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At least 595 records · Page 33Linked to original sources

PubMed1999

Sodium cyanate alters glutathione homeostasis in rodent brain: relationship to neurodegenerative diseases in protein-deficient malnourished populations in Africa.

Sodium cyanate, a neurotoxic chemical in rodents, primates and humans, is implicated in neurodegenerative disorders in protein-deficient populations subsisting in parts of Africa on the cyanogenic plant cassava. The molecular and cellular mechanisms of cyanate neurotoxicity are not understood. This study investigates the effect of sodium cyanate on glutathione (GSH) homeostasis in rodent brain and liver in vitro and in vivo. GSH levels in mouse brain were rapidly, time- and dose-dependently decreased following intraperitoneal administration of 100, 200 or 300 mg/kg sodium cyanate. By contrast, GSH disulfide (GSSG) levels were increased and GSH/GSSG ratios were decreased in a dose-dependent manner in rat brain. Sodium cyanate depleted GSH levels in all regions of mouse brain. Brain glutathione reductase activity was dose-dependently inhibited, while glutathione peroxidase activity was not affected by sodium cyanate. The disruption of GSH homeotasis, as evidenced by reduced tissue GSH/GSSG ratios, likely results from cyanate-induced inhibition of glutathione reductase activity. The results of this study suggest that cyanate neurotoxicity, and perhaps cassava-associated neurodegenerative diseases, are mediated in part by disruption of glutathione homeostasis in neural tissue.

Africa↗

PubMed1999

Alteration of iron homeostasis following chronic exposure to manganese in rats.

Recent studies suggest that manganese-induced neurodegenerative toxicity may be partly due to its action on aconitase, which participates in cellular iron regulation and mitochondrial energy production. This study was performed to investigate whether chronic manganese exposure in rats influenced the homeostasis of iron in blood and cerebrospinal fluid (CSF). Groups of 8-10 rats received intraperitoneal injections of MnCl2 at the dose of 6 mg Mn/kg/day or equal volume of saline for 30 days. Concentrations of manganese and iron in plasma and CSF were determined by atomic absorption spectrophotometry. Rats exposed to manganese showed a greatly elevated manganese concentration in both plasma and CSF. The magnitude of increase in CSF manganese (11-fold) was equivalent to that of plasma (10-fold). Chronic manganese exposure resulted in a 32% decrease in plasma iron (p<0.01) and no changes in plasma total iron binding capacity (TIBC). However, it increased CSF iron by 3-fold as compared to the controls (p<0.01). Northern blot analyses of whole brain homogenates revealed a 34% increase in the expression of glutamine synthetase (p<0.05) with unchanged metallothionein-I in manganese-intoxicated rats. When the cultured choroidal epithelial cells derived from rat choroid plexus were incubated with MnCl2 (100 microM) for four days, the expression of transferrin receptor mRNA appeared to exceed by 50% that of control (p<0.002). The results indicate that chronic manganese exposure alters iron homeostasis possibly by expediting unidirectional influx of iron from the systemic circulation to cerebral compartment. The action appears likely to be mediated by manganese-facilitated iron transport at brain barrier systems.

Animals↗

PubMed2003

Calcium-phosphorus-magnesium homeostasis in pregnant women after renal transplantation.

