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At least 613 records · Page 34Linked to original sources

PubMed2002

Interactions of oxidative stress with thiamine homeostasis promote neurodegeneration.

Thiamine-dependent processes are diminished in brains of patients with several neurodegenerative diseases. The decline in thiamine-dependent enzymes can be readily linked to the symptoms and pathology of the disorders. Why the reductions in thiamine linked processes occur is an important experimental and clinical question. Oxidative stress (i.e. abnormal metabolism of free radicals) accompanies neurodegeneration and causes abnormalities in thiamine-dependent processes. The vulnerability of thiamine homeostasis to oxidative stress may explain deficits in thiamine homeostasis in numerous neurological disorders. The interactions of thiamine with oxidative processes may be part of a spiral of events that lead to neurodegeneration, because reductions in thiamine and thiamine-dependent processes promote neurodegeneration and cause oxidative stress. The reversal of the effects of thiamine deficiency by antioxidants, and amelioration of other forms of oxidative stress by thiamine, suggest that thiamine may act as a site-directed antioxidant. The data indicate that the interactions of thiamine-dependent processes with oxidative stress are critical in neurodegenerative processes.

Animals↗

PubMed1999

Metabolic aspects of phosphate replacement therapy for hypophosphatemia after renal transplantation: impact on muscular phosphate content, mineral metabolism, and acid/base homeostasis.

Hypophosphatemia caused by renal phosphate loss occurs frequently after kidney transplantation. In assumption of systemic phosphorus depletion, the presumed deficit commonly is replaced by oral phosphate supplements. However, such treatment is debatable, because intracellular phosphorus stores have not been assessed in this setting and may not be accurately reflected by serum phosphate concentrations. Moreover, disturbances in mineral metabolism from chronic renal failure, such as hypocalcemia and hyperparathyroidism, may be prolonged with oral phosphate supplements. Conversely, a neutral phosphate salt might improve renal acid excretion and systemic acid/base homeostasis for its properties as a urinary buffer and a poorly reabsorbable anion. Twenty-eight patients with mild early posttransplantation hypophosphatemia (0.3-0.75 mmol/L) were randomly assigned to receive either neutral sodium phosphate (Na(2)HPO(4)) or sodium chloride (NaCl) for 12 weeks and examined with regard to (1) correction of serum phosphate concentration and urinary phosphate handling; (2) muscular phosphate content; (3) serum calcium and parathyroid hormone (PTH); and, (4) renal acid handling and systemic acid/base homeostasis. Mean serum phosphate concentrations were similar and normal in both groups after 12 weeks of treatment; however, more patients in the NaCl group remained hypophosphatemic (93% versus 67%). Total muscular phosphorus content did not correlate with serum phosphate concentrations and was 25% below normophosphatemic controls but was completely restored after 12 weeks with and without phosphate supplementation. However, the percentage of the energy-rich phosphorus compound adenosine triphosphate (ATP) was significantly higher in the Na(2)HPO(4) group, as was the relative content of phosphodiesters. Also, compensated metabolic acidosis (hypobicarbonatemia with respiratory stimulation) was detected in most patients, which was significantly improved by neutral phosphate supplements through increased urinary titratable acidity. These benefits of added phosphate intake were not associated with any adverse effects on serum calcium and PTH concentrations. In conclusion, oral supplementation with a neutral phosphate salt effectively corrects posttransplantation hypophosphatemia, increases muscular ATP and phosphodiester content without affecting mineral metabolism, and improves renal acid excretion and systemic acid/base status.

Acid-Base Equilibrium↗

PubMed1997

Calcium homeostasis and yeast phagocytosis in hemocytes of the colonial ascidian Botryllus schlosseri.

