Excretion Of Amino Acids Research Articles

Current knowledge on mycolic acids in Corynebacterium glutamicum and their relevance for biotechnological processes

Corynebacterium glutamicum is the world's largest producer of glutamate and lysine. Industrial glutamate overproduction is induced by empirical processes, such as biotin limitation, supplementation with specific surfactants or addition of sublethal concentration of certain antibiotics to the culture media. Although Gram-positive bacteria, C. glutamicum and related bacterial species and genera contain, in addition to the plasma membrane, an outer permeability membrane similar to that of Gram-negative microorganisms. As the amino acids have to cross both membranes, their integrity, composition and fluidity influence the export process. While the precise mechanism of the export of the amino acids by C. glutamicum is not fully understood, the excretion of amino acids through the inner membrane involved at least a major export system mechanosensitive channel MscS family (MscCG) encoded by NCgl1221. As the various industrial treatments have been shown to affect the lipid content of the bacterial cell, it is strongly believed that defects in the hallmark of the outer membrane, 2-alkyl, 3-hydroxylated long-chain fatty acids (mycolic acids), could be key factors in the glutamate overproduction. This review aims at giving an overview of the current knowledge on mycolic acids structure, biosynthesis and transfer in C. glutamicum and their relevance for amino acid biotechnological production.

Differential cystine and dibasic amino acid handling after loss of function of the amino acid transporter b0,+AT (Slc7a9) in mice

Cystinuria is an autosomal recessive disease caused by mutations in SLC3A1 (rBAT) and SLC7A9 (b(0,+)AT). Gene targeting of the catalytic subunit (Slc7a9) in mice leads to excessive excretion of cystine, lysine, arginine, and ornithine. Here, we studied this non-type I cystinuria mouse model using gene expression analysis, Western blotting, clearance, and brush-border membrane vesicle (BBMV) uptake experiments to further characterize the renal and intestinal consequences of losing Slc7a9 function. The electrogenic and BBMV flux studies in the intestine suggested that arginine and ornithine are transported via other routes apart from system b(0,+). No remarkable gene expression changes were observed in other amino acid transporters and the peptide transporters in the intestine and kidney. Furthermore, the glomerular filtration rate (GFR) was reduced by 30% in knockout animals compared with wild-type animals. The fractional excretion of arginine was increased as expected (∼100%), but fractional excretions of lysine (∼35%), ornithine (∼16%), and cystine (∼11%) were less affected. Loss of function of b(0,+)AT reduced transport of cystine and arginine in renal BBMVs and completely abolished the exchanger activity of dibasic amino acids with neutral amino acids. In conclusion, loss of Slc7a9 function decreases the GFR and increases the excretion of several amino acids to a lesser extent than expected with no clear regulation at the mRNA and protein level of alternative transporters and no increased renal epithelial uptake. These observations indicate that transporters located in distal segments of the kidney and/or metabolic pathways may partially compensate for Slc7a9 loss of function.

Severe renal tubulopathy in a newborn due to BCS1L gene mutation: Effects of different treatment modalities on the clinical course

Very early onset Toni–Debré–Fanconi Syndrome, a disorder of proximal renal tubules of the kidney which results in the increased urinary excretion of glucose, amino acids, uric acid, phosphate and bicarbonate, could be the manifestation of various inborn errors. Defects of oxidative phosphorylation are a heterogeneous group of disorders with various clinical presentations. Recently, patients with early liver failure, renal tubulopathy and encephalopathy due to the mutations in the BCS1L gene coding for a structural protein in mitochondrial complex III have been described.Ten-day-old female newborn was referred to our clinic because of intractable acidosis. Physical examination revealed severe hypotonia, and hepatomegaly. The laboratory examinations revealed lactic acidosis, increased blood alanine, alanine aminotransferase and aspartate aminotransferase levels, generalized aminoaciduria and glucosuria. The tubular reabsorption of phosphate was reduced. Because of multisystem involvement, mitochondrial disease was suspected and the mutational analysis of the BCS1L gene revealed homozygous P99L mutation. As the patient was unresponsive to bicarbonate replacement, oral dichloroacetate and peritoneal dialysis, continuous high dose intravenous sodium bicarbonate therapy with a dose up to 1.25mEq/kg/h was started. The patient got on well until the age of 9months when she died of sepsis.It was stressed that high dose intravenous continuous sodium bicarbonate therapy could be an alternative treatment option in patients with severe acidosis and renal tubulopathy resistant to dichloroacetate and peritoneal dialysis. Patients with BCS1L mutations should be considered in the differential diagnosis of severe tubulopathy in the newborn period.

