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Biomedical subjects

M C Ruiz

Publications and source records attributed to M C Ruiz.

At least 19 recordsLinked to original sources
PubMed2006

Effect of statin treatment on oxidative stress and renal function in renal transplantation.

The beneficial action of statins on the lipid profile, cardiovascular disease, and death is well known. Besides their lipid-lowering role, these drugs have pleiotropic action that derive from their prevention of the synthesis of isoprenoids, mediators in cell signaling. Thus, due to their antioxidant capacity, statins can decrease the production of reactive oxygen species by inhibiting NAD(P)H oxidase activity. Previous studies by our group have described increased oxidative stress status in renal transplantation that might benefit from HMG CoA reductase inhibitor therapy. The aim of this study was to assess the influence of statins on stress parameters and their relevance to renal function in kidney transplantation. In 58 transplanted patients a first blood sample was obtained, without statins followed by 21 patients treated with statins (group 1) and 37 patients without drug (group 0) for a 6-month study period. We collected clinical data as well biochemical results on lipid profile, creatinine and oxidative stress. Lipid profile reduction was significant among group 1 compared with group 0. An increased glutathione peroxidase (GPx) among observed in all patients was greater in the statin-treated group (P = .006). No differences in creatinine or Cockroft-Gault values were observed between before versus after drug administration. In conclusion, statin treatment in renal transplantation improves the lipid profile and may increase GPx-measured antioxidant capacity but appears to have no short-term effect on renal function.

Humans↗
PubMed2005

Modulation factors of oxidative status in stable renal transplantation.

Reactive oxygen species (ROS) trigger a biomolecular alteration that causes functional and structural changes. In renal transplantation, there is an increase in oxidative phenomena related to endothelial dysfunction, inflammation, and atherosclerosis, the main cause of cardiovascular complications and chronic allograft failure. The present study was designed to assess the oxidative state of transplant patients with stable renal function, in order to establish differences in oxidative, biochemical, and clinical parameters between patients treated with tacrolimus versus cyclosporine. We studied 67 stable kidney transplant patients treated with calcineurin inhibitors who were not receiving cholesterol-lowering therapy, and 14 healthy subjects. Data were collected on biochemical parameters: lipid profile (apoA, apoB, total cholesterol and fractions, and triglycerides); urea; and creatinine; oxidative parameters: malondialdehyde (MDA) as a lipid peroxidation marker, glutathione peroxidase (GPx), catalase, superoxide dismutase (SOD), glutathione reductase (GR), and antibodies against oxidized LDL; and clinical variables. Transplanted patients showed a higher oxidative status (MDA increase and GPx decrease) than healthy subjects. The oxidative status did not differ between the cyclosporine and tacrolimus cohorts. Some factors during the posttransplant period, such as delayed graft function, cytomegalovirus infection, and microalbuminuria, which may damage renal function, produce a decreased antioxidant capacity (lower GPx).

Cholesterol↗
PubMed2005

Relationship between oxidative stress parameters and atherosclerotic signs in the carotid artery of stable renal transplant patients.

Reactive oxygen species (ROS) may participate in atheroma plaque formation, which may be noninvasively diagnosed by Doppler ultrasound of carotid artery. We sought to determine the relationship between the presence of carotid artery lesions and oxidative parameters to identify factors that may influence these lesions in renal transplant patients. Fifty renal transplanted patients with stable renal function and without diabetes mellitus were studied for more than 1 year posttransplantation. Echo Doppler examination of the carotid artery was performed to assess the intimal media thickness (IMT), atheroma plaques, calcification, and stenosis. Data were collected on oxidative parameters: malondialdehyde (MDA), glutathione peroxidase (GPx), catalase, superoxide dismutase (SOD), glutathione reductase (GR), and lipid profile. The serum GPx level among patients without atheroma plaques, calcification, or stenosis was higher than in those with ultrasound signs. The LDL cholesterol fraction was lower in patients with no ultrasound signs of atherosclerotic lesions; total cholesterol values showed the same behavior. In conclusion, transplanted patients with atheromatous plaques, calcification, and carotid stenosis have a greater degree of hypercholesterolemia and lower antioxidant activity (lower GPx). Recipient age was the principal risk factor for the presence of increased IMT, atheroma plaque, calcification, and/or stenosis of carotid artery in renal transplant patients.

Adult↗
PubMed2004

Environmental behavior of cement-based stabilized foundry sludge products incorporating additives.

