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At least 487 records · Page 27Linked to original sources
PubMed1992

Effects of altered calcium homeostasis on the expression of glutathione S-transferase isozymes in primary cultured rat hepatocytes.

The effects of altered Ca2+ homeostasis on glutathione S-transferase (GST) isozyme expression in cultured primary rat hepatocytes were examined. Isolated hepatocytes were cultured on Vitrogen substratum in serum-free modified Chee's essential medium and treated with Ca2+ ionophore A23187 at 120 hr post-plating. GST activity increased slightly, albeit significantly, in a concentration-dependent manner in A23187-treated hepatocytes relative to untreated controls. Western blot analysis using GST class alpha and mu specific antibodies showed an approximately 1.6- and 1.5-fold increase in the class alpha, Ya and Yc subunits, respectively, whereas no significant increase (approximately 1.2-fold) in class mu GST expression was observed following A23187 treatment. Northern blot analysis revealed an approximately 5-fold increase in GST class alpha and an approximately 7-fold increase in class mu GST mRNA levels in ionophore-treated hepatocytes compared to untreated cells. Results of the Western and Northern blot analyses of the ionophore-treated hepatocytes were compared with those obtained for tert-butyl hydroperoxide-treated cells. Immunoblot analysis showed a significant increase in the expression of GST class alpha, Ya and Yc subunits, approximately 1.8- and 1.7-fold, respectively, for tert-butyl hydroperoxide-treated hepatocytes as compared to controls, with little or no increase in class mu GSTs. Northern blot analysis showed approximately 3- and 2-fold increases, respectively, in class alpha and mu GST mRNA levels, following the tert-butyl hydroperoxide treatment. The results of the present investigation show that alterations in Ca2+ homeostasis produced by either Ca2+ ionophore A23187 or tert-butyl hydroperoxide treatment of hepatocytes enhanced the expression of GST isozymes in primary cultured rat hepatocytes.

Animals↗
PubMed1995

Ethanol and nerve growth factor effects on calcium homeostasis in cultured embryonic rat medial septal neurons before and during depolarization.

Ethanol and nerve growth factor (NGF) affect the survival of cholinergic neurons in the rat medial septum. To investigate whether calcium (Ca2+) homeostasis in these neurons is affected by ethanol or NGF treatment, changes in intracellular free Ca2+ concentration ([Ca2+]i) were studied in embryonic (E21) cultured medial septal neurons before stimulation (basal) and during stimulation with high potassium (K+). Changes in [Ca2+]i across time were measured in cultures of neurons treated without ethanol or with 100, 200, 400, or 800 mg% ethanol with NGF (+NGF) or without NGF (-NGF). Changes in [Ca2+]i were analyzed from fluorescence images, using indo-1. The effect of ethanol or NGF treatment was to reduce the rise in basal [Ca2+]i. The combination of ethanol and NGF treatment in +NGF neurons led to increases in basal [Ca2+]i with the greatest increase in basal [Ca2+]i occurring with 200 mg% ethanol. The effect of ethanol or NGF was to increase [Ca2+]i during stimulation with high K+. The greatest increases in [Ca2+]i occurred with 100 and 800 mg% ethanol. Together, ethanol and NGF treatment in +NGF-treated neurons led to significantly greater increases or decreases in K+ stimulated changes in [Ca2+]i compared to similarly treated -NGF neurons. We conclude that in medial septal neurons (before and during depolarization) changes in Ca2+ homeostasis occur in the presence of ethanol or NGF. The changes in [Ca2+]i following ethanol treatment are greater when NGF is present.

Animals↗
PubMed1983

Alterations in renal cortex cation homeostasis during mercuric chloride and gentamicin nephrotoxicity.