Clinical, biochemical, molecular and therapeutic aspects of 2 new cases of 2-aminoadipic semialdehyde synthase deficiency

Our aim was to report two new cases of hyperlysinemia type I describing the clinical, biochemical and molecular features of the disease and the outcome of lysine restriction. Two children presented with febrile seizures followed by developmental delay, clumsiness and epilepsy. At age 2 and 8years a biochemical and genetic diagnosis of hyperlysinemia type I was confirmed and lysine-restricted diet was started in both cases. Three years after initiation of lysine restriction, case 1 had not suffered further seizures. In case 2, tremor and dysmetria improved, but fine motor clumsiness persisted. Mild cognitive impairment was present in both patients despite dietary treatment. Laboratory studies: Plasma, urine and cerebrospinal fluid amino acid concentrations were measured by ion exchange chromatography. Mutation analysis of the AASS gene was performed by directly sequencing the PCR products.The plasma lysine values were higher than 1200μmol/L in both cases. Additionally, an increase in dibasic aminoaciduria was observed. Lysine restriction decreased plasma lysine values and nearly normalised dibasic aminoaciduria. Mutational screening of the AASS gene revealed that case 1 was a compound heterozygote for c.2662+1_2662+5delGTAAGinsTT and c.874A>G and that case 2 was a compound heterozygote for c.976_977delCA and c.1925C>G.In conclusion, we present two children with hyperlysinemia type I and neurological impairment in which implementation of lysine-restricted diet achieved a mild improvement of symptoms but did not reverse cognitive impairment. The partial decrease of lysine concentrations and the normalisation of urine excretion of dibasic amino acids after lysine restriction further reinforce the possibility of this therapeutic intervention, although further investigations seem necessary.

The relationship between aerobic fitness level and metabolic profiles in healthy adults

Application of metabolomics to nutrition and health research is increasing and while much effort has been invested in understanding factors that influence the metabolomic profile there is relatively little known about the impact of fitness level. This study aimed to examine the relationship between fitness level, substrate oxidation rates, and the metabolic profile. Two hundred and fourteen healthy adults (18-60 years) were recruited and 65 subjects were selected based on their estimated maximal oxygen consumption levels. Metabolomic analysis was performed. The subjects were split into fitness groups according to their maximal oxygen consumption levels (mL/kg/min) and analysis revealed significant differences in normalized fat and carbohydrate oxidation levels between the groups. Urinary metabolomic analysis revealed significantly different profiles in the groups with 15 amino acids significantly higher in the low fitness groups. Effects of fitness level in the plasma metabolic profiles were also demonstrated. This study demonstrates a relationship between fitness level and the amino acid profile. Moreover, the metabolite changes show that a reduced excretion of amino acids in adults is associated with increased fitness levels and an increased fat oxidation rate during exercise. Interestingly, higher levels of branched chain amino acids were associated with lower fitness levels and higher insulin resistance.

Hyperexcretion of homocitrulline in a Malaysian patient with lysinuric protein intolerance

