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J V Anderson

Publications and source records attributed to J V Anderson.

At least 37 records · Page 2Linked to original sources
PubMed1992

Purification of Multiple Forms of Glutathione Reductase from Pea (Pisum sativum L.) Seedlings and Enzyme Levels in Ozone-Fumigated Pea Leaves.

Glutathione reductase was purified from pea seedlings using a procedure that included 2',5'-ADP Sepharose, fast protein liquid chromatography (FPLC)-anion exchange, and FPLC-hydrophobic interaction chromatography. The purified glutathione reductase was resolved into six isoforms by chromatofocusing. The isoform eluting with an isoelectric point of 4.9 accounted for 18% of the total activity. The five isoforms with isoelectric points between 4.1 and 4.8 accounted for 82% of the activity. Purified glutathione reductase from isolated, intact chloroplasts also resolved into six isoforms after chromatofocusing. The isoform eluting at pH 4.9 constituted a minor fraction of the total activity. By comparing the chromatofocusing profile of the seedling extract with that of the chloroplast extract, we inferred that the least acidic isoform was extraplastidic and that the five isoforms eluting from pH 4.1 to 4.8 were plastidic. Both the plastidic (five isoforms were pooled) and extraplastidic glutathione reductases had a native molecular mass of 114 kD. The plastidic glutathione reductase is a homodimer with a subunit molecular mass of 55 kD. Both glutathione reductases had optimum activity at pH 7.8. The K(m) for the oxidized form of glutathione (GSSG) was 56.0 and 33.8 mum for plastidic and extraplastidic glutathione reductase, respectively, at 25 degrees C. The K(m) for NADPH was 4.8 and 4.0 mum for plastidic and extraplastidic isoforms, respectively. Antiserum raised against the plastidic glutathione reductase recognized a 55-kD polypeptide from purified antigen on western blots. In addition to the 55-kD polypeptide, another 36-kD polypeptide appeared on western blots of leaf crude extracts and the purified extraplastidic isoform. The lower molecular mass polypeptide might represent GSSG-independent enzyme activity observed on activity-staining gels of crude extracts or a protein that has an epitope similar to that in glutathione reductase. Fumigation with 75 nL L(-1) ozone for 4 h on 2 consecutive days had no significant effect on glutathione reductase activity in peas (Pisum sativum L.). However, immunoblotting showed a greater level of glutathione reductase protein in extracts from ozone-fumigated plants compared with that in control plants at the time when the target concentration was first reached, approximately 40 min from the start of the fumigation, and 4 h on the first day of fumigation.

Journal Article↗
PubMed1992

Seasonal variation in the antioxidant system of eastern white pine needles : evidence for thermal dependence.

Antioxidant metabolites in eastern white pine (Pinus strobus L.) needles increased two- to fourfold from the summer to the winter season. Antioxidant enzymes in needle tissue increased between 2- and 122-fold during this same period. These seasonal changes were determined by monitoring ascorbate and glutathione concentrations and the activity of ascorbate peroxidase, glutathione reductase (GR), and superoxide dismutase. Levels of antioxidant metabolites and enzymes were observed always to be lowest during the summer, or active growing season, and highest during the winter, or dormant season. These data correlated well with the thermal kinetic window for purified GR obtained from summer needles. The minimum, apparent K(m,NADPH) for two isoforms of GR (GR(A) and GR(B)) occurred at 5 and 10 degrees C, respectively. The upper limit of the thermal kinetic window (200% of the minimum K(m)) for GR(A) and GR(B) was 20 and 25 degrees C, respectively, indicating that needle temperatures exceeding 25 degrees C may result in impairment of antioxidant metabolism. The needle content and kinetic properties of GR, the increased activities of other enzymes, and the high substrate concentrations observed during the winter are consistent with the protective function this pathway may provide against photooxidative, winter injury.

Journal Article↗
PubMed1992

Prevalence of gastritis in patients with acromegaly: untreated and during treatment with octreotide.