A series of experiments were conducted to stabilize the inorganic and organic pollutants in a foundry sludge from a cast iron activity using Portland cement as binder and three different types of additives, organophilic bentonite, lime and coal fly ash. Ecotoxicological and chemical behavior of stabilized mixes of foundry sludge were analyzed to assess the feasibility to immobilize both types of contaminants, all determined on the basis of compliance leaching tests. The incorporation of lime reduces the ecotoxicity of stabilized mixes and enhances stabilization of organic pollutants obtaining better results when a 50% of cement is replaced by lime. However, the alkalinity of lime increases slightly the leached zinc up to concentrations above the limit set under neutral conditions by the European regulations. The addition of organophilic bentonite and coal fly ash can immobilize the phenolic compounds but are inefficient to reduce the ecotoxicity and mobility of zinc of final products.

Calcium Compounds↗
PubMed2003

Environmental assessment of cement/foundry sludge products.

This work deals with the environmental assessment of products based on cement and a waste from a cast iron activity. The waste is a foundry sludge from wastewater treatment previously characterized. This industrial waste shows a high water content (62.4%) and a hazardous behavior due to its metallic content mainly Zn (16.5%), together with a low fraction of organic pollutants, mainly phenolic compounds. The feasibility of immobilizing both typs of contaminants was studied using Portland cement as binder at different cement/waste ratios. The parameters of environmental control were the ecotoxicity and mobilization of zinc and phenolic compounds, all determined on the basis of compliance leaching tests. The acid neutralization capacity of the cement/waste products was measured in order to obtain information on their buffering capacity. Experimental results from chemical analysis of leachates led to a non ecotoxic character of cement/waste products Although the metallic ions were mobilized within the cement mattices, the organic matter did not allow the formation of monolithic forms and an efficient immobilization of phenolic compounds. Concerning the acid neutralization capacity, this parameter was shown to depend mainly on the quantity of cement, although a decrease in alkalinity was observed when the amount of water in the cement/waste products increased.

Construction Materials↗
PubMed2001

Simultaneous measurement and imaging of intracellular Ca(2+) and H(+) transport in isolated rabbit gastric glands.

1. Activation of H(+) secretion in the intracellular canaliculi of parietal cells occurs on an unknown time scale with ill-defined kinetics for the coupling of H(+) secretion and the elevation of intracellular calcium ([Ca(2+)](i)) stimulated by secretagogues. 2. We developed a method to determine H(+) secretion in isolated rabbit gastric glands with spatio-temporal resolution, using the fluorescent indicator Lysosensor Yellow-Blue (LYB). Glands accumulated the dye exclusively in the intracellular canaliculi of parietal cells and the gland lumen. Dye fluorescence in the acid spaces of the glands increased upon stimulation of acid secretion by carbachol, histamine and forskolin. Simultaneous fluorescence measurements of acid secretion and [Ca(2+)](i) at 1 s resolution were made by joint loading of LYB and Fluo-3. 3. Carbachol-stimulated H(+) secretion was detected in the gland lumen as early as 3 s after the onset of the [Ca(2+)](i) spike. H(+) accumulation appeared to be transient and paralleled the release component of the [Ca(2+)](i) spike. Short and repetitive stimulations with carbachol elicited repetitive responses in [Ca(2+)](i) and H(+) secretion. 4. Histamine or forskolin stimulated H(+) secretion with a delayed onset (around 2 min) and a sustained response. Acid secretion was temporally unrelated to the oscillatory Ca(2+) responses. 5. The striking difference in the kinetics of activation of H(+) secretion by cholinergic and cAMP-dependent secretagogues indicates that two distinct mechanisms are operating in the final stimulation of the pump, in spite of both eliciting a [Ca(2+)](i) response.

Animals↗
PubMed2001

Environmental assessment of lubricants before and after wire drawing process.

Iron wire drawing processes involve the use of solid lubricants made of powdered raw materials, which lead to industrial wastes after being used. These wastes, based on stearates, have a negative effect on the environment. This study deals with the environmental assessment of some lubricants before and after the wire drawing process in a Spanish factory. The parameters evaluated for this study have been total organic carbon (TOC), mobility of zinc and lead, and ecotoxicity (EC(50)). Results show that wastes have more ecotoxicity than the original lubricants due to the content of metals that lubricants pick up from the wire, as pickling, patenting and galvanising take part in the manufacture. The capture of metallic particles leads to a reduction of TOC and an increase in ecotoxicity.

Biological Assay↗
PubMed2001

Correlation of fatty acid unsaturation of the major liver mitochondrial phospholipid classes in mammals to their maximum life span potential.