Lysinuric protein intolerance (LPI; MIM 222700) is an inherited aminoaciduria with an autosomal recessive mode of inheritance. Biochemically, affected patients present with increased excretion of the cationic amino acids: lysine, arginine, and ornithine. We report the first case of LPI diagnosed in Malaysia presented with excessive excretion of homocitrulline. The patient was a 4-year-old male who presented with delayed milestones, recurrent diarrhea, and severe failure to thrive. He developed hyperammonemic coma following a forced protein-rich diet. Plasma amino acid analysis showed increased glutamine, alanine, and citrulline but decreased lysine, arginine and ornithine. Urine amino acids showed a marked excretion of lysine and ornithine together with a large peak of unknown metabolite which was subsequently identified as homocitrulline by tandem mass spectrometry. Molecular analysis confirmed a previously unreported homozygous mutation at exon 1 (235 G > A, p.Gly79Arg) in the SLC7A7 gene. This report demonstrates a novel mutation in the SLC7A7 gene in this rare inborn error of diamino acid metabolism. It also highlights the importance of early and efficient treatment of infections and dehydration in these patients. The diagnosis of LPI is usually not suspected by clinical findings alone, and specific laboratory investigations and molecular analysis are important to get a definitive diagnosis.

Potential Diagnostic Assay for Cystinuria by Capillary Electrophoresis Coupled to Mass Spectrometry

Cystinuria is an autosomal recessive genetic disorder characterized by abnormal intestinal and renal tubular transport of L-cystine as well as of L-lysine, L-arginine and L-ornithine. This leads to excessive urinary excretion of amino acids, with the formation of kidney stones caused by the low solubility of L-cystine in the urine. In this study, an analytical method for simultaneous determination of these four amino acids in urine by capillary electrophoresis coupled to electrospray ionization mass spectrometry (CE-ESI-MS) was developed and validated. Using standard solutions of L-cystine, L-lysine, L-arginine and L-ornithine, the amino acid detection limits by this method were 114.2, 61.3, 72.7 and 86.7 µmol L-1. Standard solutions were injected in a silica capillary column (50 µm i.d. and 70 cm length) under 2 psi of pressure by 10 s. The separation occurred at 300 V cm-1, using 1.0 mol L-1 formic acid in 10% methanol in water as the background electrolyte. The method was applied to the urine of a patient clinically diagnosed as a cystinuria carrier, which revealed the presence of 900.5 ± 5, 600.0 ± 2, 700.2 ± 1 and 500.0 ± 3 µmol L-1 of amino acid, respectively, and 75.3 ± 1 µmol L-1 of creatinine. The CE-ESI-MS method described here for analyzing L-cystine and other cystinuria-related amino acids is a sensitive and reliable diagnostic tool for characterizing and monitoring this disease.

Urea Excretion in Isoparorchis hypselobagri (Billet, 1898)

The amount of excretion of amino acid is lower when the flukes are kept in vitro in the incubation media without glucose (control) than in the incubation media with glucose. The amount of excreted amino acid shows highly significant values than that of control in vitro condition. In the swim bladder washings of host Wallago attu amino acids are also present in significant amounts. Tyrosine, arginine, tryptophan, phenylalanine, cysteine, methionine, proline, hydroxyproline were identified in the excretory materials. So, amino acid is one of the important excretory products in Isoparorchis hypselobagri.

Renal uptake and tolerability of a 2′-O-methoxyethyl modified antisense oligonucleotide (ISIS 113715) in monkey

The primary target organ for uptake of systemically administered phosphorothioate oligonucleotides is the kidney cortex and the proximal tubular epithelium in particular. To determine the effect of oligonucleotide uptake on renal function, a detailed renal physiology study was performed in cynomolgus monkeys treated with 10–40mg/kg/week ISIS 113715 for 4 weeks. The concentrations of oligonucleotide in the kidney cortex ranged from 1400 to 2600μg/g. These concentrations were associated with histologic changes in proximal tubular epithelial cells that ranged from the appearance of cytoplasmic basophilic granules to atrophic and degenerative changes at higher concentrations. However, there were no renal functional abnormalities as determined by the typical measurements of blood urea nitrogen, serum creatinine, creatinine clearance, or urine specific gravity. Nor were there changes in glomerular filtration rate, or renal blood flow. Specific urinary markers of tubular epithelial cell damage, such as N-acetyl-glucosaminidase, and α-glutathione-s-transferase were not affected. Tubular function was further evaluated by monitoring the urinary excretion of amino acids, β2-microglobulin, or glucose. Renal function was challenged by administering a glucose load and by examining concentrating ability after a 4-h water deprivation. Neither challenge produced any evidence of change in renal function. The only change observed was a low incidence of increased urine protein/creatinine ratio in monkeys treated with ≥40mg/kg/week which was rapidly reversible. Collectively, these data indicate that ISIS 113715-uptake by the proximal tubular epithelium has little or no effect on renal function at concentrations of 2600μg/g.