OBJECTIVE: It has previously been suggested that acromegalic patients treated with the somatostatin analogue octreotide invariably have chronic gastritis. We have examined the prevalence of gastritis in a large group of acromegalic patients, untreated and during treatment with octreotide. DESIGN: We studied three groups of acromegalic patients: (A) untreated; (B) octreotide-treated; (C) a subgroup of these studied both before and during octreotide therapy. PATIENTS: Forty-eight patients, grouped as above, with active acromegaly were examined for the presence of gastritis. MEASUREMENTS: Gastroscopy and histological examination of gastric biopsies for the presence of gastritis and Helicobacter organisms were undertaken. The principal outcome was quantification of the prevalence of gastritis in the various study groups. RESULTS: Group A: 10 of the 33 patients (30%) had gastritis before any therapy with octreotide. Group B: 17 of 36 patients (47%) on octreotide treatment for 6-59 months (mean 20.5) had gastritis, and this was present in five out of the sub-group of eight patients (62%) treated for over 3 years. Group C: three of 21 patients (14%) developed gastritis during treatment with octreotide for between 6 and 23 months (mean 12.4). There was a highly significant association between the presence of gastritis and the presence of Helicobacter pylori organisms. CONCLUSIONS: Octreotide therapy of acromegaly may predispose to the development of gastritis, but this remains statistically unproven. Certainly, gastritis is not an invariable consequence of octreotide therapy, even after prolonged periods of treatment. The presence of gastritis is associated with H. pylori infection.

Acromegaly↗
PubMed1992

Possible mechanism and treatment of o,p'DDD-induced hypercholesterolaemia.

Ortho,para,dichlorodiphenyl dichloroethane (o,p'DDD, Mitotane (Roussell)) is used as an adrenolytic drug to reduce adrenocortical mass and circulating cortisol levels in Cushing's syndrome but has the unwanted side-effect of inducing hypercholesterolaemia. This paper examined the mechanism of that effect in 30 patients with Cushing's syndrome treated with o,p'DDD during the past 10 years. o,p'DDD increased serum cholesterol by 68 per cent, mainly by increasing LDL-cholesterol. The latter effect was not due to impaired binding of LDL to its receptor, as shown in vitro using cultured fibroblasts. Increases in plasma mevalonic acid during o,p'DDD administration were suggestive of increased cholesterol synthesis, this effect being reversed by simvastatin. These findings suggest that o,p'DDD causes hypercholesterolaemia by increasing cholesterol synthesis. It is proposed that this effect is due to the drug's known ability to block cytochrome P450-mediated reactions, thus impairing the formation of oxysterols responsible for down-regulating hepatic cholesterol synthesis. Treatment with simvastatin, an inhibitor of cholesterol synthesis, reverses the hyperlipidaemia and enables o,p'DDD therapy to be maintained without increasing cardiovascular risk.

Adult↗
PubMed1991

Human atrial natriuretic factor and renin-aldosterone in paracetamol induced fulminant hepatic failure.

It has been postulated that deficiency of a putative natriuretic factor, or resistance to such a factor, may contribute to sodium retention in fulminant hepatic failure. Levels of plasma human atrial natriuretic factor (h-ANF), plasma renin activity, and aldosterone concentration were measured in 33 patients with fulminant hepatic failure due to paracetamol overdose, and 12 healthy control subjects. Levels of h-ANF were raised only in patients with evidence of severe renal impairment (serum creatinine greater than 300 mumol/l and urine output less than 100 ml/24 hours). h-ANF values were median 4.15, range 2-9 pmol/l and 10.1, 1-25 pmol/l for the control and severe renal impairment groups respectively (p less than 0.001). In the latter plasma renin activity was raised compared to that in control subjects (median 19.8, range 1.04-41.7 and 2.86, 1.87-5.9 pmol/l/h respectively, p less than 0.02). Plasma aldosterone concentration was also raised in patients (2176, 199-6894 pmol/l compared to 368, 133-578 pmol/l in control subjects, p less than 0.01). Haemodialysis induced changes in circulating h-ANF which correlated with volume and right atrial pressure changes (p less than 0.001 and p less than 0.05 respectively). In six patients with no or mild renal failure infusion of 900 ml 5% human albumin solution caused a significant increase in plasma h-ANF (p less than 0.05) without natriuresis or diuresis, a finding compatible with the hypothesis that there may be resistance to h-ANF in this group. The present findings indicate that there is no deficiency of h-ANF in fulminant hepatic failure and that known mechanisms of h-ANF release are not impaired.

