriesterases to enhance the breakdown of poor substrates is desirable for the purposes of bioremediation. A limiting factor in the identification of phosphotriesterase mutants with increased activity is the ability to effectively screen large mutant libraries. To this end, we have investigated the possibility of coupling phosphotriesterase activity to cell growth by using methyl paraoxon as the sole phosphorus source. The catabolism of paraoxon to phosphate would occur via the stepwise enzymatic hydrolysis of paraoxon to dimethyl phosphate, methyl phosphate, and then phosphate. The Escherichia coli strain DH10B expressing the phosphotriesterase from Agrobacterium radiobacter P230 (OpdA) is unable to grow when paraoxon is used as the sole phosphorus source. Enterobacter aerogenes is an organism capable of growing when dimethyl phosphate is the sole phosphorus source. The enzyme responsible for hydrolyzing dimethyl phosphate has been previously characterized as a nonspecific phosphohydrolase. We isolated and characterized the genes encoding the phosphohydrolase operon. The operon was identified from a shotgun clone that enabled E. coli to grow when dimethyl phosphate is the sole phosphorus source. E. coli coexpressing the phosphohydrolase and OpdA grew when paraoxon was the sole phosphorus source. By constructing a short degradative pathway, we have enabled E. coli to use phosphotriesters as a sole source of phosphorus.

Amino Acid Sequence↗
PubMed1974

The acute effect of 25-hydroxycholecalciferol on renal handling of phosphorus. Evidence for a parathyroid hormone-dependent mechanism.

The acute effect of i.v. and direct intrarenal arterial infusion of 25-hydroxycholecalciferol (25HCC) and 1,25-dihydroxycholecalciferol (1,25-DHCC) on renal handling of phosphorus was evaluated in the following groups of rats: (a) intact animals, (b) parathyroidectomized (PTX) hypocalcemic rats, (c) PTX rats in which normocalcemia was maintained with calcium supplements and (d) PTX animals in which urinary phosphorus was augmented by (i) i.v. sodium phosphate, (ii) expansion of the extracellular fluid volume with normal saline, and (iii) i.v. parathyroid hormone (PTH). Clearances of inulin (C(In)), phosphorus (C(P)), and fractional clearances of phosphorus (C(P)/C(In)) of the experimental groups were compared with those of the corresponding control groups, and the clearances of the infused kidneys with those of the contralateral kidneys. In intact animals, i.v. 25HCC decreased C(P)/C(In) from 0.29+/-0.04 (mean +/-SE) to 0.19+/-0.04, and i.v. 1,25-DHCC decreased C(P)/C(In) from 0.25+/-0.04 to 0.15+/-0.02. The intrarenal infusion of both 25HCC and 1,25DHCC into intact animals failed to produce a unilateral change; however, it decreased C(P)/C(In) bilaterally. i.v. and intrarenal infusions of 25HCC or 1,25DHCC in PTX hypocalcemic and normocalcemic rats, and i.v. infusions of 25HCC in PTX rats receiving either sodium phosphate or normal saline, all failed to produce significant changes in C(P)/C(In). In contrast, 24HCC given i.v. to PTX animals receiving exogenous PTH was associated with a significant fall in C(P)/C(In), from 0.34+/-0.08 to 0.13+/-0.02. These results indicate that 25HCC enhances tubular reabsorption of phosphorus in rats, only in the presence of either endogenous or exogenous circulating PTH, but not in its absence and thus imply a PTH-dependent mechanism of 25HCC action on the kidney. This effect does not appear to be related to the conversion of 25HCC into 1,25DHCC, since the latter fails to affect tubular reabsorption of phosphorus in PTX rats.

Animals↗