Profile of serum amino acids in patients on peritoneal dialysis

Patients on peritoneal dialysis (PD) are predisposed to disturbances in amino acid metabolism and development of malnutrition which are unfavorable prognostic factors. Studying the serum level of essential amino acids in patients on PD. The total of 56 PD patients (mean age 42.4±11.5 years, treatment duration 24.0±14.2 months) was examined simultaneously with 12 practically healthy volunteers (mean age 39.4±10.7 years). Analysis of the dietary interviews and 3-day dietary journals was carried out. The levels of essential and conditionally essential amino acids in both serum and daily volume of peritoneal dialysis solution were determined using liquid chromatography. Dietary protein consumption in PD patients was 1.06±0.09 vs. 1.21±0.05 g/kg/day (р<0.05) in the control group. Decreased serum levels of 6 essential amino acids were registered (valine, lysine, threonine, and tyrosine – almost 2 fold (р<0.05), leucine and isoleucine – by 28 and 34% (р<0.05), accordingly, as well as normal concentration of phenylalanine and methionine – 0.6±2.3 and 9.4±2.1 mg/L, correspondingly, vs. 11.1±0.8 and 11.3±0.8 mg/L in the control (р>0.05), and increased level of histidine – 32.7±6.8 vs. 14.6±0.5 mg/L in the control. The ratios essential/nonessential amino acids and branched/replaceable amino acids as well as Fisher’s index were 0.54±0.05, 0.25±0.05 and 2.0±05, correspondingly, vs. 1.35±0.15, 0.55±0.05 and 3.2±0.2 in the control (р<0.05). Daily excretion of essential amino acids with dialysis solution fluctuated between 314 and 522 mg, and that of conditionally essential amino acids – between 156 and 337 mg. Direct correlation was revealed between daily excretion of essential amino acids, on the one hand, and both peritoneal transport (р=0.001) and daily excretion of isoleucine, threonine, histidine, and their serum levels, on the other (р=0.04, р=0.001, and р=0.01, accordingly). Direct correlation between daily excretion of essential amino acids and that of tyrosine and its serum level was only near reliable value (р=0.055). PD patients are characterized by the markedly unbalanced level of essential amino acids. The deficiency of the majority of essential amino acids in PD patients is due to their high loss through dialysis solution and insufficient protein consumption.

Changes in cell hydration and amino acid efflux related to chronically higher water intake in healthy young men

Cell hydration is integral to endocrine, immune, neural, cardiovascular, gastrointestinal, muscle, and skeletal function. Acute cell dehydration is associated with a wide variety of adverse outcomes under extreme conditions and in critical illness. Biomarkers of chronic cell hydration are needed to test for longer‐term effects under daily life conditions. In vitro, cells adapt to chronic cell dehydration by increasing protein breakdown to increase intracellular concentrations and counter the osmotic gradient. Once adapted, cells overswell if exposed to hypoosmotic conditions, and release accumulated amino acids. In vivo, in chronically stressed animals, hypoosmotic amino acid efflux is measurable in urine. This study explored for changes in cell hydration and urinary amino acid excretion in 5 healthy men (20–25y) with habitually low total water intake (&lt;2L/d) who increased water intake to 3.5L/d over 4 wks by drinking water. Each week, urine was collected after a 750ml bolus of drinking water. Higher water intake was associated with increased urine volume, decreased urine ADH and osmolality, a downward shift in the distribution of red cell deformability over the osmolality range, and altered post‐bolus urinary amino acid excretion. More work is needed on amino acid efflux as a possible biomarker of chronic cell hydration.Funded by Danone Research, NIH #UL1 RR024131 &amp; #5UL1RR024131‐05, and RAS #A106017.