To help better understand the role of changes in cellular cation homeostasis in the pathogenesis of renal tubular cell injury, the alterations in cation content of renal cortex and isolated renal cortical mitochondria occurring during models of nephrotoxicity secondary to gentamicin and HgCl2 were determined both during a developing phase of injury prior to the appearance of cell necrosis and after advanced injury when cell necrosis was present. At 3 hr after 5 mg/kg HgCl2 or after 4 daily doses of 100 mg/kg gentamicin, tubular cell integrity was still intact but mitochondrial functional changes were present. There were no alterations of renal cortex tissue electrolytes at this stage in the HgCl2 model but tissue K+, and more prominently, tissue Mg2+ were decreased in the gentamicin model. K+ and Mg2+ contents of isolated mitochondria were slightly reduced after HgCl2. Only K+ content was slightly reduced after gentamicin. No evidence for tissue or mitochondrial Ca2+ overload was present in either model. At 12 hr after 5 mg/kg HgCl2 or after 10 daily 100 mg/kg doses of gentamicin, widespread areas of tubular cell necrosis were present and the function of isolated mitochondria was severely compromised. Tissue electrolytes at this stage of injury in both models were characterized predominantly by a twofold increase in Na+ content and five- to sixfold increases in Ca2+. Isolated mitochondria showed marked decreases in K+ content and marked increases in content of Na+ and Ca2+. These data suggest that neither cellular and mitochondrial Ca2+ overload nor substantial changes in cellular Na+ and K+ homeostasis can be implicated in the early stages of renal tubular cell injury produced by gentamicin and HgCl2.

Animals↗
PubMed1981

Thyroid homeostasis as studied by computer simulation.

Physico-chemical factors alone may account for much of the thyroid gland homeostasis and by inference for homeostasis of basal energy metabolism in mammals. Computer simulations indicate that changes of several of the important rate constants for thyroid function have little effect on circulating thyroid hormone concentrations. This was especially true of the rate constants for thyroid hormone release from the thyroid gland and to a lesser extent of the rate constants governing thyroid hormone metabolism and excretion. The rate at which thyroid hormone levels in blood respond to changes was rather slow indicating that transient changes in dietary iodine or in the rate constants governing thyroid function would have little effect. If changes taking place over several days, such as during the initiation of lactation, the parameters of thyroid function change at a corresponding rate.

Animals↗
PubMed1994

Effect of chronic IL-1 beta infusion on glucose homeostasis and pancreatic insulin secretion.

The present studies examined the effects of chronic interleukin-1 (IL-1 beta) infusion on glucose homeostasis and insulin secretion in male Sprague Dawley rats. IL-1 beta (4 micrograms per day) or saline was infused over a six day period using mini-osmotic pumps, surgically inserted under light ether anesthesia. Saline-infused rats were fed the amount of food consumed by their respective pair in the IL-1 beta group on the previous day. IL-1 beta infusion resulted in decreased food intake and significant body weight loss as well as increased liver and kidney weights. IL-1 beta infusion resulted in fasting hypoglycemia as well as elevated blood glucose levels in response to an oral glucose load compared to controls. Glucose-induced insulin secretion from the isolated perfused pancreas was significantly lower in IL-1 beta treated rats compared to controls. These data demonstrate that chronic IL-1 beta administration alters glucose homeostasis and impairs glucose-induced insulin secretion.

Animals↗
PubMed1996

Calcium homeostasis in aged neurones.

Mechanisms of cytoplasmic calcium homeostasis were investigated in peripheral and central neurones isolated from neonatal, adult and old Wistar rats and in granule neurones in acutely prepared cerebellar slices of adult and old CBA mice. The cytoplasmic calcium concentration ([Ca2+]i) was measured by either indo-1-or fura-2-based microfluorimetry. The resting [Ca2+]i was significantly higher in senile neurones. The depolarization-induced [Ca2+]i transients were markedly altered in old neurones when compared with adult ones: the age-associated changes in stimulus-evoked [Ca2+]i signalling comprised of (i) significant decrease of the amplitudes of [Ca2+]i transients; (ii) prolongation of the rising phase and (iii) prominent deceleration of the recovery of the [Ca2+]i elevation towards the resting level after the end of depolarization. The amplitudes of calcium release from caffeine/Ca(2+)-sensitive endoplasmic reticulum calcium stores became significantly smaller in old central neurones, whereas they remained unaffected in peripheral neurones. Based on our observations we can conclude that ageing of the nervous system is associated with significant changes in mechanisms of [Ca2+]i homeostasis in individual neurones. These changes lead to a stable increase in the resting [Ca2+]i and to a substantial prolongation of stimulus-evoked [Ca2+]i signals. We could suggest also that the ability of the old neurones to handle Ca2+ loads is diminished, which may determine higher vulnerability of aged neurones to excess of calcium ions.

