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Biomedical subjects

D Perrett

Publications and source records attributed to D Perrett.

At least 127 records · Page 7Linked to original sources
PubMed1978

Elevation of rat erythrocyte nucleotide levels following acute renal failure induced by glycerol or mercuric chloride.

Biochemical changes in the blood following induction of renal failure by glycerol or mercuric chloride have been studied in 16 rats. Plasma creatinine, urea and Pi levels indicated that renal impairment followed the same time course in both renal failure models, with the severest effects on day 3 and returning to normal by day 7. Erythrocyte ATP and guanine triphosphate (GTP) levels were significantly elevated above contorl values on day 1 and remained elevated in both models. ATP/ADP and GTP/GDP ratios also increased in both models. In renal failure the increased purine 'salvage' in the erythrocyte may be attributed to accumulation of purine metabolites in the serum associated with increased P-ribose-PP levels due to elevated cellular Pi. Nucleotide changes in both these models are analogous to those found in chronic renal failure in man.

Acute Kidney Injury↗
PubMed1977

An outline of D-penicillamine metabolism.

In a study using 14C-D-penicillamine in a normal subject only 50% of the D-penicillamine was absorbed from the gut. The major urinary metabolites are cysteine-penicillamine and penicillamine disulphide. S-methyl-D-penicillamine is the only biochemically transformed metabolite so far identified.

Amino Acids↗
PubMed1976

Simplified low-pressure high-resolution nucleotide analyser.

A simple nucleotide analyser was constructed from commercially available components. A 20 cm X 0.4 cm I.D. column of pellicular anion exchanger operating at approximately 20 p.s.i. was found to perform identically with published methods using high-pressure equipment. The eluant was monitored using a variable-wavelength UV monitor. A very simple device for producing variable gradients was employed. The nucleotide analyser was trouble free to operate and the results were both linear and reproducible. Applications to the rapid analysis of nucleotides and the high-sensitivity analysis (approx. 10 pmoles) of cyclic 3',5'-adenosine monophosphate and cyclic 2',3'-guanosine monophosphate and tissue nucleotides are described.

Anion Exchange Resins↗
PubMed1976

Studies on adenine and adenosine metabolism by intact human erythrocytes using high performance liquid chromatography.

Adenine and adenosine metabolism has been studied in intact human erythrocytes in vitro using high performance liquid chromatography, isotopic labeling and electrophoresis. Their metabolism to nucleotides was controlled by phosphoribose diphosphate synthesis which was phosphate dependent. Adenosine formed hypoxanthine or IMP depending upon Pi concentration, but adenosine kinase and deaminase activities were not affected by P levels. Free [14C]adenine and [14C]hypoxanthine were found in cellular extracts. Rapid interconversions occurred to give a distribution for ATP : ADP : AMP of 10 : 1 : 0.1. Marked decomposition of ATP to ADP and AMP occurred during incubations in plasma and Earle's media in air on nitrogen, but ATP levels remained stable in phosphate buffers and in the presence of oxygen. At physiological Pi (1 mM) adenosine kinase activity grossly exceeded adenine phosphoribosyltransferase activity. The latter was approximately 7 fold that of hypoxanthine phosphoribosyltransferase activity. These differences decreased with increasing Pi levels. No significant increase in corresponding nucleotides was obtained by incubation with high levels (0.5 mM) of adenine, guanine or guanosine at physiological Ii, ATP increased by 10% independently of the substrate employed and significant amounts of IMP and GTP were formed adenosine and guanosine, respectively. The existence of a bound intracellular pool of ATP is suggested.

Adenine↗
PubMed1976

Enhanced preservation of the ischaemic kidney with inosine.

The function of rat kidneys subjected to 60 minutes of warm ischaemia at body-temperature was notably protected by the prior administration of the purine nucleoside inosine as a 40 mg/ml solution maintained at 37 degrees C. With direct intrarenal arterial perfusion of the kidney at the onset of ischaemia or with intraperitoneal (i.p.) injection 40 minutes before ischaemia, the plasma-creatinine at 24 hours was significantly lower (P less than 0-001) than that of untreated 60-minute-ischaemia controls and not significantly different from that of non-ischaemic unilateral-nephrectomy controls. Intravenous inosine 20 minutes beforehand also afforded significant (P less than 0-01) protection. 7-day survival was 100% in 30 inosine-pretreated rats and 65% in 45 rats with all other types of pre-treatment (P less than 0-001). Although i.p. adenosine was better (P less than 0-05) than no treatment, i.p. inosine was better (P less than 0-02) than i.p. adenosine. Allopurinol, phenoxybenzamine, A.T.P., or cyclic A.M.P. caused no improvement over controls. Kidneys perfused with inosine maintained higher purine-nucleotide levels during ischaemia and rapidly resynthesised A.T.P. when blood-flow was restored in vivo.