Modification of tryptophan transport system and its impact on production of l-tryptophan in Escherichia coli

The production of l-tryptophan through chemical synthesis, direct fermentation, bioconversion and enzymatic conversion has been reported. However, the role of transport system for aromatic amino acids in l-tryptophan producing strains has not been fully explored. In this study, the fact was revealed that l-tryptophan production and cell growth were affected by the modification of transport systems based on YddG functioning as aromatic amino acid excretion and AroP functioning as general aromatic amino acid permease. Through comparing glucose conversion rates of recombinant strains such as Escherichia coli TRTH ΔaroP, E. coli TRTH-Y, and E. coli TRTH ΔaroP-Y, the moderate modification of transport system resulted in the metabolic flux redistribution of l-tryptophan biosynthesis pathway. In the fed-batch fermentation by E. coli TRTH and E. coli TRTH-Y in 30-liter fermentor, the final production of l-tryptophan fermented by E. coli TRTH-Y was 36.3g/L, which was 12.6% higher than fermentation by E. coli TRTH.

돈모 단백질의 급여가 닭의 영양소 대사에 미치는 영향

Two experiments were conducted to investigate the effect of feeding hog hair protein (HHP) on the nutritional value for poultry. In experiment 1, twenty roosters of Hanhyup-3 strain were alloted, and metabolizability of HHAA was measured. In experiment 2, forty roosters of Hanhyup-3 strain were alloted to 0, 3, 7.6 and 15.1% of HHAA treatments, 10 birds per treatment, and measured feed utilization and blood parameters. In experiment 1, no trend was found in excretion of amino acid, high in glysine and glutelin, low in valine, threonine, and methionine. HHAA metabolizability of serine, phenylalanine, alanine, and isoleucine was more higher than that of lysine, cystine, asparagine, and tyrosine. In experiment 2, as the HHAA level increased, feed intake decreased significantly in 15.1% treatment, but water intake increased significantly in 15.1% traetment. Dry matter and nitrogen metabolizability decreased in 7.6 and 15.1% treatments. Although no significant difference was found among three treatments(0, 3, and 5.7%), as the HHAA level increased, dry matter and nitrogen metabolizability decreased. Serum creatinine level was significantly increased in 15.1% treatment. In conclusion, it is considered that proper level to substitute soybean meal by HHAA was 10%.

Quantitative urine amino acid analysis using liquid chromatography tandem mass spectrometry and aTRAQ ® reagents

Ion-exchange chromatography (IEC) is the most widely used method for amino acid analysis in physiological fluids because it provides excellent separation and reproducibility, with minimal sample preparation. The disadvantage, however, is the long analysis time needed to chromatographically resolve all the amino acids. To overcome this limitation, we evaluated a novel liquid chromatography tandem mass spectrometry (LC–MS/MS) method, which utilizes aTRAQ ® reagents, for amino acid analysis in urine. aTRAQ ® reagents tag the primary and secondary amino groups of amino acids. Internal standards for each amino acid are also labeled with a modified aTRAQ ® tag and are used for quantification. Separation and identification of the amino acids is achieved by liquid chromatography tandem mass spectrometry using retention times and mass transitions, unique to each amino acid, as identifiers. The run time, injection-to-injection, is 25 min, with all amino acids eluting within the first 12 min. This method has a limit of quantification (LOQ) of 1 μmol/L, and is linear up to 1000 μmol/L for most amino acids. The Coefficient of Variation (CV) was less than 20% for all amino acids throughout the linear range. Method comparison demonstrated concordance between IEC and LC–MS/MS and clinical performance was assessed by analysis of samples from patients with known conditions affecting urinary amino acid excretion. Reference intervals established for this method were also concordant with reference intervals obtained with IEC. Overall, aTRAQ ® reagents used in conjunction with LC–MS/MS should be considered a comparable alternative to IEC. The most attractive features of this methodology are the decreased run time and increased specificity.

Aphid-host plant interactions: does aphid honeydew exactly reflect the host plant amino acid composition?