OBJECTIVE: The aim of the study was the assessment of calcium-phosphorus-magnesium homeostasis in pregnant women after renal transplantation. METHODS: The study covered 64 pregnant women in the third trimester of gestation including: 33 women after renal transplantation (the study group) and 31 healthy pregnant women (the control group). Women from both groups were at the similar age: 30.8+/-4.7 vs. 31.3+/-5.0 years (NS) and at the same gestational age 34.8+/-2.4 vs. 35.3+/-2.6 weeks (NS). The mean body mass index (BMI) in the women from the study group before pregnancy was 21.49+/-2.81 vs. 22.1+/-3.02 in the control group (NS), BMI before delivery was 25.43+/-3.05 vs. 26.0+/-3.35 (NS), the percentage of the BMI increase during pregnancy was 18.7+/-7.68 vs. 17.65+/-7.13 (NS) and BMI increase during gestation was 3.93+/-1.56 vs. 3.90+/-1.54, respectively (NS). Arterial blood pressure at the time of blood samples collection for biochemical tests was 151.4+/-26.8/92.5+/-16.9 in women from the study group comparing to 115.0+/-6.0/68.0+/-7.0 mmHg (P<0.001) in the patients from the control group. The maximal blood pressure during pregnancy was 169.2+/-20.7/102.7+/-14.0 vs. 118.0+/-7.0/70.0+/-8.0 mmHg (P<0.001), respectively. We estimated serum levels of: total Ca, ionized Ca(2+), inorganic phosphorus (P(i)), Mg, total protein, albumin and blood morphology. Moreover, urine levels of Ca, P(i), Mg and protein were assessed. RESULTS: The pregnant women after renal transplantation presented increases in serum concentrations of total Ca (2.54+/-0.20 vs. 2.16+/-0.10 mmol/l; P<0.001) and ionized Ca(2+) (1.322+/-0.104 vs. 1.12+/-0.07 mmol/l; P<0.001) and the decrease in P(i) level (1.013+/-0.211 vs. 1.10+/-0.16 mmol/l; P<0.05), total protein (59.3+/-7.0 vs. 65+/-5 g/l; P<0.001) and albumin (461.6+/-65.65 vs. 493.2+/-59 micromol/l; P<0.05). Moreover, in the study group drop in red blood cells count to 3.71+/-0.56 vs. 4.01+/-0.35 x 10(12)/l (P<0.02) in the control group was detected. Despite increased volume of 24-h urine collection in the kidney recipients we observed significantly decreased urine 24-h calcium excretion 2.47+/-0.92 vs. 6.72+/-3.49 mmol (P<0.001) and simultaneous increase in urine Mg excretion 3.422+/-1.025 vs. 2.18+/-0.52 mmol/24 h (P<0.001). There was no difference in urine 24-h P(i) excretion between the study and the control group. The pregnant renal transplant recipients presented proteinuria of 1.19+/-1.9 g/24 h. CONCLUSIONS: Women after kidney grafting present vital aberrations in calcium-phosphorus-magnesium homeostasis during pregnancy. The most significant changes are associated with calcium metabolism (high increase in serum Ca levels and impairment of renal elimination of calcium). The observed changes may be influenced by the doses of immunosuppressive agents and disturbed renal function.

Adult↗

PubMed1998

Second trimester calcium-phosphorus-magnesium homeostasis in women with threatened preterm delivery.

OBJECTIVE: The effect of threatened preterm delivery on calcium, phosphorus, magnesium homeostasis in the second trimester of pregnancy was investigated. METHODS: Serum concentrations of total and ionized calcium, inorganic phosphorus, magnesium, total protein, albumin, total estrogens and human placental lactogen were determined in women with threatened preterm delivery at 23-28 weeks of gestation (the studied group) and in women with uncomplicated pregnancy of the same duration (the control group). Additionally activities of total alkaline phosphatase and heat-stable alkaline phosphatase fraction were measured. RESULTS: Patients of the studied group compared to the control group showed decreased concentration of total calcium (2.15 +/- 0.073 vs. 2.25 +/- 0.11 mmol/l, P < 0.001), inorganic phosphorus (1.21 +/- 0.26 vs. 1.34 +/- 0.22 mmol/l, P < 0.01) and magnesium (0.63 +/- 0.053 vs. 0.71 +/- 0.12 mmol/l, P < 0.001), total protein (64.0 +/- 5.4 vs. 68.6 + 1.0 g/l, P < 0.001), albumin (546.3 +/- 55.1 vs. 579.6 +/- 49.3 micromol/l, P < 0.003) and placental lactogen (3664 +/- 1806 vs. 4651 +/- 1858 ng/ml, P < 0.02); they also demonstrated decreased activity of total alkaline phosphatase (42.17 +/- 16.99 vs. 50.66 +/- 6.56 IU/l, P < 0.001) and its heat stable fraction (22.65 +/- 7.89 vs. 31.89 +/- 9.09 IU/l, P < 0.001). Patients of the studied group showed normal values of ionized calcium and total estrogens. CONCLUSIONS: Premature uterine contractility in women in the second trimester is accompanied by lowered serum concentrations of total calcium, inorganic phosphorus, magnesium, total protein and albumin. There is also decreased activity of total alkaline phosphatase, its heat-stable fraction and placental lactogen which may have diagnostic value. Premature uterine contractility in women in the second trimester may be related to the disturbances of calcium-phosphorus-magnesium homeostasis and calcium supplementation should be considered.