Acetaminophen↗
PubMed1991

Atrial natriuretic peptide in physiological doses does not inhibit the ACTH or cortisol response to corticotrophin-releasing hormone-41 in normal human subjects.

Whilst it has been postulated that atrial natriuretic peptide (ANP) may modulate pituitary hormone release, several investigations in non-human species have reported conflicting results when looking for an effect on the hypothalamo-pituitary-adrenal axis. However, in a recent study significant inhibition of corticotrophin-releasing hormone (CRH)-stimulated ACTH in cultured rat anterior pituitary cells occurred only with the complete peptide alpha-ANP(1-28). We have therefore investigated whether this form of ANP can inhibit CRH-stimulated ACTH and cortisol release in human subjects. Six healthy male volunteers received human alpha-ANP or placebo, and human CRH or placebo, on four separate occasions. ANP was infused at a rate of 0.01 micrograms/kg per min in order to achieve levels in the high physiological range. CRH was given as a bolus dose of 100 micrograms 30 min into the ANP infusion. Cortisol and ANP were measured by radioimmunoassay, the latter after extraction. ACTH was measured by immunoradiometric assay. The data were analysed by Student's paired t-test on basal, peak and incremental levels. Basal levels of ANP were within the normal range (2-5 pmol/l). With ANP infusion, mean +/- S.E.M. peak ANP levels were 29.6 +/- 3.1 pmol/l. There were no significant differences in mean basal cortisol and ACTH levels on each of the 4 study days. Mean peak cortisol and ACTH levels after CRH and ANP did not significantly differ from those achieved with CRH and placebo ANP. We thus conclude that at high physiological doses, circulating ANP does not inhibit CRH-stimulated ACTH or cortisol release.

Adrenocorticotropic Hormone↗
PubMed1990

Single, total paracentesis for tense ascites: sequential hemodynamic changes and right atrial size.

Hemodynamic changes induced by a single, total paracentesis were evaluated in 21 patients with tense ascites from whom 4 to 16 L of ascites were drained over 2 to 8 hr with no serious complications. At 60 min, compared to baseline, there was an increase in cardiac output (7.7 +/- 0.5 to 8.5 +/- 0.6 L/min, p less than 0.02) and a tendency for right atrial pressure to decrease (9.3 +/- 0.8 to 7.50 +/- 0.8 mm Hg, NS), with no change in pulmonary capillary wedge pressure (10.9 +/- 0.9 to 10.7 +/- 0.9 mm Hg). Between 3 and 12 hr later, there was a drop in right atrial pressure, pulmonary capillary wedge pressure and cardiac output to 5.6 +/- 0.6 (p less than 0.02), 7.2 +/- 0.8 mm Hg (p less than 0.002) and 7.2 +/- 0.6 L/min (NS) respectively, indicative of the development of relative hypovolemia and suggesting that therapeutic plasma expansion is appropriate at this time. Two-dimensional echocardiography before paracentesis (n = 8) showed a reduction in the right to left atrium area ratio as compared with values in patients with minimal ascites (0.54 +/- 0.04 vs 0.82 +/- 0.02, p less than 0.0001). This technique may help in identifying patients with right atrial compression caused by tense ascites.

Adult↗
PubMed1990

Structural and functional analysis of the rat testis-specific histone H1t gene.