Free radical damage is considered a determinant factor in the rate of aging. Unsaturated fatty acids are the tissue macromolecules that are most sensitive to oxidative damage. Therefore, the presence of low proportions of fatty acid unsaturation is expected in the tissues of long-lived animals. Accordingly, the fatty acid compositions of the major liver mitochondrial phospholipid classes from eight mammals, ranging in maximum life span potential (MLSP) from 3.5 to 46 yr, show that the total number of double bonds is inversely correlated with MLSP in both phosphatidylcholine (PtdCho) and phosphatidylethanolamine (PtdEtn) (r = 0.757, P < 0.03, and r = 0.862, P < 0.006, respectively), but not in cardiolipin (P = 0.323). This is due not to a low content of unsaturated fatty acids in long-lived animals, but mainly to a redistribution between kinds of fatty acids on PtdCho and PtdEtn, shifting from arachidonic (r = 0.911, P < 0.002, and r = 0.681, P = 0.05, respectively), docosahexaenoic (r = 0.931 and r = 0.965, P < 0.0001, respectively) and palmitic (r = 0.944 and r = 0.974, P < 0.0001, respectively) acids to linoleic acid (r = 0.942, P < 0.0001, for PtdCho; and r = 0.957, P < 0.0001, for PtdEtn). For cardiolipin, only arachidonic acid showed a significantly inverse correlation with MLSP (r = 0.904, P < 0.002). This pattern strongly suggests the presence of a species-specific desaturation pathway and deacylation-reacylation cycle in determining the mitochondrial membrane composition, maintaining a low degree of fatty acid unsaturation in long-lived animals.

Animals↗
PubMed2000

Relationship between toxicokinetics of carbaryl and effect on acetylcholinesterase activity in Pomacea patula snail.

The 96-h LC(50) value of carbaryl was 14.6 microg/mL for the snail Pomacea patula. Organisms were exposed for 72 h to a low sublethal concentration (0.1 of LC(50)) using a semistatic contamination system; bioconcentration and elimination experiments were performed evaluating simultaneously acetylcholinesterase (ACHase) activity. The inhibition of the digestive gland ACHase reached 76% when the carbaryl concentration in tissue was 3.2 microg/g. The increased enzyme inhibition was observed concomitantly with the bioconcentration of carbaryl until 7 h. ACHase inhibition was linearly dependent on the uptake and bioconcentration of carbaryl (r(2)=0.87). The transfer of snails to carbaryl-free water after 72 h of exposure was followed by rapid monophasic elimination with a half-life of 1.0 h. However, ACHase activity levels never returned to control values. These results revealed that the bioconcentration might play a critical role in contributing to the toxicity of carbaryl.

Animals↗
PubMed2000

Role of Ca2+in the replication and pathogenesis of rotavirus and other viral infections.

Ca2+ plays a key role in many pathological processes, including viral infections. Rotavirus, the major etiological agent of viral gastroenteritis in children and young animals, provides a useful model to study a number of Ca2+ dependent virus-cell interactions. Rotavirus entry, activation of transcription, morphogenesis, cell lysis, particle release, and the distant action of viral proteins are Ca2+ dependent processes. In the extracellular medium, Ca2+ stabilizes the structure of the viral capsid. During entry into the cell the low cytoplasmic Ca2+ concentration induced the solubilization of the outer protein layer of the capsid and transcriptase activation. Viral protein synthesis modifies Ca2+ homeostasis which, in turn, favours viral morphogenesis and induces cell death. The generation of diarrhea is a multifactorial process involving Ca2+ dependent secretory processes of mediators and water and electrolytes, as well as the induction of cell death in the different cell types that compose the intestinal epithelium. The discovery of the non-structural viral protein NSP4 as a viral enterotoxin and the possible participation of the enteric nervous system in the pathogenesis of diarrhea represent significant advances in its understanding. Ca2+ also plays a role in the replication cycles and pathogenesis of other viral diseases such as poliovirus, Coxsackie virus, cytomegalovirus, vaccinia and measles virus and HIV.

Animals↗
PubMed1999

Characterization of a membrane calcium pathway induced by rotavirus infection in cultured cells.

Some viruses induce changes in membrane permeability during infection. We have shown previously that the porcine strain of rotavirus, OSU, induced an increase in the permeability to Na+, K+, and Ca2+ during replication in MA104 cells. In this work, we have characterized the divalent cation entry pathway by measuring intracellular Ca2+ in fura-2-loaded MA104 and HT29 cells in suspension. The permeability to Ca2+ and other cations was evaluated by the change of the intracellular concentration following an extracellular cation pulse. Rotavirus infection induced an increase in permeability to Ca2+, Ba2+, Sr2+, Mn2+, and Co2+. The rate of cation entry decreased over time as the intracellular concentration increased during the first 20 s. This indicates that regulatory mechanisms, including channel inactivation, are triggered. La3+ did not enter the cell and blocked the entry of the divalent cations in a dose-dependent manner. Metoxyverapamil (D600), a blocker of L-type voltage-gated channels, partially inhibited the entry of Ca2+ in virus-infected MA104 and HT29 cells. The results suggest that rotavirus infection of cultured cells activates a cation channel rather than nonspecific permeation through the plasma membrane. This activation involves the synthesis of viral proteins through mechanisms yet unknown. The increase in intracellular Ca2+ induced by the activation of this channel may be related to the increase in cytoplasmic and endoplasmic reticulum Ca2+ pools required for virus maturation and cell death.