This paper reports the effects of drugs affecting the homeostasis of cytosolic-free calcium on in vitro yeast phagocytosis by hemocytes of the colonial ascidian Botryllus schlosseri. Significant inhibition of phagocytosis is observed after exposure of hemocytes to 10 microM or higher concentrations of thimerosal, which is known to deplete intracellular calcium stores in mammalian cells. The two calcium channel blockers nifedipine and verapamil significantly decrease the phagocytic index, the minimum effective concentrations being 10 and 50 microM, respectively. As these substances have no effects at lower concentrations, they probably act through the inhibition of Ca(2+)-ATPase activity, required to restock intracellular calcium stores, due to their interaction with calmodulin. Analogously, pimozide, which suppresses ATPase activity by interacting with calmodulin, and thapsigargin, which inhibits Ca(2+)-ATPase activity, significantly reduce the phagocytic index. Moreover, nifedipine, by altering cytosolic calcium homeostasis, also lowers the production of superoxide anion associated with phagocytosis. Results indicate that in ascidians, as in mammals, a rise in intracellular calcium is required for phagocyte activation and induction of the respiratory burst.

Animals↗

PubMed1997

Activation of heme oxygenase-1 expression by disturbance of endoplasmic reticulum calcium homeostasis in rat neuronal cell culture.

Evidence has been presented that disturbances of endoplasmic reticulum (ER) calcium homeostasis contribute to neuronal injury induced by transient cerebral ischemia. The present series of experiments was designed to study whether the expression of heme oxygenase-1 (HO-1), which is markedly increased after transient cerebral ischemia, is also activated by a disturbance of ER calcium homeostasis. ER calcium pools were depleted by a 30 min exposure of primary cortical and hippocampal neurons to thapsigargin (Tg), an irreversible inhibitor of ER Ca2+-ATPase. In cortical neurons, HO-1 mRNA levels (analysed by quantitative polymerase chain reaction (PCR)) were significantly increased (22-fold) 12 h after exposure to Tg but had decreased again to only nine times control levels by 24 h after treatment. In hippocampal neurons, a significant increase in HO-1 mRNA levels was already apparent 4 h after treatment (8.3-fold over controls), levels rose further to 27-fold over controls after 6 h, and stayed high for up to 24 h after treatment (34-fold over controls). The similarity between the pattern of changes in HO-1 mRNA levels induced by transient ischemia and depletion of ER calcium stores suggests common underlying mechanisms.

Animals↗

PubMed1998

The effects of beta/A4-amyloid and its fragments on calcium homeostasis, glial fibrillary acidic protein and S100beta staining, morphology and survival of cultured hippocampal astrocytes.

Aggregated beta/A4-amyloid is known to increase intraneuronal calcium by various mechanisms and to lead eventually to the death of the cultured neuron. This study deals with the role of beta/A4-amyloid and several of its fragments in calcium homeostasis, glial fibrillary acid protein and S100beta staining, morphology and survival of cultured rat hippocampal astrocytes as determined by Fura imaging, indirect immunofluorescence and life/death assays. In contrast to cultured neurons, none of the 12 different beta/A4 fragments tested caused an increase in intra-astrocytic free calcium. However, among the compounds evaluated, the fragments 10-20mer, 25-35mer and the full-length peptides (1-40, 1-42 and 1-43mer), at 5 and 10 microM, decreased free intra-astrocytic calcium statistically significantly after the cells had been incubated for 48 and 72 h. This occurred both for astrocytes treated with vehicle alone or the reversed sequence of the 1-40mer, i.e. the 40-1mer. However, survival was not altered under the conditions examined, even when there was a change in free intracellular calcium. Concomitant with the decrease in intracellular free calcium, the shape of the astrocytes became more spider-like, normally an indication of activated astrocytes, and markedly more intense anti-S100beta and anti-glial fibrillary acidic protein staining was seen. The functional relevance of altered calcium homeostasis for apolipoprotein E secretion, potentially relevant for neuronal plasticity in general and in Alzheimer's disease, is discussed.

Amyloid beta-Protein Precursor↗

PubMed1999

Expression profile of the copper homeostasis gene, rAtox1, in the rat brain.