Plants provide aphids with unbalanced and low concentrations of amino acids. Likely, intracellular symbionts improve the aphid nutrition by participating to the synthesis of essential amino acids. To compare the aphid amino acid uptakes from the host plant and the aphids amino acid excretion into the honeydew, host plant exudates (phloem + xylem) from infested and uninfested Vicia faba L. plants were compared to the honeydew produced by two aphid species (Acyrthosiphon pisum Harris and Megoura viciae Buckton) feeding on V. faba. Our results show that an aphid infestation modifies the amino acid composition of the infested broad bean plant since the global concentration of amino acids significantly increased in the host plant in response to aphid infestations. Specifically, the concentrations of the two amino acids glutamine and asparagine were strongly enhanced. The amino acid profiles from honeydews were similar for the two aphid species, but the concentrations found in the honeydews were generally lower than those measured in the exudates of infested plants (aphids uptakes). This work also highlights that aphids take large amounts of amino acids from the host plant, especially glutamine and asparagine, which are converted into glutamic and aspartic acids but also into other essential amino acids. The amino acid profiles differed between the host plant exudates and the aphid excretion product. Finally, this study highlights that the pea aphid, a “specialist” for the V. faba host plant, induced more important modifications into the host plant amino acid composition than the “generalist” aphid M. viciae.

Amino acid absorption and homeostasis in mice lacking the intestinal peptide transporter PEPT1

The intestinal peptide transporter PEPT1 mediates the uptake of di- and tripeptides derived from dietary protein breakdown into epithelial cells. Whereas the transporter appears to be essential to compensate for the reduced amino acid delivery in patients with mutations in amino acid transporter genes, such as in cystinuria or Hartnup disease, its physiological role in overall amino acid absorption is still not known. To assess the quantitative importance of PEPT1 in overall amino acid absorption and metabolism, PEPT1-deficient mice were studied by using brush border membrane vesicles, everted gut sacs, and Ussing chambers, as well as by transcriptome and proteome analysis of intestinal tissue samples. Neither gene expression nor proteome profiling nor functional analysis revealed evidence for any compensatory changes in the levels and/or function of transporters for free amino acids in the intestine. However, most plasma amino acid levels were increased in Pept1(-/-) compared with Pept1(+/+) animals, suggesting that amino acid handling is altered. Plasma appearance rates of (15)N-labeled amino acids determined after intragastric administration of a low dose of protein remained unchanged, whereas administration of a large protein load via gavage revealed marked differences in plasma appearance of selected amino acids. PEPT1 seems, therefore, important for overall amino acid absorption only after high dietary protein intake when amino acid transport processes are saturated and PEPT1 can provide additional absorption capacity. Since renal amino acid excretion remained unchanged, elevated basal concentrations of plasma amino acids in PEPT1-deficient animals seem to arise mainly from alterations in hepatic amino acid metabolism.

Lysinuric protein intolerance: Reviewing concepts on a multisystem disease

Lysinuric protein intolerance (LPI) is an inherited aminoaciduria caused by defective cationic amino acid transport at the basolateral membrane of epithelial cells in intestine and kidney. LPI is caused by mutations in the SLC7A7 gene, which encodes the y(+)LAT-1 protein, the catalytic light chain subunit of a complex belonging to the heterodimeric amino acid transporter family. LPI was initially described in Finland, but has worldwide distribution. Typically, symptoms begin after weaning with refusal of feeding, vomiting, and consequent failure to thrive. Hepatosplenomegaly, hematological anomalies, neurological involvement, including hyperammonemic coma are recurrent clinical features. Two major complications, pulmonary alveolar proteinosis and renal disease are increasingly observed in LPI patients. There is extreme variability in the clinical presentation even within individual families, frequently leading to misdiagnosis or delayed diagnosis. This condition is diagnosed by urine amino acids, showing markedly elevated excretion of lysine and other dibasic amino acids despite low plasma levels of lysine, ornithine, and arginine. The biochemical diagnosis can be uncertain, requiring confirmation by DNA testing. So far, approximately 50 different mutations have been identified in the SLC7A7 gene in a group of 142 patients from 110 independent families. No genotype-phenotype correlation could be established. Therapy requires a low protein diet, low-dose citrulline supplementation, nitrogen-scavenging compounds to prevent hyperammonemia, lysine, and carnitine supplements. Supportive therapy is available for most complications with bronchoalveolar lavage being necessary for alveolar proteinosis.