A 6.86 kb rat genomic DNA fragment containing the testis-specific histone H1t gene and the histone H4t gene has been sequenced. S1-nuclease protection analyses of total cellular RNA from rat liver and testis showed that histone H1t mRNA was present only in testis. Examination of various highly enriched populations of rat testis cell types revealed that H1t mRNA was found exclusively in a fraction enriched in pachytene spermatocytes. When protein, DNA interactions within the proximal promoter region of the histone H1t gene were examined by electrophoretic mobility shift assays, only minor differences were found in mobility shift patterns of the H1t promoter in assays comparing binding of nuclear proteins from pachytene spermatocytes and early spermatids. However, major differences in binding were observed upon comparing nuclear proteins from rat pachytene spermatocytes to liver. Comparison of binding patterns of rat testis, rat hepatoma H4 cells, HeLa cells, and COS-1 cells also revealed dramatic differences. Transcriptional activity of the histone H1t promoter was examined by measuring H1t promoted chloramphenicol acetyltransferase (CAT) mRNA levels in transient expression assays in transfected rat hepatoma H4 cells, HeLa cells, and COS-1 cells. These assays revealed that the histone H1t promoted CAT gene functioned poorly in HeLa cells and COS-1 cells compared to expression with the parent SV40 promoted vector pSV2CAT. The H1t promoted CAT gene apparently did not work at all in transfected rat hepatoma H4 cells, which is consistent with testis germinal cell specific expression of the histone H1t gene.

Animals↗
PubMed1990

Purification, characterization, and immunological properties for two isoforms of glutathione reductase from eastern white pine needles.

Glutathione reductase (EC 1.6.4.2) was purified from Eastern white pine (Pinus strobus L.) needles. The purification steps included affinity chromatography using 2', 5'-ADP-Sepharose, FPLC-anion-exchange, FPLC-hydrophobic interaction, and FPLC-gel filtration. Separation of proteins by FPLC-anion-exchange resulted in the recovery of two distinct isoforms of glutathione reductase (GR(A) and GR(B)). Purified GR(A) had a specific activity of 1.81 microkatals per milligram of protein and GR(B) had a specific activity of 6.08 microkatals per milligram of protein. GR(A) accounted for 17% of the total units of glutathione reductase recovered after anion-exchange separation and GR(B) accounted for 83%. The native molecular mass for GR(A) was 103 to 104 kilodaltons and for GR(B) was 88 to 95 kilodaltons. Both isoforms of glutathione reductase were dimers composed of identical subunit molecular masses which were 53 to 54 kilodaltons for GR(A) and 57 kilodaltons for GR(B). The pH optimum for GR(A) was 7.25 to 7.75 and for GR(B) was 7.25. At 25 degrees C the K(m) for GSSG was 15.3 and 39.8 micromolar for GR(A) and GR(B), respectively. For NADPH, the K(m) was 3.7 and 8.8 micromolar for GR(A) and GR(B), respectively. Antibody produced from purified GR(B) was reactive with both native and denatured GR(B), but was cross-reactive with only native GR(A).

Journal Article↗
PubMed1989

Comparison of the structural organization and expression of germinal and somatic rat histone H4 genes.

A rat somatic histone H4 gene was isolated by screening a rat genomic library using a cloned cell-cycle-regulated human histone H4 gene as a probe. The somatic histone H4 gene was subcloned and the nucleotide sequence was determined. The structural organization and expression of the somatic histone H4 gene and the rat germinal histone H4t gene were compared. Although the predicted amino-acid sequences of the two histones were identical, 49 out of 102 codons differed. The leader sequence of the germinal histone H4t mRNA was 17 bases compared to 40 bases for the somatic histone H4 mRNA, and the 3' terminal sequence of the germinal histone H4t mRNA was 52 bases compared to 75 bases for the somatic histone H4 mRNA. The germinal histone H4 gene also lacked a consensus purine-rich motif which was present in the 5' noncoding region of the somatic histone H4 gene. Northern blot analyses and S1-nuclease protection analyses revealed that the germinal histone H4t and H1t genes were expressed during spermatogenesis in rat pachytene spermatocytes, and the somatic histone H4 gene was expressed only in nongerminal rat cells and tissues. The histone H4t gene was also expressed in some other rat cell types. The differences in expression of the histone H4t and H1t genes may reflect differences in transcription, differences in turnover rates of the mRNAs, or a combination of these factors.