In humans the regulation of cellular copper homeostasis is essential for proper organ development and function. A novel cytosolic protein, named Atox 1, was recently identified in yeast that functions in shuttling intracellular mononuclear copper [Cu(I)] to copper-requiring proteins. Atox 1 and its human homolog, hAtox1, are members of an emerging family of proteins termed copper chaperones that are involved in the maintenance of copper homeostasis. Northern blot analysis demonstrates that Atox 1 is widely expressed at varying levels in a variety of rat tissues including brain. Using in situ hybridization histochemistry, we characterized the expression profile for the rat homolog of Atox1 (rAtox1) in the normal adult rat brain. There is widespread expression within the brain that appears to be primarily neuronal. The highest levels of Atox1 message consists of distinct neuronal subtypes that are also characterized by their high levels of metals like copper, iron, and zinc, which include the pyramidal neurons of the cerebral cortex and hippocampus in addition to the neurons of the locus coeruleus. The high levels of a metal chaperone like Atox1 in subsets of neurons that also sequester metals suggests that Atox1 may be important in maintaining the functionality of metal requiring enzymes. A detailed analysis of the restricted expression profile for a novel copper chaperone, rAtox1, is described in the adult rat CNS. Further analysis shows that Atoxl expression is associated with neuronal populations that sequester copper.

Animals↗

PubMed2002

Assessment of the disturbances in metabolic homeostasis: a hypothesis of synergism.

Based on the hypothesis that a synergistic interaction between triiodothyronine (T(3)) and insulin contributes to abnormalities in glucose and other metabolic pathways, the mechanisms underlying the impairment of metabolic homeostasis (MH) and the development of type-2 diabetes (DM) were investigated via a proposed homeostatic model, [(FG*TG)/T3*FI)]. The MH model characterizes the relationship between T(3) and insulin and the levels of triglycerides (TG), fasting insulin (FI), and fasting glucose (FG) and is introduced as a clinical method to assess insulin sensitivity and the status of metabolic homeostasis in lieu of current screening models advocated by the by American Diabetic Association (ADA). The present study validated the hypothetical model in a sample of 110 African-American women.

Black or African American↗

PubMed2001

Monitoring of early postnatal glucose homeostasis and cerebral function in newborn infants of diabetic mothers. A pilot study.

The aims of this pilot study were to evaluate a new technique in the monitoring of postnatal glucose homeostasis (microdialysis) and also to study possible associations between early postnatal hypoglycaemia and influences on cerebral function monitoring (CFM) in 12 newborn infants of diabetic mothers. In order to study the postnatal glucose homeostasis, frequent dialysate samples were obtained from a subcutaneous microdialysis catheter for measurements of glucose. In addition, we also received samples of dialysate lactate and glycerol. Dialysate glucose concentrations were correlated to capillary blood glucose levels, measured by a glucose oxidase method. The cerebral function monitor was applied postnatally and a registration was obtained continuously. Capillary blood glucose decreased initially, and seven newborns received intravenous glucose infusions due to glucose concentrations less than 2.2 mmol/l. Dialysate glucose concentrations were, on average, 0.4 mmol/l higher than corresponding concentrations in capillary blood. The correlation coefficient between the two measurements was 0.63 and the coefficient of variation was 19.2%. Dialysate lactate and glycerol levels increased significantly, with peak values 3-4 h postnatally. No significant overall influence of hypoglycaemia was detectable in the CFM tracing. We conclude that a relatively poor correlation was observed between glucose measurements in capillary samples and microdialysis. However, using the microdialysis technique saw indication of marked lipolysis and increased lactate production, which may be of importance for cerebral postnatal adaptation. The mild postnatal hypoglycaemia in infants of diabetic mothers does not seem to give visually detectable influences on CFM.

Adult↗

PubMed2001

Use of rat models to mimic alterations in iron homeostasis during human alcohol abuse and cirrhosis.