Aging↗
PubMed1987

Glucose homeostasis in magnesium-deficient rats.

Glucose homeostasis was studied in rats fed diets containing 750,200, or 100 mg/kg Mg for 6 to 8 weeks, from the age of 4 weeks. Weight gain of the rats receiving 200 and 100 mg/kg diets was decreased. This resulted from both a lower food intake and reduced effectiveness of the ingested food. Fed or fasting plasma glucose levels were similar in the three groups. During an intravenous glucose tolerance test, the rate of glucose disappearance was higher in Mg 100 rats than in controls. By contrast, during an oral glucose tolerance test, the rise in plasma glucose was greater and more sustained in Mg 100 rats. During both tests, the insulin response was markedly lower in Mg-deficient rats than in controls. This could be partially due to the reduced insulin content of the pancreas of these animals. The impairment of tolerance to oral glucose was corrected by 5 weeks on a high-Mg diet. After intravenous injection of insulin, the fall in plasma glucose levels was also slightly more pronounced in Mg 100 rats. During no test did we observe a significant difference between glucose or insulin responses in Mg 200 or Mg 750 rats. These results, thus, show that chronic Mg deficiency alters several parameters of glucose homeostasis in the rat.

Animals↗
PubMed1993

Restoration of nitrogen homeostasis in a man with ornithine transcarbamylase deficiency.

We evaluated the hypothesis that sodium phenylbutyrate-induced phenylacetylglutamine biosynthesis in a man with partial ornithine transcarbamylase (OTC) deficiency has a dual effect; it provides an additional vehicle for waste nitrogen excretion, and in the process it suppresses the patient's residual urea N synthesis, which then may be available for N homeostasis if the need arises. A 38-year-old man was studied over three periods. Period I was a control period during which he received a fixed caloric and N intake plus L-citrulline. Phenylbutyrate was added in period II and was maintained during period III, during which his N intake was increased. Plasma levels of ammonium and glutamine and net urea N synthesis were measured in each period; phenylacetylglutamine N synthesis was measured in periods II and III. These studies demonstrated that phenylbutyrate administration led to a 73% decrease in net de novo urea N synthesis during period II, which subsequently increased threefold in period III in response to the increased N intake. Phenylacetylglutamine N synthesis was 2.27 g/d, similar to his estimated maximum net urea N synthesis of 2.65 g/d. During periods II and III, his plasma levels of ammonium and glutamine improved as compared with period I when they were abnormally high. We conclude that sodium phenylbutyrate treatment of patients with urea cycle disorders who have significant residual enzyme activity results in both an improvement in waste N excretion and improved N homeostasis as a result of the generation of a reserve urea N synthetic capacity. This therapeutic approach may be useful in other nitrogen accumulation decreases, eg, portal-systemic encephalopathy.

Adult↗
PubMed1988

bis-(beta-chloroethyl)sulfide (BCES)-induced changes in epidermal cell homeostasis in vitro.

