Biomedical subjects

R Rodrigo

Publications and source records attributed to R Rodrigo.

At least 19 recordsLinked to original sources

PubMed2006

Mass spectrometrical analysis of galectin proteins in primary rat cerebellar astrocytes.

Galectins are a family of animal lectins with specificity for beta-galactosides and are involved in a host of cellular activities, ranging from development to cancer. The molecules are expressed by neural and non-neural cells intracellularly as well as extracellularly. Using two-dimensional gel electrophoresis coupled to tandem mass spectrometry, the present work aimed to identify and characterize galectins in primary rat cerebellar astrocytes. The protein-chemical method identified nine spots representing two members of the galectin family, namely galectin-1 and galectin-3. These findings suggest that high abundant expression of galectin in astrocytes is limited to the two abundant galectin family members. As these family members are linked to human astrocytic tumors, their reliable detection in astrocytes by proteomic techniques would enable us to further understand their role in neural development, injury, and regeneration in general and astrocytoma in particular.

Amino Acid Sequence↗

PubMed2005

In situ measurements of the physical characteristics of Titan's environment.

On the basis of previous ground-based and fly-by information, we knew that Titan's atmosphere was mainly nitrogen, with some methane, but its temperature and pressure profiles were poorly constrained because of uncertainties in the detailed composition. The extent of atmospheric electricity ('lightning') was also hitherto unknown. Here we report the temperature and density profiles, as determined by the Huygens Atmospheric Structure Instrument (HASI), from an altitude of 1,400 km down to the surface. In the upper part of the atmosphere, the temperature and density were both higher than expected. There is a lower ionospheric layer between 140 km and 40 km, with electrical conductivity peaking near 60 km. We may also have seen the signature of lightning. At the surface, the temperature was 93.65 +/- 0.25 K, and the pressure was 1,467 +/- 1 hPa.

Journal Article↗

PubMed2005

Bile duct ligation plus hyperammonemia in rats reproduces the alterations in the modulation of soluble guanylate cyclase by nitric oxide in brain of cirrhotic patients.

Modulation of soluble guanylate cyclase (sGC) by nitric oxide (NO) is altered in brain from cirrhotic patients. The aim of this work was to assess whether an animal model of cirrhosis, bile duct ligation, alone or combined with diet-induced hyperammonemia for 7-10 days reproduces the alterations in NO modulation of sGC found in brains from cirrhotic patients. sGC activity was measured under basal conditions and in the presence of NO in cerebellum and cerebral cortex of the following groups of rats: controls, bile duct ligation without or with hyperammonemia and hyperammonemia without bile duct ligation. In cerebellum activation of sGC by NO was significantly lower in bile duct ligated rats with (12 +/- five-fold) or without (14 +/- six-fold) hyperammonemia than in control rats (23 +/- seven-fold). In cerebral cortex activation of sGC by NO was higher in rats with bile duct ligation with hyperammonemia (124 +/- 30-fold) but not without hyperammonemia (59 +/- 15-fold) than in control rats (66 +/- 11-fold). The combination of bile duct ligation and hyperammonemia reproduces the alterations in the modulation of soluble guanylate cyclase by NO found in cerebral cortex and cerebellum of cirrhotic patients while bile duct ligation or hyperammonemia alone reproduces the effects in cerebellum but not in cerebral cortex.

Animals↗

PubMed2005

Increased immunohistochemical expression of thrombomodulin at placental perivascular myofibroblast in severe preeclampsia (PE).

The presence of pro-coagulant and anti-coagulant components of the placental vascular endothelium and syncytiotrophoblast are essential for homeostasis. Vascular endothelium prevents blood clot formation in vivo by involving a cell surface thrombin-binding glycoprotein, thrombomodulin (TM), that activates plasma anti-coagulant protein C. The TM levels increase during pregnancy, but the fibrinolytic capacity diminishes. Since vascular lesions with placental coagulation disorders can be associated with preeclampsia (PE), we hypothesized that TM expression in the stem villous vasculature and syncytiotrophoblast of the placenta are impaired in PE. Plasma and placental tissue samples were collected from PE (n=12) and normotensive pregnant patients (n=11). Patient's gestational age was 35.7+/-1.2 (normotensive) and 30.6+/-1.5 weeks (PE). Blood samples were drawn 30 min before delivery. Serum PAI-1 and PAI-2 antigens were determined by enzyme-linked immunoabsorbent assay (ELISA). A monoclonal antibody specific for TM was used for immunohistochemical tissue staining (ABC) and the staining was quantified by semi quantitative scores. Results show no intensity differences at the apical syncytiotrophoblast between the two groups. However, in preeclamptic placenta, TM expression diminished in the endothelium of the stem villi arteries and increased in the perivascular and stromal myofibroblats in cases of severe PE. TM changes were associated with an increased PAI-1/PAI-2 ratio. It is suggested that in severe PE, the decreased placental blood flow may be due to structural and functional impairment of the endothelium of the stem villi vessels and the surrounding perivascular and stromal myofibroblast, by increasing TM expression which may modulate fetal blow flow in the villous tree.