Amino Acid Sequence↗
PubMed1989

Plasma atrial natriuretic peptide in human fetus: response to intravascular blood transfusion.

To investigate whether atrial natriuretic peptide is present in the human fetal circulation and changes in response to fetal blood volume expansion, the concentration of plasma atrial natriuretic peptide was measured by radioimmunoassay in samples obtained by cordocentesis. Twenty-four patients referred for intravascular blood transfusion because of red cell isoimmunization at 21 to 35 weeks' gestation were studied. Plasma atrial natriuretic peptide concentrations in fetal blood (median, 8.0 pmol/L; range, 1 to 27.3) were significantly higher than those of 25 young 18- to 32-year-old adult control subjects (median, 4.5 pmol/L; range, 1 to 11.3, p less than 0.002 but similar to those found in the umbilical cord blood of 10 normal neonates immediately after delivery (median, 7.35 pmol/L; range, 2.7 to 15.5). In seven patients in whom fetal and maternal plasma atrial natriuretic peptide was measured simultaneously, all fetal concentrations were higher (p less than 0.01). The concentration of fetal atrial natriuretic peptide before and immediately after blood transfusion (n = 12) rose significantly (p less than 0.05), and the rise correlated positively with the transfusion rate (p less than 0.05). We conclude that atrial natriuretic peptide is present in plasma of the human fetus as early as 21 weeks' gestation and that its concentration increases promptly in response to vascular volume expansion. These findings suggest that atrial natriuretic peptide may play a role in fetal volume homeostasis.

Adolescent↗
PubMed1989

Atrial natriuretic peptide: physiological release associated with natriuresis during negative pressure breathing in man.

1. Negative pressure breathing was one of the first physiological tools used to study the renal effects of redistribution of the blood volume from the peripheries to the thorax. The recent discovery of a putative natriuretic hormone (atrial natriuretic peptide, ANP) in cardiac atrial tissue has rekindled interest in the effect of the cardiovascular system on renal function. We have therefore studied the effects of this physiological manoeuvre on plasma ANP concentrations and renal responses. 2. Plasma concentrations of ANP, plasma renin activity and plasma aldosterone concentration were measured during an 80 min period of negative pressure breathing at -12 cmH2O pressure in six hydrated normal subjects. Identical control studies were performed in the same subjects at at least 1 week apart. 3. Negative pressure breathing resulted in a natriuresis and diuresis which were associated with a significant rise in plasma ANP concentration. The natriuresis occurred despite an increase in plasma renin activity and in plasma aldosterone concentration. 4. These findings, under specific carefully controlled conditions, support the previously contentious postulate that negative pressure breathing enhances sodium excretion, in addition to its well-recognized diuretic effect. They add further weight to the hypothesis that expansion of the central blood volume is an important stimulus to the release of ANP from the heart (acting by way of atrial distension), and suggest that changes of plasma ANP concentration may have induced the natriuresis which occurred in the face of a modest activation of the sodium-retaining renin-aldosterone system.

Adult↗
PubMed1989

Plasma atrial natriuretic factor and graft function in renal transplant recipients.

In order to determine the relationships between allograft function and the recipient's plasma concentrations of atrial natriuretic factor (ANF), plasma ANF was measured by radioimmunoassay for 14 days after cadaveric renal transplantation in 9 patients aged 19-64 years. All received immunosuppression with prednisolone, azathioprine, and cyclosporine. No patient was in heart failure. During the study period, six grafts functioned, and three were nonfunctioning--two due to rejection and one to acute tubular necrosis. Plasma ANF concentration at the time of transplantation was 48 +/- 16 pmol/L (mean +/- SEM) range 15-145 pmol/L. In the six patients with functioning grafts, ANF declined in parallel with the fall in serum creatinine (658 +/- 35 to 210 +/- 34 mumol/L). In the three with nonfunctioning grafts, serum creatinine and plasma ANF concentration both increased. There was overall a significant linear relation between serum creatinine and plasma ANF (r = 0.527, P less than 0.001). The changes in plasma ANF after renal transplantation bore no relationship to changes in body weight or blood pressure. However, plasma ANF concentration was related to allograft fractional sodium excretion (r = 0.687, p less than 0.001). We conclude that elevated plasma ANF concentrations in end-stage renal disease are restored to normal by successful renal transplantation, implying that renal function is a determinant of plasma ANF concentration. Circulating plasma ANF may also have a direct effect on allograft sodium excretion.