Calcium↗

PubMed1976

Recent advances in calcium metabolism. I. Mechanisms of calcium homeostasis.

Within recent years newly acquired knowledge has provided a clearer understanding of some aspects of the complex mechanisms that collectively maintain calcium homeostasis within body fluids and it is our intent to define current concepts of the interrelationship of these various factors to the end that fuller understanding may be available concerning the maintenance of calcuim homeostasis in health as well as features which result in its disruption and the consequent effects of imbalances of calcium in various disease states. In this first section dealing with the physiologic state, there are included descriptions of: (1) the metabolism of vitamin D, the synthesis of its active metabolites, 25 OHD3 and1.25(OH)2D3, and the metabolic actions of the active vitamin D metabolite and analogues upon gastrointestinal, bone, and kidney functions; (2) the synthesis, secretion, and metabolic activity of parathyroid hormone and the difficulties with the radioimmunoassay of PTH related to the number of PTH-like peptides in the circulation; and (3) the chemistry, metabolism, and biologic activities of calcitonin, a hypocalcemic principle derived from the parafollicular cells of the thyroid gland. It is emphasized that under normal circumstances these humoral mechanisms act in an integrated manner to maintain serum concentrations of total and ionized calcium within narrowly defined limits.

Adolescent↗

PubMed1986

Role of atrial natriuretic peptide in sodium homeostasis in premature infants.

To examine the possible involvement of atrial natriuretic peptide (ANP) in sodium homeostasis in premature infants, two groups of low birth weight infants with different dietary sodium regimens were studied. Sodium balance and plasma concentration of ANP were measured at weekly intervals for 5 weeks. At 1 week of age the study was started by dividing infants into two groups, group 1 with low and group 2 with increased sodium intake. Mean plasma concentrations of ANP were 47.7 +/- 7.6 and 51.4 +/- 9.5 fmol/ml, respectively. A steady decrease in plasma ANP concentration to 18.8 +/- 2.9 fmol/ml was observed in infants with sodium intake 1.5 mmol/kg/d (group 1), which was related to the decrease in serum sodium concentration in this group. In contrast, supplementation with NaCl 4.6 mmol/kg/d (group 2) was associated with a 30% increase in plasma ANP concentration, significantly different (P less than 0.025) from that in infants not given supplement, and was also higher than the values in full-term neonates. Our data suggest that altered sodium homeostasis induces regulatory changes in plasma ANP levels. ANP may provide a sensitive and important hormonal system for the control of sodium balance, even in premature neonates.

Atrial Natriuretic Factor↗

PubMed2003

Functional role of alpha7 nicotinic receptor in physiological control of cutaneous homeostasis.

Non-neuronal nicotinic acetylcholine receptors (nAChRs) are abundantly expressed in skin and their function remains to be elucidated. Herein, we report that cutaneous alpha7 nAChR plays a role in the physiological control of cutaneous homeostasis. We studied in vitro effects of functional inactivation of alpha7 receptor on the expression of apoptosis regulators in keratinocytes (KC) lacking alpha7 nAChR, and extracellular matrix regulators in the skin of alpha7 knockout (KO) mice. Elimination of the alpha7 component of nicotinergic signaling in KC decreased relative amounts of the pro-apoptotic Bad and Bax at both the mRNA and the protein levels, suggesting that alpha7 nAChR is coupled to stimulation of keratinocyte apoptosis. The skin of alpha7 KO mice featured decreased amounts of the extracellular matrix proteins collagen 1alpha1 and elastin as well as the metalloproteinase-1. Taken together, these results suggest an important role for alpha7 nAChR in mediating plethoric effects of non-neuronal acetylcholine on cutaneous homeostasis.

