Prevalence of Toxoplasma gondii antibodies in cats in the western part of Great Buenos Aires, Argentina, 1993.

The serological prevalence of Toxoplasma gondii was determined, using indirect haemagglutination assay, in the sera of 169 cats. Classification by age, sex, alimentary, hunting and roaming habits was made in conjunction with the number of cats living in each house. An important prevalence was detected (19.5%) from 1 year of age and statistical significance was found in those animals that had predatory habits or lived in groups.

Lipid changes in hepatic microsomes and its relationship to P-nitrophenol glucuronidation in an experimental model of portal hypertension.

The liver is responsible for the most important metabolic pathway of non polar compounds. The aim of the present work was to study the p-nitrophenol glucuronidation and its relationship with lipidic composition of microsomal membrane in a model of hepatic portal hypertension and hepatocellular damage induced by monocrotaline. A global increment in liver microsomal phospholipids as well as changes in the phospholipid pattern (phosphatidylethanolamine and sphingomyelin increased up to 156 +/- 13 and 195 +/- 14% respectively) were detected in monocrotaline intoxicated rats when it were compared to control rats. The microsomal cholesterol content showed a decrease in monocrotaline intoxicated rats. (4.1 +/- 0.7 against 6.6 +/- 1.5 micrograms/mg of microsomal protein, in control rats). When p-nitrophenol activity was measured, Km from monocrotaline intoxicated rats was 0.137 mM, and Vmax was 2.9 nmol of p-nitrophenol/mg microsomal protein since in control group Km was 0.322 mM, and Vmax was 4.5 nmol of p-nitrophenol/mg microsomal protein. It is concluded that monocrotaline intoxicated rats showed a different behavior in the kinetics of p-nitrophenol UDP-glucuronyltransferase, as well as a different microsomal lipidic profile, when compared to control group.

[Benzodiazepine metabolism in experimental extrahepatic cholestasis]. / Metabolismo de benzodiacepinas en colestasis extrahepática experimental.

The aim of the present study was to determine the effect of bile flow impairment on hepatic lorazepam detoxication and its relationship with the liver microsomal membrane phospholipid composition. It was observed a decrease of phosphatidylcholine, phosphatidylinositol, phosphatidylethanolamine and sphingomyelin content and an increase of phosphatidylserine and phosphatidylglycerol. A similar activity on lorazepam detoxication was observed when cholestatic rats were compared to controls. These results suggest that there is a different modulation than the phospholipid environment play the key role in lorazepam metabolism, independently of membrane.

[Increase of acetaminophen conjugation ability in experimental cholestasis]. / Aumento de la capacidad de conjugación del acetaminofene en colestasis experimental.

Acetaminophen glucuronidation ability and its relationship to hepatic microsomal phospholipid changes were studied during experimental extrahepatic cholestasis. This study included two groups of Wistar rats: 1) normal rats and 2) cholestatic rats. UDP-Glucuronyltransferase activity (UDP-GT) towards acetaminophen resulted increased in 38% (p < 0.05) in the cholestatic group when compared to normal rats. We also found important changes in hepatocyte microsomal phospholipid profile. When phosphatidylcholine fatty acid composition was analysed, all of them resulted diminished except for an increment on oleic acid content (36%). This fatty acid increase in the main membrane phospholipid had a parallel behaviour with acetaminophen glucuronidation activity. This fact could support an activation role for oleic acid over this enzymic system.

[Fluidity of hepatic microsomal membrane and its relation with aging]. / Fluidificación de la membrana microsomal hepática y su relación con el envejecimiento.

The effect of aging on hepatic microsomal membrane phospholipid composition was studied composition was studied in both young (2 months) and mature (6 months) Wistar rats. When total microsomal phospholipid content was analysed the aged group showed a significant increment (73%). Microsomal phospholipid pattern also showed a different behavior between both groups, with a significative increase in phosphatidylcholine (62%), phosphatidylserine (124%), phosphatidylinositol (31%) and sphingomyelin (10%) and appearance of phosphatidylethanolamine and phosphatidylglycerol in the six-month group. A higher microsomal membrane fluidity in the aged animals was revealed by the increase in PC/EM index (47%). This increment jin fluidity during aging process may reflect an adaptative response resulting in changes on the enzyme activities responsible for drug and carcinogen metabolism.

[Phospholipid composition of the hepatic microsomal membrane and its relationship to bilirubin UDP glucuronyltransferase in human cholestasis]. / Composición fosfolipídica de la membrana microsomal hepática y su relación con la actividad de la bilirrubina UDP-glucuroniltransferasa en colestasis humana.

A number of morphological and functional changes on liver cells were reported during experimental cholestasis. Some specific metabolic pathways catalyzed by "membrane bound" enzymes were described to be altered by lipid microenvironment changes. The purpose of he present study is to establish Bilirubin UDP-Glucuronyltransferase activity--a microsomal integral enzyme responsible for bilirubin conjugation--and microsomal phospholipid profile in cholestatic and normal patients. Surgical liver biopsies were taken fron five patients suffering prolonged extrahepatic cholestasis, and five patients submitted to abdominal surgery excluding hepato-biliary diseases that were considered as controls. The following biochemical parameters were determined in both groups: bilirubin concentration, alkaline phosphatase, gamma-glutamyltranspeptidase, oxalacetic and pyruvic transaminases, and pseudo-cholinesterase activities. Serum cholestatic markers showed significative increments in cholestatic patients (Table 1). Total Bilirubin UDP-Glucuronyltransferase activity was similar comparing normal and cholestatic individuals (1.11 +/- 0.66 and 1.93 +/- 0.82 nmol conjugated bilirubin/mg protein in 10 min. respectively). When final reaction product was analysed, the normal group showed 80% of bilirubin diglucuronide; but resulted undetectable in cholestatic patients yielding 100% of bilirubin monoglucuronide. Microsomal phospholipid analysis showed a decrease in phosphatidylcholine and phosphatidylethanolamine contents in the cholestatic group; probably due to the action of bile acids accumulated into the hepatic cells. Simultaneously we found an increment in phosphatidylserine and sphingomyelin levels in cholestatic patients compared to normals (Figure 1). This fact could be explained by the existence of special sites in the membrane for the latter phospholipids, protected against bile acids detersive action.(ABSTRACT TRUNCATED AT 250 WORDS)