Actins↗

PubMed2001

Oxidative stress, microsomal and peroxisomal fatty acid oxidation in the liver of rats treated with acetone.

Parameters of oxidative stress, microsomal cytochrome P450 activity and peroxisomal fatty acid oxidation were studied in liver of rats following acetone (1% v/v) consumption for 7 days. Acetone treatment increased the activity of catalase and decreased the activities of superoxide dismutase (SOD) and glutathione peroxidase (GTPx), but did not significantly modify the liver content of malondialdehyde (MDA) and reduced glutathione. Also, acetone increased the total content of cytochrome P450, the microsomal lauric acid hydroxylation, aminopyrine N-demethylation and the peroxisomal beta-oxidation of palmitoyl CoA. These effects were similar to those found previously in starved and ethanol-treated rats, supporting the hypothesis that ketone bodies would be the common inducer of microsomal and peroxisomal fatty acid oxidation in these metabolic states.

Acetone↗

PubMed2001

Red wine raises plasma HDL and preserves long-chain polyunsaturated fatty acids in rat kidney and erythrocytes.

The effects of red wine and ethanol on plasma lipoproteins and the fatty acid composition of kidney lipids and erythrocytes phospholipids were studied. Lipid peroxidation is one of the main deleterious effects of oxidant attack on biomolecules, due to the disruption of the structural integrity of membranes. The vulnerability of the kidney to oxidative damage has been partly attributed to its high content of long-chain polyunsaturated fatty acids. Antioxidants, such as flavonoids, would be a means of reducing the risk of oxidative damage to membranes. Nutritional sources rich in antioxidants, including those provided by wine, are expected to attenuate the effects of oxidative challenges. Adult rats were fed red wine rich in flavonols, ethanol (125 ml/l), or alcohol-free red wine. The control group drank water. After 10 weeks, blood samples served to measure plasma lipoproteins and antioxidant capacity. Kidney lipids and erythrocyte phospholipids were extracted. The samples were assayed by GLC. Energy intake did not differ between all the groups, but the weight gain of the ethanol group was less than the other three groups. Blood HDL and triacylglycerols were increased by both ethanol and red wine. Ethanol decreased arachidonic and docosahexaenoic acids in both kidney lipids and erythrocyte phospholipids, as compared with either water, red wine or alcohol-free red wine groups. These results indicate that non-alcoholic components of red wine could contribute to avoiding the unfavourable effects of ethanol on plasma lipoproteins, kidney lipids and membrane erythrocyte phospholipids.

Animals↗

PubMed2000

Bile duct ligation and oxidative stress in the rat: effects in liver and kidney.

In the liver, seven days of bile duct ligation (BDL) decreases the cytochrome P-450 content and the UDP-glucuronyl transferase activity. Also, a decrease in the water soluble antioxidant mechanism reflected in the activities of the enzymes superoxide dismutase (SOD), catalase and the glutathione peroxidase (GTPx) was found in the liver but not in the kidney. Despite an increase in the amount of the GSH in the liver, increased lipid peroxidation is produced in the BDL rats, as indicated by the levels of malondialdehyde (MDA). The kidney responded in a different way to cholestasis, decreasing only the UDP-glucuronyl transferase activity and increasing the levels of GSH and MDA. In the red blood cells the activity of the antioxidant enzymes SOD, GTPx and catalase and the content of GSH were not modulated by cholestasis. In conclusion, disturbance of the oxidant-antioxidant balance might be responsible for cholestatic liver injury and impaired renal function in BDL rats.

Animals↗

PubMed1999

Effects of bromoethylamine on antioxidant capacity, lipid peroxidation, and morphological characteristics of rat liver.