A rat cutaneous keratinocyte culture system was developed to study the effects of the vesicant bis-(beta-chloroethyl)sulfide (BCES) on the homeostasis of cell proliferation and differentiation. Lectins were used to reveal cell surface carbohydrate changes as the keratinocytes differentiate. In the newborn rat epidermis, the isolectin, Griffonia simplicifolia I-B4 (GS I-B4), binds to basal cell surfaces. Ulex europeus agglutinin I (UEA) binds to the surfaces of spinous and lower granular cells and is therefore considered an indicator of keratinocyte differentiation. A fluorometric assay was developed which determines the ratio of bound UEA to bound GS I-B4 (the UEA/B4 ratio) in primary monolayer cultures of rat cutaneous keratinocytes maintained in low Ca2+ medium. The UEA/B4 ratio was found to be a representation of the relative sizes of the differentiating and proliferating cell compartments in the monolayer cultures, respectively (W.W. Ku and I.A. Bernstein, 1988, Exp. Cell Res., 175, 298-316). Monolayer cultures exposed for 1 hr to BCES at Day 1 exhibited a dose-related increase in the UEA/B4 ratio at Day 7 when compared to solvent controls. The results from the analysis of lectin binding sites showed a decrease in GS I-B4 binding with little or no change in UEA binding as a result of BCES exposure, contributing to the increase in the UEA/B4 ratio. BCES-exposed monolayers also showed early perturbations in replicative DNA synthesis as revealed by autoradiography. Subsequent to the perturbations in replicative DNA synthesis was an inability of BCES-exposed cultures to produce cells into the monolayer through mitosis. In addition to an increase in the UEA/B4 ratio, BCES-exposed monolayers also showed a dose-related loss of DNA, with the appearance of enlarged cells at Day 7. These enlarged cells failed to show evidence of DNA synthesis, with groups of these cells showing intense UEA staining with only faint GS I-B4 staining. Overall, exposure to low concentrations of BCES appeared to disrupt the normal homeostasis of cell proliferation and differentiation in this monolayer culture system. This disruption was primarily through a reduction in the fraction of germinative (basal) cells with concomitant retention of some early differentiated cells, presumably early spinous or spinous cells.

Alkylating Agents↗
PubMed1988

Altered calcium homeostasis in the pathogenesis of myocardial ischemic and hypoxic injury.

Pathological calcification, observed in infarcted myocardium under certain conditions, is the most severe manifestation of abnormal calcium (Ca2+) homeostasis induced by ischemia and related forms of myocardial injury. Specialized techniques for measurement of intracellular electrolytes, i.e., electron probe X-ray microanalysis, and intracellular free Ca2+, i.e. carboxylate indicators including fura-2, are providing new insights into regulation of intracellular Ca2+ and the role of altered Ca2+ homeostasis in the pathogenesis of myocardial cell injury. Several lines of investigation indicate that increased intracellular Ca2+ develops in association with other electrolyte alterations, altered cell volume regulation, and altered membrane phospholipid composition during the progression of myocardial cell injury.

Arrhythmias, Cardiac↗
PubMed1996

Mechanism of zinc homeostasis.

Homeostatic equilibrium of a nutrient is characteristic of a healthy body. For zinc, phytate has been shown to alter that equilibrium in several monogastric species including man. The pancreas is an important organ in the maintenance of zinc homeostasis. Elevated calcium has been shown to be a synergistic agent in affecting the rate of onset and rate of homeostatic change. In the studies described, rats were depleted of zinc to differing extents, zinc was injected intraperitoneally to label the endogenous zinc pool. Phytate- and nonphytate-containing protein diets were fed and feces were collected. Feces were counted for radioactivity. The ratios of radioactivity (phytate:nonphytate) indicated that the major effect of phytate was on the endogenous secreted pool. Evidence is included to indicate that two, pancreatic labile pools of zinc are secreted, one is stable complexes not affected by phytate and two, a labile pool of zinc readily available for complexation. A mathematical model is included that fits all nutritional models for zinc homeostasis.

Absorption↗
PubMed1993

beta-Amyloid precursor protein metabolites and loss of neuronal Ca2+ homeostasis in Alzheimer's disease.