With alcoholism, there are marked disturbances in iron homeostasis that are linked to alterations in serum transferrin and ferritin concentrations. This study identifies rat models of alcohol abuse that closely mimic these disturbances. Male rats were placed in one of the following three protocols: (1) pair-feeding of liquid diets for 1-8 weeks; (2) agar-block feeding for 8 weeks; or (3) generation of cirrhosis with CCl(4). Serum samples were analyzed for ferritin, transferrin, and iron levels, and the transferrin iron saturation and ferritin/transferrin ratios were calculated. Liver iron concentrations were also determined. Serum transferrin levels were elevated in animals fed alcohol for 8 weeks in pair-feeding and agar-block feeding protocols, but reduced in rats with cirrhosis. Serum ferritin concentration was reduced in rats fed ethanol in the liquid diet, but increased in rats consuming ethanol in agar blocks, in rats pair-fed the liquid control diet, and in rats with cirrhosis. This finding was mirrored by liver nonheme iron concentrations in all experimental groups, but not in the corresponding control groups. Serum iron levels were significantly elevated only in rats fed the liquid control diet. There was a progressive decrease in transferrin iron saturation and ferritin/transferrin ratios for animals fed ethanol in the liquid diet, but not when ethanol was ingested from agar blocks. The development of cirrhosis resulted in elevated liver iron concentrations and doubled ferritin/transferrin ratios. It is concluded that these models may be used to study disturbances in iron homeostasis that occur during alcohol abuse and the (subsequent) development of liver disease.

Alcoholism↗

PubMed1998

Acute effect of ethanol on lens cation homeostasis.

This study examined the effect of ethanol on the calcium homeostasis of the bovine lens. After acute exposure of the whole lens to physiologically related ethanol concentration, the calcium content of the lens cortex increased from 0.345 +/- 0.075 to 0.476 +/- 0.047 micromol/g (p < 0.05). In contrast, other cation levels such as sodium, potassium, and magnesium did not change. In the study of the lens calcium transport, ethanol caused an increase in the calcium permeability of the lens lipid membrane by about 12% at 30 mM ethanol. Ethanol did not alter the calcium pump activity at ethanol concentration up to 400 mM. Above 600 mM ethanol, the calcium pump was almost completely inhibited. It has been suggested that moderate to heavy alcohol consumption is a risk factor for cataracts. This study indicates that acute ethanol exposure can cause a loss in the lens calcium homeostasis, which maybe one of the cellular mechanisms to contribute to the cataract development in the alcoholic individual.

Animals↗

PubMed2005

[FGF23, a "new" hormone regulating phosphate homeostasis and vitamin D metabolism].

Until recently, the action of two hormones - parathyroid hormone (PTH) and calcitriol - on three target tissues - bone, kidney, and gut - has been thought to regulate the closely linked homeostasis of calcium and phosphates. In this system, an increase in the plasma concentration of one ion often leads to a reciprocal change in the concentration of the other and PTH stimulates 1 alpha-hydroxylase activity and calcitriol synthesis in renal proximal tubular cells. A second phosphate regulation system was recently identified. It involves one or more phosphaturic hormones, called "phosphatonins", that is, circulating factors with potent phosphaturic activity. The key phosphatonin appears to be a fibroblast growth factor, known as FGF23. It is now established that FGF23 regulates not only phosphate homeostasis, but also vitamin D metabolism. In contrast to PTH, however, FGF23 inhibits rather than stimulates 1 alpha-hydroxylase activity and calcitriol synthesis.

Fibroblast Growth Factor-23↗

PubMedDate not supplied

The toxicity of H2O2 on the ionic homeostasis of airway epithelial cells in vitro.