Animals↗

PubMed1996

Influence of a diet regimen on glucose homeostasis and serum lipid levels of male elite athletes.

Physical training affects carbohydrate metabolism and results in an increased insulin-stimulated glucose disposal. To investigate if carbohydrate and lipid metabolism would be affected by nutritional factors in optimally trained elite athletes, during a 1-year period we studies elite ice-hockey players on two Swedish top-performance teams. Players on one team were subjected to extensive dietary monitoring and intervention, whereas players on the second team continued their ordinary diet. Blood levels of insulin, C-peptide, glucose, hemoglobin A1C (HbA1c), lipids, and lipoproteins were measured repeatedly. Basal insulin levels and insulin resistance (IR) were significantly lower among athletes on both teams compared with a sedentary group, and muscle weight and body mass index were significantly higher. During the course of the study in the intervention group, insulin levels decreased (3.6 +/- 0.3 v 6.2 +/- 0.6 [mean +/- SEM], P <.05) in conjunction with a decreased relative fat energy content, but returned toward baseline levels when relative fat energy content increased. IR decreased in parallel (0.59 +/- 0.05 v l.12 +/- 0.12, P <.05) and followed a similar pattern, reverting toward baseline levels. Also, levels of HbA1c changed during dietary manipulation. No changes in these parameters were observed among the elite players from the team not participating in the diet regimen. In contrast to the parameters for glucose homeostasis, no significant changes were found in serum lipid or lipoprotein levels in either team during the course of the study. The results verify the presence of an improved carbohydrate metabolism in elite athletes. The observed changes in glycemic control and glucose homeostasis as a consequence of dietary modification demonstrate further that nutritional factors may affect carbohydrate metabolism also in well-trained athletes.

Adult↗

PubMed1999

1,25(OH)2D3 only affects long-term levels of plasma Ca2+ but not the rapid minute-to-minute plasma Ca2+ homeostasis in the rat.

Results from our lab have shown previously that parathyroid hormone (PTH) is not the key factor in the rapid regulation of plasma Ca2+. The possible role of 1,25(OH)2D3 in the rapid minute-to-minute regulation of plasma Ca2+, as addressed by a possible rapid non-genomic action of 1,25(OH)2D3, was therefore studied in vivo in rats. The rapid calcemic recovery from induction of hypocalcemia by a brief EGTA infusion was examined in vitamin D-depleted rats with intact parathyroid glands and in vitamin D depleted rats 1 h after parathyroidectomy (PTX). The influence of different levels of plasma 1,25(OH)2D3 on the rapid calcemic recovery from hypocalcemia was examined in PTX rats treated with 1,25(OH)2D3 for two days at two different doses of 0.2 microg/day, 0.05 microg/day or vehicle, and in PTX rats being BNX for two days, as well. Additionally, the long-term effect of 1,25(OH)2D3 on plasma Ca2+ homeostasis was examined. Plasma Ca2+ recovered significantly (P<0.05) 10 min after discontinuing EGTA in vitamin D-depleted rats with or without parathyroid glands. Plasma Ca2+ increased significantly (P<0.05) and at the same rate after induction of hypocalcemia in PTX rats with different levels of plasma 1,25(OH)2D3. The final levels of plasma Ca2+ obtained were set by 1,25(OH)2D3 in a dose-related manner. 1,25(OH)2D3 did not affect the rapid calcemic recovery from EGTA induced hypocalcemia, but only had an effect on the long-term plasma Ca2+ homeostasis in the rat.

Animals↗

PubMed2004

Telomere length homeostasis is achieved via a switch between telomerase- extendible and -nonextendible states.

Telomerase counteracts telomere erosion that stems from incomplete chromosome end replication and nucleolytic processing. A precise understanding of telomere length homeostasis has been hampered by the lack of assays that delineate the nonuniform telomere extension events of single chromosome molecules. Here, we measure telomere elongation at nucleotide resolution in Saccharomyces cerevisiae. The number of nucleotides added to a telomere in a single cell cycle varies between a few to more than 100 nucleotides and is independent of telomere length. Telomerase does not act on every telomere in each cell cycle, however. Instead, it exhibits an increasing preference for telomeres as their lengths decline. Deletion of the telomeric proteins Rif1 or Rif2 gives rise to longer telomeres by increasing the frequency of elongation events. Thus, by taking a molecular snapshot of a single round of telomere replication, we demonstrate that telomere length homeostasis is achieved via a switch between telomerase-extendible and -nonextendible states.