The effect of previous exposure to dietary microbial phytase on the endogenous excretions of energy, nitrogen and minerals from turkeys

1. A precision feeding experiment was conducted with turkeys, which had previously been fed diets with or without phytase, to study the effects on the excretions of endogenous energy (EEL), nitrogen (ENL), amino acids (EAAL) and minerals. 2. Female turkeys (BUT 6) which had been fed one of 4 experimental diets (low P maize-soya diets (control, C), C + 250 international units of phytase/kg diet (FTU), C + 500 FTU and C + 2500 FTU) were used in this study. All birds were fasted and then given 50 mL of glucose solution at 46 d of age. Birds were allocated to individual metabolism cages in a randomised block design with 8 replicates for each of the 4 previously-fed diets. 3. The response of EEL and ENL to phytase pre-exposure was linear. An increase of 100 FTU reduced the EEL and ENL by approximately 1·6 kJ and 20 mg respectively. The results suggest that a minimum activity of phytase of 500 FTU is needed to initiate the reduction of these losses. 4. Pre-exposure to phytase reduced the EAAL, which was best described as a linear response with increasing phytase dose in the pre-study period. An increase of 100 FTU reduced the losses of total endogenous amino acids by approximately 225 mg. 5. In contrast to the results for endogenous energy losses, turkeys pre-exposed to phytase linearly increased their excretions of Ca and Mg with increasing phytase activity in the pre-study period. 6. The effects of feeding turkeys with supplementary phytase continued for at least 4 d after the diets were withdrawn. This suggests that exposure to phytase alters the functionality and secretions of the gastrointestinal tract, which may influence the nutritive value of diets fed immediately after.

Growth and biochemical characterization of associations between cyanobionts and wheat seedlings in co-culturing experiments

AbstractN2-fixing cyanobacteria are unique in their capacity to form symbiotic associations with a wide range of eukaryotic hosts belonging to different plant groups. The present study was undertaken to analyze the interactions of the cyanobiont PI 01 (from Azolla pinnata) and Nostoc PCC 9229 (from Gunnera monoika) with wheat seedlings, in co-culturing experiments. Each of the cyanobionts enhanced significantly the volume of root and shoot biomass in the experimental cultures. The transverse sections of roots in the co-cultured seedlings revealed the presence of aseriate packets of cyanobionts below the root epidermis. The investigated cyanobionts excreted amino acids (His, Met, Val) and sugars into the medium, while indoleacetic acid was detected when the cyanobionts were grown in a tryptophan containing medium. During the co-culturing, sugars and proline were detected in the extracellular filtrates. It can be hypothesized that these sugars and amino acids may serve as signal substances in the development of functional associations between the relevant cyanobionts and the wheat seedlings.

Vitamin D Deficiency Rickets Mimicking Pseudohypoparathyroidism-Case Report

Vitamin D deficiency rickets (VDDR) is a disorder biochemically characterized by elevated serum alkaline phosphatase (ALP) activity, normal or decreased serum calcium (Ca) and inorganic phosphate concentrations, secondary hyperparathyroidism and decreased serum 25−hydroxyvitamin D (25(OH)D) levels. In stage 1 VDDR, urinary amino acid and phosphate excretion are normal with minimal or no findings of rickets on radiographs. Pseudohypoparathyroidism (PHP) is an inherited disorder characterized by end−organ resistance to parathormone (PTH). VDDR occasionally resembles PHP type 2 in clinical presentation and biochemical features, creating difficulties in the differential diagnosis of these two entities. Here we report an infant diagnosed with VDDR. In addition to inadequate vitamin D intake, usage of antiepileptic drugs (AED) may have led to the worsening of the vitamin D deficiency. The patient presented with a history of febrile convulsions, for which he received phenobarbital treatment. The initial findings of hypocalcemia, hyperphosphatemia and normal tubular reabsorption of phosphate, mimicking PHP 2, responded well to vitamin D and oral Ca treatment with normalization of serum Ca, phosphorus (P), ALP and PTH levelsConflict of interest:None declared.