Recent findings link altered processing of beta-amyloid precursor protein (beta APP) to disruption of neuronal Ca2+ homeostasis and an excitotoxic mechanism of cell death in Alzheimer's disease. A major pathway of beta APP metabolism results in the release of secreted forms of beta APP, APPss. These secreted forms are released in response to electrical activity and can modulate neuronal responses to glutamate, suggesting roles in developmental and synaptic plasticity. beta APP is upregulated in response to neural injury and APPss can protect neurons against excitotoxic or ischemic insults by stabilizing the intracellular Ca2+ concentration [Ca2+]i. An alternative beta APP processing pathway liberates intact beta-amyloid peptide, which can form aggregates that disrupt Ca2+ homeostasis and render neurons vulnerable to metabolic or excitotoxic insults. Genetic abnormalities (e.g. certain beta APP mutations or Down syndrome) and age-related changes in brain metabolism (e.g. reduced energy availability or increased oxidative stress) may favor accumulation of [Ca2+]i-destabilizing beta-amyloid peptide and diminish the release of [Ca2+]i-stabilizing, neuroprotective APPss.

Alzheimer Disease↗
PubMed1993

Neuropeptide Y: a central regulator of energy homeostasis.

Neuropeptide Y (NPY) is a 36 amino acid peptide belonging to the pancreatic polypeptide family of neuroendocrine hormones. It is the most abundant peptide yet discovered in the mammalian brain and is widely expressed by neurons in the central and peripheral nervous systems as well as adrenal medullary cells. Recently, a large number of studies have focussed on the potential roles played by NPY within the hypothalamus and pituitary with respect to the control of food intake and energy homeostasis. It is now clear that NPY is a potent stimulator of food intake in models of hyperphagia, that hypothalamic NPY also regulates sympathetic neural activity and it appears that NPY may also influence the glucocorticoid, growth hormone and thyroid hormone axes. Taken together, current data suggest that hypothalamic and pituitary NPY-expressing cells represent an important and critical site of integration of peripheral hormonal signals with regulation of energy homeostasis.

Amino Acid Sequence↗
PubMed1988

L-type lipase activity in ovaries of superovulated rats. Relation to cholesterol homeostasis.

The impact of lowering the ovarian L(iver)-type lipase activity on cholesterol homeostasis in the ovaries was studied in superovulated rats. L-type lipase activity increased rapidly after injection with chorionic gonadotrophin (HCG) (day 0), its activity remained high between days 3 and 8. During this period plasma progesterone and 20 alpha-hydroxyprogesterone were raised. The ovarian content of unesterified cholesterol remained constant during this period while cholesterol esters increased. Lowering of the L-type lipase activity by in vivo treatment with anti-liver lipase (ALLA) during 4-5 h did not affect plasma hormones or ovarian cholesterol contents. However, de novo cholesterol synthesis in the ovaries was significantly increased by about 40%. After pretreatment of the rats with aminogluthetimide, ALLA administration led to a 250% increase in de novo cholesterol synthesis in the unesterified cholesterol fraction, but was without effect on plasma hormones and on the ovarian cholesterol content. Administration of the cholesterol synthesis inhibitor Simvastatin led to a 25% lowering in ovarian cholesterol synthesis without effect on plasma hormones or ovarian cholesterol content. Additional administration of ALLA affected only the plasma progesterone (-30%). These results indicate that L-type lipase is involved in ovarian cholesterol homeostasis.

Aminoglutethimide↗
PubMed1991

Effect of exogenous carnitine on carnitine homeostasis in the rat.