Oxygen species may be formed in the air spaces of the respiratory tract in response to environmental pollution such as particulate matter. The mechanisms and target molecules of these oxidants are still mainly unknown but may involve modifications of the ionic homeostasis in epithelial cells. Cytosolic concentrations of Ca2+ (Fura2) and Na+ (SBFI) and short-circuit current (Isc) were followed in primary cultures of human nasal epithelial cells and in the cell line 16HBE14o- after exposure to H2O2 or *OH (H2O2 + Fe2+). Cells were grown on glass coverslips for ionic imaging or on permeable snapwell inserts for Isc studies. Exposure of the apical as well as the basal side of the cultures to H2O2 or *OH induced a concentration-dependent transient increase in Isc which is due to a transient secretion of Cl-. Cai also increased transiently with approximately the same kinetics. The response was dependent on the release of calcium from intracellular stores. Nai on the contrary increased steadily over more than an hour. When the apical membrane was permeabilized with gramicidin, *OH inhibited the Na+ current (a measure of Na(+)-K(+)-ATPase activity in the baso-lateral membrane). The arrest of the pump was significant after 30 min exposure to oxidant. On the other hand no increase in the apical or baso-lateral sodium conductances could be detected. The progressive arrest of the Na+/K(+)-pump may contribute to the sustained elevation of Nai. This strong modification in the cellular ionic homeostasis may participate in the stress response of the respiratory epithelium through alterations in signal transduction pathways.

Calcium↗

PubMed1999

Controlling the sugar bowl. Regulation of glucose homeostasis in children.

In this article, the authors have attempted to provide a reasonable, working, and dynamic model incorporating a number of factors that are known to be involved in the regulation of glucose homeostasis in infants, children, and adults. Through the understanding of this model and its application, it is hoped that some of the authors' speculations regarding the pathophysiology of hyperglycemia and hypoglycemia might be challenged and either supported or rejected. In the meantime, the model can provide a framework for several of the facts and observations about the regulation of glucose homeostasis.

Blood Glucose↗

PubMed2001

Correlation between the glucose clamp technique and the homeostasis model assessment in hypertension.

The homeostasis model assessment (HOMA) has been extensively used as a reliable surrogate marker for measuring insulin resistance in patients with diabetes mellitus and in normal subjects. Comparative data in another insulin resistance state, hypertension, is lacking. The goal of the present study was to obtain that information by testing the correlation of HOMA with the euglycemic hyperinsulinemic clamp in 36 hypertensive and 27 normotensive subjects. Clamp-derived insulin sensitivity was calculated as the glucose disposal rate over steady-state plasma insulin concentration. Homeostasis model assessment was computed using the formula (fasting glucose x fasting insulin)/22.5. There was significant correlation between the clamp and HOMA for both the hypertensive (r = -0.64, P < .0001) and normotensive subjects (r = -0.58, P = .002). The HOMA can be used reliably as a less expensive and less cumbersome alternative for measuring insulin resistance in hypertension.

Adult↗

PubMed1994

Volume homeostasis in normal pregnancy and pre-eclampsia: physiology and clinical implications.

The pieces of the jigsaw puzzle of volume homeostasis in human pregnancy are being put together gradually. This chapter has focused on recent advances in our understanding of factors controlling extracellular fluid volume in normal pregnancy and their disturbance in women who develop pre-eclampsia. We have explored the clinical implications of these guidelines for management of patients with pre-eclampsia. Clearly there is still much to be learned. Studies of the cellular and subcellular handling of sodium are still in their infancy and will add much to our understanding of the physiology of volume homeostasis in normal pregnancy and its disturbance in pre-eclampsia and other causes of hypertension in pregnancy.

Adult↗

PubMed2000

Cardiovascular homeostasis during inhalational general anesthesia: a clinical comparison between sevoflurane and isoflurane. On behalf of the Italian Research Group on sevoflurane.