Animals↗
PubMed1999

Diabetes induces an impairment in the proteolytic activity against oxidized proteins and a heterogeneous effect in nonenzymatic protein modifications in the cytosol of rat liver and kidney.

It is assumed that increased oxidative stress contributes to the development of complications in diabetes. In this study, several markers of protein structural modifications directly induced by free radicals were investigated in the liver and kidney cytosolic fractions of rats with streptozotocin-induced diabetes. Sulfydryl residue and side-chain amino group analyses, as well as immunoblotting and chromatographic measurements of protein-bound carbonyl, suggest that protein oxidative modification is not increased by diabetes, with the exception of sulfydryl groups in renal cytosol. The levels of the glycation-derived carbonyl N epsilon-fructosyl-lysine are significantly increased by diabetes. Furthermore, unchanged proteolytic activity against in vivo-oxidized proteins, significant decreases both in activity against H2O2-modified proteins and in proteasome activity, measured by the degradation of a specific fluorogenic substrate, suggest that the unchanged oxidative protein modification in the diabetic state cannot be attributed to an increased cytosolic proteolytic activity in these tissues. These results provide evidence against a generalized increase in protein oxidative damage and demonstrate a diabetes-induced alteration in cytosolic proteolytic pathways, suggesting that proteasome activity may be impaired in these organs.

Animals↗
PubMed1998

Oncosis in MA104 cells is induced by rotavirus infection through an increase in intracellular Ca2+ concentration.

Rotavirus infection modifies the metabolism and ionic homeostasis of the host cell. First, there is an induction of viral synthesis with a parallel shutoff of cell protein production, followed by an increase of plasma membrane Ca2+ permeability, thereby inducing an increase of free cytoplasmic and sequestered Ca2+ concentrations. Cell death follows at a later stage. We studied the role of the increase in Ca2+ concentration in cell death. An elevation of extracellular Ca2+ concentration during infection induced an increase in [Ca2+]i and potentiated cell death. Buffering the increases in [Ca2+]i with BAPTA added at 6 h p.i. reduced the cytopathic effect without inhibiting viral protein synthesis and infectious particle production. Metoxyverapamil (D600), a Ca2+ channel inhibitor, added at 1 h p.i. reduced Ca2+ permeability, the increases in [Ca2+]i, and cell death produced by infection without modifying viral protein synthesis and infectious titer. Thapsigargin, the inhibitor of Ca(2+)-ATPase of endoplasmic reticulum, potentiated the increase of [Ca2+]i and accelerated the time course of cell death. Double staining with fluorescein diacetate and ethidium bromide or acridine orange and ethidium bromide showed that infected MA104 cells had lost plasma membrane integrity without DNA fragmentation or formation of apoptotic bodies. These results support the hypothesis that the increase in [Ca2+]i due to a product of viral protein synthesis triggers the chain of events that leads to cell death by oncosis.

Animals↗
PubMed1998

The Pzh1 protein phosphatase and the Spm1 protein kinase are involved in the regulation of the plasma membrane H+-ATPase in fission yeast.

We have previously shown that the mutation of the Schizosaccharomyces pombe PPZ-like protein phosphatase encoded by the gene pzh1+ results in increased tolerance to sodium and in hypersensitivity to potassium ions. A similar phenotype has also been reported for deletants in the spm1/pmk1 gene, encoding a mitogen-activated protein (MAP) kinase. We have found that the sodium tolerance phenotype of pzh1 deletants is stronger than that of spm1 mutants, and both effects are additive. Therefore, most probably both gene products mediate different pathways on sodium tolerance. In our hands, mutation of the kinase does not alter the tolerance to potassium, but it yields cells more tolerant to magnesium ions. While in budding yeast the mutations are synthetically lethal, fission yeast cells lacking both the phosphatase and the kinase genes are viable. Interestingly, their ability to export H+ to the medium is greatly impaired (although not that of pzh1 or spm1 single mutants). We have observed that, although the amount of the H+-ATPase in the plasma membrane is not altered, the activity of the enzyme is lower than normal and cannot be induced by glucose. These observations suggest that the activity of the H+-ATPase in fission yeast might be regulated by phospho-dephosphorylation mechanisms that might involve the pzh1+ and spm1+ gene products.

Biological Transport↗