The interaction of exogenous carnitine with whole body carnitine homeostasis was characterized in the rat. Carnitine was administered in pharmacologic doses (0-33.3 mumols/100 g body weight) by bolus, intravenous injection, and plasma, urine, liver, skeletal muscle and heart content of carnitine and acylcarnitines quantitated over a 48 h period. Pre-injection urinary carnitine excretion was circadian as excretion rates were increased 2-fold during the lights-off cycle as compared with the lights-on cycle. Following carnitine administration, there was an increase in urinary total carnitine excretion which accounted for approx. 60% of the administered carnitine at doses above 8.3 mumols/100 g body weight. Urinary acylcarnitine excretion was increased following carnitine administration in a dose-dependent fashion. During the 24 h following administration of 16.7 mumols [14C]carnitine/100 g body weight, urinary carnitine specific activity averaged only 72 +/- 4% of the injection solution specific activity. This dilution of the [14C]carnitine specific activity suggests that endogenous carnitine contributed to the increased net urinary carnitine excretion following carnitine administration. 5 min after administration of 16.7 mumol carnitine/100 g body weight approx. 80% of the injected carnitine was in the extracellular fluid compartment and 5% in the liver. Plasma, liver and soleus total carnitine contents were increased 6 h after administration of 16.7 mumols carnitine/100 g body weight. 6 h post-administration, 37% of the dose was recovered in the urine, 12% remained in the extracellular compartment, 9% was in the liver and 22% was distributed in the skeletal muscle. In liver and plasma, short chain acylcarnitine content was increased 5 min and 6 h post injection as compared with controls. Plasma, liver, skeletal muscle and heart carnitine contents were not different from control levels 48 h after carnitine administration. The results demonstrate that single, bolus administration of carnitine is effective in increasing urinary acylcarnitine elimination. While liver carnitine content is doubled for at least 6 h following carnitine administration, skeletal muscle and heart carnitine pools are only modestly perturbed following a single intravenous carnitine dose. The dilution of [14C]carnitine specific activity in the urine of treated animals suggests that tissue-blood carnitine or acylcarnitine exchange systems contribute to overall carnitine homeostasis following carnitine administration.

Acylation↗
PubMed1989

The supraoptic nucleus: afferents from areas involved in control of body fluid homeostasis.

Physiological evidence indicates that the supraoptic nucleus may be an important integrating region for information relating to body fluid homeostasis. It is known that the supraoptic nucleus receives neural influences from brain receptive zones for plasma osmolality and angiotensin II, as well as from relay centers for blood pressure and blood volume. It is also known that these influences interact to modulate vasopressin release from the supraoptic nucleus. Therefore, a detailed investigation of the neurochemical afferents to the supraoptic nucleus from regions of the lamina terminalis and the brainstem was undertaken. Injection of a fluorescent retrograde tracer, doxorubicin, into the supraoptic nucleus was combined with histochemistry of angiotensin II and catecholamines. Following supraoptic nucleus injection, retrograde label was found in forebrain neurons of the subfornical organ, median preoptic nucleus, and organum vasculosum of the lamina terminals. Some labeled cells in the subfornical organ and organum vasculosum of the lamina terminalis were also found to contain angiotensin II immunoreactivity. In the brainstem, retrograde label was found in neurons of the A1, A2 and A6 cell groups. Many of these cells were also found to contain catecholamine fluorescence or tyrosine hydroxylase immunoreactivity. Corroboration of the A2 projection was obtained by lesions of this nucleus, which reduced catecholamine fluorescence in the supraoptic nucleus. These findings provide an anatomical basis for the functional observations that the supraoptic nucleus plays a key integrative role in the maintenance of body fluid homeostasis.

Angiotensin II↗
PubMed1991

Unattainable homeostasis in healing leads to interstitial and vascular intimal fibroses: a unified hypothesis of their pathogenesis.

Homeostasis, or the maintenance of constant internal environment in the organism, is disrupted by injury. In this case, pathological defence reactions such as inflammation and healing take place in order to restore it. They succeed if etiological harmful factors are eliminated. In the opposite case, constant injury leads to continuous healing and fibrosis. Both interstitial and vascular intimal fibroses have similar pathogeneses and may be provoked by the same etiological factors. It may be concluded, therefore, that in spite of their apparent differences, both fibroses are only the different expressions of the same process by which injury should be healed and homeostasis restored. Fibrosis itself may become dangerous for the patient, depending on its extent and on the affected organ. In this case, the inhibition of healing reaction by antiangiogenesis may be envisaged as a life-saving measure.

Animals↗