Base Sequence↗

PubMed2000

Glucose homeostasis in the micropremie.

This article evaluates the current knowledge of the kinetics of glucose homeostasis in the micropremie. Glucose production, glucose use, and glucose oxidation are reviewed in detail. This article also evaluates the developmental regulation of glucose homeostasis relative to some of the fundamental differences known to exist in the neonate compared to the adult.

Glucose↗

PubMed1996

Prolonged exercise in pregnancy: glucose homeostasis, ventilatory and cardiovascular responses.

This study was designed to assess glucose homeostasis in pregnant women in their third trimester of gestation in response to exercise. Specifically, this study was designed to (1) compare the extend and rate at which blood glucose levels decrease in pregnant (22 to 33 weeks of gestation) versus that which occurs in nonpregnant women; and (2) determine the pattern of changes of the substrates (glucose, lactate, beta-hydroxybutyrate, and free fatty acids, and hormones (insulin), that contribute to the glucose homeostasis of pregnant (N = 10), and nonpregnant (N = 10) women in response to 1-hour prolonged moderate intensity exercise (at 55% of their VO2max). Each subject was tested for the determination of their maximal oxygen consumption (VO2max) and, based on their VO2max, they performed 60 minutes of prolonged moderate intensity exercise. Blood was collected before, during, and after the exercise bout. The results indicated that blood glucose levels of pregnant women decrease at a faster rate and to a significantly lower level post exercise (P < .05). Insulin levels of pregnant women also decreased to a significantly lower level post exercise, and lactate levels were maintained at a lower level 15 minutes after exercise. beta-hydroxybutyrate level was not different between the two groups, but demonstrated a different pattern of changes during exercise (P < .05). Furthermore, the results suggest that blood glucose levels of the late pregnant women decrease lower than those of nonpregnant women; also, there are differences in the rate and kinetics of blood glucose between pregnant and nonpregnant women. The results also indicate significant differences in the level of circulating substrates and hormones between pregnant and nonpregnant women in response to exercise.

3-Hydroxybutyric Acid↗

PubMed2002

Interleukin-15 and the regulation of lymphoid homeostasis.

Interleukin-15 (IL-15) is a cytokine that plays unique roles in both innate and adaptive immune cell homeostasis. While early studies suggested that IL-15 resembled IL-2, more recent work suggests that IL-15 may play multiple unique roles in immune homeostasis befitting its pleiotropic expression pattern. This review will focus on recent studies that highlight some of these functions.

Animals↗

PubMed1999

Angiotensin II and connective tissue: homeostasis and reciprocal regulation.

As a concept traditionally applied to integrative organ physiology, homeostasis likewise applies to self-regulated growth and structure of loose, dense and specialized connective tissues. De novo generation and co-induction of signals, either stimulatory or inhibitory to the formation of these tissues, provide for a reciprocal regulation of their composition; angiotensin (Ang) II is a growth stimulator. Components involved in AngII generation and its biological activity, including angiotensin converting enzyme (ACE) and AngII receptors, are expressed by mesenchymal cells responsible for connective tissue turnover. ACE inhibition or AT1 receptor antagonism attenuate the formation of these connective tissues. The concept of circulatory homeostasis, and the endocrine properties of plasma AngII involved in maintaining same, need each be broadened to encompass auto- and paracrine effects of AngII produced within connective tissues, where it contributes to their homeostatic regulation of structure and composition.

Angiotensin II↗

PubMed2000

Oxidative glutamate toxicity involves mitochondrial dysfunction and perturbation of intracellular Ca2+ homeostasis.