Administration of bromoethylamine (BEA, 1.2 mmol/kg) to fed rats induced a significant diminution in the activity of hepatic superoxide dismutase (at 1 h after treatment), catalase, and glutathione peroxidase and in the content of nonprotein sulfhydryls (at 15 h after treatment). The content of thiobarbituric acid reactants by the liver was enhanced by 1.9 times over control values (at 3 h). Light microscopy studies revealed that BEA (72 h after treatment) induced periportal fatty accumulation, focal liver cell necrosis, and diffuse inflammatory infiltrates, in addition to hypertrophic Kupffer cells and mitotic hepatocytes. Also, hypertrophic middle tunic or hypertrophic smooth muscle layers of arterioles was observed in the periportal space, with dilated sinusoidal capillaries and free macrophage infiltration. It is concluded that BEA induces a derangement in the antioxidant status of the liver with the consequent lipid peroxidation response, which may constitute a significant hepatotoxic mechanism of the haloaklylamine.

Animals↗

PubMed1998

Modulation of peroxisomal and microsomal fatty acid oxidation by acetone. A comparative study between liver and kidney.

The effect of acetone consumption on some microsomal and peroxisomal activities was studied in rat kidney and these results were compared with data from former investigations in liver. Acetone increased the microsomal lauric acid hydroxylation, the aminopyrine N-demethylation catalyzed by cytochrome P450 and the microsomal UDP-glucuronyltransferase activity. Also, acetone increased the peroxisomal beta-oxidation of palmitoyl CoA and catalase activities in kidney. These studies suggest that acetone is a common inducer of the microsomal and peroxisomal fatty acid oxidation, as previously shown in both starved and ethanol treated rats. Our results support the hypothesis that microsomal fatty acid omega-hydroxylation results in the generation of substrates being supplied for peroxisomal beta-oxidation. We propose that the final purpose of these linked fatty acid oxidations could be the catabolism of fatty acids or the generation of a substrate for the synthesis of glucose from fatty acids. This pathway would be triggered by acetone treatment in a similar way in liver and kidney.

Acetone↗

PubMed1998

Effects of chronic ethanol consumption on extramitochondrial fatty acid oxidation and ethanol metabolism by rat kidney.

1. We evaluated the effects of chronic ethanol consumption on microsomal and peroxisomal fatty acid oxidation and on ethanol oxidation by the kidney. 2. When mature rats were fed 20% ethanol for 10 weeks, an increase in alcohol dehydrogenase and catalase activities were observed in the kidney. 3. Renal microsomal and peroxisomal oxidation of fatty acids also increased by the treatment, but total cytochrome P450 content did not. 4. We concluded that chronic ethanol consumption results in an increased extramitochondrial disposition of fatty acids and ethanol oxidation by the kidney.

Alcohol Dehydrogenase↗

PubMed1998

Acute and chronic effect of ethanol on (Na + K)-ATPase activity and cyclic AMP response to vasopressin in rat papillary collecting duct cells.

1. We evaluated the effects of ethanol on (Na + K)-ATPase activity and cAMP response to vasopressin in native and cultured rat papillary collecting duct (PCD) cells. 2. A significant increase in (Na + K)-ATPase and Mg(2+)-ATPase activities was found in PCD cells either isolated from chronic ethanol-fed rats or cultured in the presence of ethanol. 3. Acute treatment with ethanol resulted in a biphasic effect on the activity of (Na + K)-ATPase, which was enhanced below 1% ethanol and inhibited at higher concentrations. 4. Chronic ethanol treatment did not change the cAMP response of PCD cells to vasopressin. Acutely, in turn, this response was enhanced by ethanol per se. 5. It is suggested that the antinatriuretic effect of ethanol could be at least in part mediated by a (Na + K)-ATPase enhancement in PCD cells. Acutely, ethanol could normalize water balance by its peripheral effects on distal nephron.

Animals↗

PubMed1998

Peroxisomal and microsomal fatty acid oxidation in liver of rats after chronic ethanol consumption.

1. Microsomal P450 and peroxisomal fatty acid oxidation activities were studied in liver of rats after long-term ethanol consumption. 2. Ethanol increased the microsomal lauric acid omega-hydroxylation and the aminopyrine N-demethylation catalyzed by cytochrome P450. 3. Ethanol increased peroxisomal beta-oxidation of palmitoyl CoA and catalase activity in liver. 4. Both microsomal and peroxisomal activities behaved in a coordinate way in the liver of rats with long-term ethanol consumption. 5. These results would support a role of microsomal omega-hydroxylation and peroxisomal beta-oxidation of fatty acids in an extramitochondrial pathway of lipid oxidation in the liver.

Alcohol Drinking↗

PubMed1998

Effect of ethanol ingestion on renal regulation of water and electrolytes.