STUDY OBJECTIVE: To obtain more information on cardiovascular homeostasis and patient discharge from the recovery area after general anesthesia with either sevoflurane or isoflurane as the main anesthetic. DESIGN: Prospective, randomized, multicenter study. SETTING: Inpatient anesthesia at 13 University Departments of Anesthesia. PATIENTS: 247 ASA physical status I, II, and III patients, aged 18 to 85 years, receiving general anesthesia for elective urological, orthopedic, ENT, vascular, and low abdominal surgery. INTERVENTIONS: General anesthesia was maintained using a 60% nitrous oxide in oxygen mixture with either isoflurane (n = 125) or sevoflurane (n = 122) adjusted according to hemodynamic variables. MEASUREMENTS AND MAIN RESULTS: Occurrence of hypotension [systolic arterial blood pressure (SBP) decrease >30% from baseline], hypertension (SBP increase >30% from baseline), bradycardia [heart rate (HR) <50 bpm], or tachycardia (HR>100 bpm) provoked stepwise changes in the inspired concentration of the study drug. If this action proved to be ineffective after an adequate stabilization period, a specific treatment was given, and the need for pharmacological treatment was recorded as a hemodynamic side effect by an independent observer. No differences in duration of anesthesia were observed between sevoflurane (126 +/- 76 min) and isoflurane patients (139 +/- 60 min). Mean duration from anesthetic discontinuation to fulfillment of discharge criteria was shorter after sevoflurane (21 min; 25(th) to 75(th) percentiles: 27 to 13 min) than isoflurane (27 min; 25(th) to 75(th) percentiles: 17 to 35 min) (p < 0.0005). Hemodynamic side effects requiring therapy occurred in 18 sevoflurane patients (14.6%) and 26 isoflurane patients (20.8%) (p = NS). The risk for hemodynamic side effects increased with age (>50 vs. < or OFFyrs: odds ratio 2.5; 95% CI 1.2 to 5.4; p = 0.015) and ASA physical status (III vs. I and II: odds ratio 2.2; 95% CI 0.9 to 5.7; p = 0.048). When only patients over 50 years of age were considered (72 in the sevoflurane group and 79 in the isoflurane group), the incidence of hemodynamic side effects was higher with isoflurane (29.1%) than with sevoflurane (15.2%) (odds ratio 2.3; 95% CI 1.0 to 5.2; p = 0.04). CONCLUSIONS: Sevoflurane provided equally safe and effective control of cardiovascular homeostasis as isoflurane, with a more rapid discharge from the recovery area. Interestingly, patients over 50 years of age showed a lower risk for hemodynamic side effects when receiving sevoflurane than isoflurane.

Adolescent↗

PubMed2002

Apoptotic DNA fragmentation and tissue homeostasis.

DNA fragmentation is a hallmark of apoptosis. The tightly controlled activation of the apoptosis-specific endonucleases provides an effective means to ensure the removal of unwanted DNA and the timely completion of apoptosis. Over the past several years, crucial progress has been made in identifying the long-awaited apoptotic endonucleases, and their importance in tissue homeostasis is beginning to unfold. Here, we focus on the most recent discoveries about the functions and mechanisms of these endonucleases in the context of apoptosis. We also discuss consequences that defective DNA fragmentation might have for tissue homeostasis and disease development.

Animals↗

PubMed2002

Solution structure of CopC: a cupredoxin-like protein involved in copper homeostasis.

The structure of the metal-free form of CopC, a protein involved in copper homeostasis, has been obtained. The fold is a Greek key beta barrel similar to that of functionally unrelated blue copper proteins but with important structural variations. The protein binds one equivalent of copper (II) with relatively high affinity and contains a cluster of conserved residues (His1, Glu27, Asp89, and His91) which could form a water-accessible metal binding site. The structure also reveals a loop containing the M(X)(n)M motif which is present in a number of proteins also involved in copper homeostasis. The present structure represents a link between copper-trafficking proteins and cupredoxins. Within a structural and genomic analysis, the role of CopC in copper trafficking is discussed.

Amino Acid Sequence↗