Glutamate toxicity on PC12 cells is mediated by oxidative stress as a consequence of the inhibition of a cystine uptake system with depletion of GSH. In this study we report that glutamate decreases PC12 cell viability, inhibiting the reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). This decrease was prevented by the antioxidants vitamin E, idebenone and L-deprenyl, which were also shown to be effective in reducing the accumulation of reactive oxygen species (ROS) in cells exposed to glutamate, decreasing the fluorescence of 2',7'-dichlorofluorescein (DCF). Incubation of PC12 cells with high glutamate concentrations induced mitochondrial dysfunction, leading to the loss of mitochondrial transmembrane potential, evaluated as a decrease in rhodamine 123 (Rh123) retention by mitochondria, and to the decrease of intracellular ATP levels. The mitochondrial dysfunction, induced by glutamate, can be involved in the observed increase of [Ca2+]i. The elevation of [Ca2+]i occurred after GSH depletion, suggesting that oxidative stress is involved in the disturbances of intracellular calcium homeostasis. In conclusion, our data indicate that glutamate, at concentrations which block cystine uptake in PC12 cells leading to GSH depletion and inducing oxidative stress, increases ROS accumulation and decreases cell survival by a mechanism involving mitochondrial dysfunction and impairment of Ca2+ homeostasis.

Animals↗

PubMed2003

Escherichia coli mechanisms of copper homeostasis in a changing environment.

Escherichia coli is equipped with multiple systems to ensure safe copper handling under varying environmental conditions. The Cu(I)-translocating P-type ATPase CopA, the central component in copper homeostasis, is responsible for removing excess Cu(I) from the cytoplasm. The multi-copper oxidase CueO and the multi-component copper transport system CusCFBA appear to safeguard the periplasmic space from copper-induced toxicity. Some strains of E. coli can survive in copper-rich environments that would normally overwhelm the chromosomally encoded copper homeostatic systems. Such strains possess additional plasmid-encoded genes that confer copper resistance. The pco determinant encodes genes that detoxify copper in the periplasm, although the mechanism is still unknown. Genes involved in copper homeostasis are regulated by MerR-like activators responsive to cytoplasmic Cu(I) or two-component systems sensing periplasmic Cu(I). Pathways of copper uptake and intracellular copper handling are still not identified in E. coli.

Copper↗

PubMed2002

New strategies to improve skin barrier homeostasis.

The uppermost thin layer, stratum corneum, plays a crucial role as a water impermeable barrier. After acute damage, it recovers automatically, but with aging or psychological stress, the recovery is delayed. Frequent damage, or damage under a dry environment, induces epidermal hyperplasia or inflammation. A specific protease inhibitor, histamine antagonist, and some magnesium salts have been demonstrated to accelerate the barrier recovery. These treatments also mitigated the epidermal hyperplasia induced by repeated barrier disruption or the damage under a dry condition. For the delay of the barrier repair induced by psychological stress, a glucocorticoid receptor antagonist or reduction of the stress by some specific odorant was significantly effective. Recently, the ion flux in the epidermis was found to be crucial for the barrier homeostasis. An external negative electric field accelerated the skin barrier recovery. These new methods to improve skin barrier homeostasis could be useful strategies to solve skin problems.

Administration, Topical↗

PubMed2000

Superantigen disruption of CD8+ T and B lymphocyte homeostasis.

Superantigens (SAgs) activate TH cells and induce their differentiation into cytokine-producing effector cells. Supranormal cytokine production is characteristic of SAg-induced polyclonal TH activation. Study of this interaction has focused upon TH cell function to the relative exclusion of other lymphocyte populations. SAgs also impact cells dependent upon TH cells for their differentiation and disrupt the normal homeostasis of the immune system. In this report, several changes in lymphocyte biology that result from SAg activation of TH cells are described. SCID mice, reconstituted with the SAg-expressing cells of DBA/2J mice, were employed as secondary recipients of SAg-reactive TH cells. Significant increases in serum IgM and IgG2a production were noted after the transfer of SAg-reactive It cells. Both B and CD8 T lymphocyte numbers increased with those of CD8 T cells surpassing levels found in normal mice. These results illustrate the ability of the TH-SAg interaction to disrupt B and CD8+ T lymphocyte homeostasis.

Animals↗