Adult↗
PubMed1989

Resistance of metastatic pancreatic endocrine tumours after long-term treatment with the somatostatin analogue octreotide (SMS 201-995).

Ten patients with metastatic pancreatic endocrine tumours were treated with the long-acting somatostatin analogue octreotide (SMS 201-995). Three patients showed no response, clinically or biochemically, and treatment was therefore withdrawn. The seven remaining patients continued treatment for a median period of 28 months (range 13-54 months). Treatment was initially effective, symptoms improved and the concentrations of tumour-related hormones were reduced. Worsening of symptoms and rising levels of tumour-related hormone concentrations occurred a median of 5 months (range 1-6 months) after the start of therapy and were initially reversed by increasing the dose of octreotide over a median of 10 months (range 6-16 months). However, after a median of 13 months (range 5-34 months) at the maximum dosage, symptoms recurred and were no longer responsive to a further increase in dosage of octreotide or other therapeutic measures. All patients died within a period of 5 months once this resistant phase of their illness had been reached.

Adenoma, Islet Cell↗
PubMed1989

Hormonal response to blood volume expansion in diabetic subjects with and without autonomic neuropathy.

The hormonal and renal response to volume expansion, produced by water immersion for 4 h, was studied in 14 insulin-dependent diabetic subjects (seven without complications, seven with autonomic neuropathy) and in 14 age-and-sex-matched normal control subjects. The diabetic subjects showed an impaired natriuretic response to volume expansion (total amount of sodium excreted 21 mmol compared to 39 mmol in normals, P less than 0.01) but the response did not differ in those with and without autonomic neuropathy. There was no significant difference in the suppression of plasma renin or aldosterone during immersion in either group. Plasma catecholamines suppressed on immersion in all groups. Basal values were lowest in the group with autonomic involvement. Atrial natriuretic peptide levels showed a twofold rise (from 4.8 to 9.6 pmol/l, P less than 0.01) on immersion. There was no significant difference in the levels of this hormone between diabetic patients and normal subjects or between those diabetics with and those without autonomic neuropathy. The present study confirms that diabetic subjects retain sodium avidly during volume expansion. This enhancement cannot be ascribed to any measurable difference in the levels of circulating hormones known to be involved in natriuresis and is not influenced by the presence of autonomic neuropathy.

Adult↗
PubMed1989

Atrial natriuretic peptide concentrations in hypoxic secondary pulmonary hypertension: relation to haemodynamic and blood gas variables and response to supplemental oxygen.

Plasma atrial natriuretic peptide concentrations, measured in samples drawn from the pulmonary artery, were raised in nine of 17 patients with hypoxic pulmonary hypertension but normal right atrial pressures at rest. No relationship was seen between atrial natriuretic peptide concentrations and mean pulmonary artery or right atrial pressure, or calculated pulmonary or systemic vascular resistance. Patients with the most severe hypoxaemia tended to have higher plasma atrial natriuretic peptide concentrations; three patients with no past history of oedema had concentrations more than twice the upper limit of normal. Treatment with supplementary oxygen for 30 minutes reduced pulmonary vascular resistance in all patients but had no significant effect on plasma atrial natriuretic peptide concentration. These findings suggest that atrial natriuretic peptide may be a factor in the control of sodium and water balance in hypoxic cor pulmonale, where the determinants of individual susceptibility to peripheral oedema are not well understood.

Aged↗