Adenosine↗
PubMed1976

Cystinuria: a new genetic variant.

1. A family is reported with an unusual type of cystinuria. 2. The propositus presented with a cystine renal stone; the renal tubular reabsorption of cystine was grossly abnormal but the tubular reabsorption of ornithine, lysine and arginine was only slightly less than normal. 3. One of the children of the propositus escreted cystine and lysine in increased amounts typical of type II heterozygotes for cystinuria. 4. The renal transport defect in this family may represent one end of the spectrum of cystinuria or it may be a form akin to isolated hypercystinuria.

Amino Acids↗
PubMed1975

A study of the renal handling and intestinal absorption of dibasic amino acids in a patient with genotype +/11 heterozygous cystinuria and idiopathic hypercalcuria.

A case is reported of a patient with idiopathic hypercalcuria who was referred for investigation of renal calculi. Studies of urinary amino acid excretion in the patient and all living members of his family, as well as studies of endogenous renal clearances of dibasic amino acids and cystine in the patient and his daughter, indicated that the patient had genotype +/11 heterozygous cystinuria. Intestinal perfusion studies showed however that the patient was able to absorb L-lysine, L-arginine normally from the jejunum and ileum. This suggests that a difference exists between renal and intestinal handling of lysine and arginine in cystinuria.

Adult↗
PubMed1975

Jejunal and ileal absorption of dibasic amino acids and an arginine-containing dipeptide in cystinuria.

Ileal transport of dibasic amino acids has not previously been studied in the intestine of healthy volunteers or cystinuric patients. Experiments have therefore been designed to compare ileal and jejunal absorption of lysine and arginine both in normal subjects and cystinuric patients. In addition, jejunal perfusion experiments have been carried out to investigate absorption of the dipeptide L-arginyl-L-leucine. The results indicate that, at the concentrations studied (4.2 mM lysine, 1 mM arginine), severe transport defects exist throughout the whole small intestine for both amino acids in cystinuria. Despite the transport defect for free arginine, cystinuric patients absorbed the dipeptide L-arginyl-L-leucine normally. Because of the transport defect for free arginine, it has been possible to show that during absorption of L-arginyl-L-leucine in cystinuria approximately 30% of dipeptide-bound arginine can be recovered from the gut lumen in the free form. These findings indicate that the prime function of specific amino acid transport systems during the absorption of protein digestion products may be as a "recapture mechanism" for amino acids liberated as a result of mucosal cell peptide hydrolysis.

Adult↗
PubMed1974

Amino acid and peptide absorption in patients with coeliac disease and dermatitis herpetiformis.

A double-lumen perfusion technique has been used to study amino acid and peptide absorption in eight normal control subjects, 13 patients with untreated adult coeliac disease, and 16 patients with dermatitis herpetiformis who had varying morphological abnormalities of the small bowel. All subjects were perfused with isotonic solutions containing 10 mM glycyl-L-alanine and 10 mM glycine + 10 mM L-alanine. Patients with adult coeliac disease had impaired absorption of glycine (p < 0.01) and L-alanine (p < 0.05) from the amino acid solution compared with the control subjects. Amino acid uptake from the dipeptide solution was not significantly impaired, although four individual patients had impaired uptake of both amino acids. In contrast to these findings, very few patients with dermatitis herpetiformis had impaired amino acid absorption from either solution. Sodium absorption was impaired from both solutions when the groups of patients with adult coeliac disease and dermatitis herpetiformis with subtotal villous atrophy and partial villous atrophy were studied, and there were patients in each group who secreted sodium and water. The results suggest that malabsorption of dietary protein is unlikely to occur in dermatitis herpetiformis but may occur and contribute to protein deficiency seen in some severe cases of adult coeliac disease. The impairment of sodium and water absorption provides evidence that there may be functional impairment of the jejunal mucosa in dermatitis herpetiformis as well as in adult coeliac disease.

Adult↗