Ethanol may alter the homeostasis of water and electrolytes before the occurrence of liver damage able to explain these disorders. How the kidney may become involved in water diuresis or sodium and potassium retention has not been well elucidated. During the last decade, an increasing body of evidence has guided interest toward the relevance of the biochemical basis of ethanol-induced injury to the kidney. Multiple functional abnormalities of renal tubules may be associated with ethanol-induced changes in membrane composition and lipid peroxidation of these epithelial cells. Ethanol interferes with the carrier function by decreasing (Na+K)-ATPase activity, but this activity is enhanced by chronic exposure. Recently, it was reported that ethanol oxidation by the kidney is favored in chronic ethanol-treated rats, thereby suggesting a pathogenic role for acetaldehyde in the nephrotoxic effect of ethanol ingestion. Also, increased reactive oxygen species, partly generated from acetaldehyde oxidation, may contribute to the occurrence of oxidative stress. The pathophysiology of renal regulation of water and electrolytes of alcoholic disease is analyzed on the basis of recent advances in our knowledge concerning the biochemical effects of ethanol on the kidney.

Alcohol Drinking↗

PubMed1997

Effects of chronic and acute ethanol exposure on renal (Na + K)-ATPase in the rat.

1. We evaluated the effects of chronic ethanol consumption on the kinetic properties of renal (Na + K)-ATPase and compared them with acute inhibition by ethanol in vitro. 2. When adult rats were fed 20% ethanol for 10 weeks, renal (Na + K)-ATPase activity increased but the sensitivity of the enzyme to ethanol inhibition in vitro was not altered. 3. Vmax was increased by ethanol consumption, whereas K0.5 and nH were not changed. The kinetic parameters of Mg(2+)-ATPase were not affected under the same conditions. 4. We concluded that ethanol-induced tolerance or enhancement of renal (Na + K)-ATPase or both can be explained on the basis of an increase in Vmax.

Adenosine Triphosphate↗

PubMed1997

Renal effects of chronic exposure to malathion in Octodon degus.

We studied the effects of chronic exposure to malathion in the kidney of Octodon degus, a caviomorph whose habitat may be exposed to pesticides currently used in Chilean agriculture. A group of adult female animals received malathion (200 ppm) as sole drinking fluid for 90 days. Kidneys showed signs of histologic damage, marked by hyperplasia and hypertrophy of tubular cells. Exposed animals had unchanged glomerular filtration rates and renal handling of sodium and chloride, but a significant increase in fractional excretion of potassium resulted from this treatment. The activities of Na+/K(+)-ATPase and Mg(2+)-ATPase in renal cortex and outer medulla were not affected by malathion exposure. This study provides evidence of both morphologic and functional renal damage elicited by chronic exposure of O. degus to a low dose of malathion. Morphologic alterations in glomerulus were accompanied by either morphologic and functional impairments of the distal nephron.

Animals↗

PubMed1996

Ablation and chemistry of meteoric materials in the atmosphere of Titan.

We compute the input of meteoric materials expected on Titan, and integrate this dust model with an ablation model and a comprehensive chemical model, investigating the effects on the atmosphere and surface. We find that a water deposition of approximately 10-100 times the expected interplanetary dust flux, or a recent large impact, is required to produce the observed CO2 abundance. Ionisation due to meteoric activity is not likely to be higher than that due to other sources.

Atmosphere↗

PubMed1996

Proteinuria and albumin homeostasis in the nephrotic syndrome: effect of dietary protein intake.

Nephrotic syndrome is analyzed in the light of interventions designed to decrease proteinuria and renal injury. The effect of dietary protein intake on urinary protein losses and albumin homeostasis are discussed on the basis of the pathophysiologic mechanisms known to account for changes in renal function of nephrotic patients. In addition, the effect of angiotensin-converting enzyme inhibitors for reduction of proteinuria is discussed in terms of the modulation of glomerular permselectivity and hemodynamics.

Albumins↗

PubMed1996

Mechanism of enhancement of renal (Na(+)+K+) ATPase activity following chronic ethanol exposure.

A method was devised to determine the nature of the mechanism of the increase in renal (Na(+)+K+)-ATPase in rats fed dilute ethanol for ten weeks. Antiserum to (Na(+)+K+)-ATPase obtained from rabbits was added to microsomal fractions of kidney and the activities of (Na(+)+K+)-ATPase and Mg2+ ATPase were determined. The addition of antiserum resulted in a same pattern of dose-related inhibition of (Na(+)+K+)-ATPase activity in control and ethanol-fed rats, whereas Mg(2+)-ATPase was not affected by the antiserum. These results suggest that the mechanism of ethanol-induced enhancement of renal (Na(+)+K+)-ATPase activity could be explained through an increase in the number of catalytic units.

Analysis of Variance↗