[Development of biochemical and histopathological parameters in paracetamol overdose in experimental cholestasis]. / Evolución de parámetros bioquímicos e histopatológicos en la sobredosis con paracetamol durante la colestasis experimental.

The aim of the present paper is to determine the effect of Paracetamol (P) acute intoxication in cholestatic rats. Four groups of animals were considered: controls, controls intoxicated with P, rats intoxicated with P and cholestatic rats. Hepatic biochemical tests and liver histology were performed in every group. It is concluded that cholestatic rats intoxicated with P showed less Liver damage than in control groups.

Enzymatic activities in brains of diabetic rats treated with vanadyl sulphate and sodium tungstate.

The hypothesis of the present study was that diabetes mellitus might affect brain metabolism. Streptozotocin (STZ)-induced diabetic rats, treated with vanadyl sulphate (V) and sodium tungstate (T) were employed to observe the aspartate aminotransferase (AST), alanine aminotransferase (ALT) and creatine kinase (CK) activities in brain homogenates. Significant increases in AST, ALT and CK activities were found in diabetic brain homogenates against controls, suggesting increments of transamination in brain and/or increases in cell membrane permeability to these enzymes. The increase in brain CK possibly expresses alterations in energy production. The decrease in CK activity caused by V and T treatment in diabetic rats suggests that both agents tend to normalize energy consumption. It is also possible that V and T-induced hypoglycemic effects cause metabolic alterations in brain.

Liver microsomal bilirubin UDP-glucuronyltransferase disturbances in bile duct ligated rats.

The activity of bilirubin UDP-Glucuronyltransferase was determined in microsomes from normal and bile duct ligated rats. It was measured after 2 and 8 days following bile duct ligation and compared with normal rats. A decrease of 33% in the total enzyme activity was observed on day 2; a fall of 70% was founded on day 8. Bilirubin diglucuronide represented approximately 20% of total conjugates in both groups of cholestatic rats, as compared with 65% found in normals. It was concluded that bilirubin microsomal conjugating capacity is markedly altered during cholestasis. This can be attributed to microsomal membrane damage produced by stagnant bile.

Protein and lipid disturbances in rat liver microsomal membranes after bile duct ligation.

An analysis of proteins, phospholipids and cholesterol from liver microsomal membranes was performed in normal and post-cholestatic rats. Bile duct ligated rats showed a progressive decrease of these membrane constituents. Minor changes in peptide analysis, a marked decrease of phosphatidylcholine and phosphatidylinositol, disappearance of phosphatidylethanolamine and sphingomyelin, and a clear increment of phosphatidylserine was observed in post-cholestatic as compared to normal group. It was concluded that extra-hepatic cholestasis produces structural changes on the liver microsomes, particularly on phospholipid profile.

Changes in liver drug glucuronidation during cholestasis are non predictable.

Liver microsomal glucuronidation of acetaminophen, chloramphenicol, salicylic acid, lorazepam, p-nitrophenol and morphine were measured in 8 days bile duct ligated rats. Compared to normals, cholestatic rats showed a decrease of 31% for p-nitrophenol glucuronidation; salicylic acid glucuronidation increased 281%; acetaminophen glucuronidation increased 38% while morphine, chloramphenicol and lorazepam values were similar to controls. We concluded that cholestasis produces non predictable changes on liver drug glucuronidation pathways.

p-Nitrophenol glucuronidation in bile duct ligated rats.

Liver microsomal glucuronidation of p-nitrophenol was measured in normal, 2 and 8 day bile duct ligated rats. At low aglycone concentration (0.24-0.8 mM) a Michaelis-Menten kinetic was registered in the three groups of animals but cholestatic rats showed a decrease of activity related to the time that cholestasis was maintained. At higher substrate concentration (1.2-2.0 mM), a very different behavior between the three groups was observed: normal rats showed a substrate inhibition phenomena; 2 day rats maintained plateau values and a remarkable activation effect of the activity was seen in the 8 day group. We concluded that cholestasis produced pronounced changes in p-nitrophenol glucuronidation pathway.

Changes in microsomal phospholipid fatty acids composition in cholestatic rats.

In the rat, the effect of the bile duct ligation on liver microsomal phospholipid fatty acid composition and on phosphatidylcholine, phosphatidylserine and phosphatidylinositol pattern were studied. After two days of cholestasis, microsomal phospholipid fatty acids showed a decrease in linoleic, stearic and arachidonic acids and an increase in oleic and docosahexaenoic ones, as compared to controls. Phosphatidylcholine showed an increment in oleic and palmitic acid content and a concomitant decrease in arachidonic acid. Phosphatidylserine showed a progressive increase while phosphatidylinositol showed a progressive decrease in all fatty acids. Eight-days post-cholestatic rats showed a marked increase in oleic acid, whereas linoleic, arachidonic, stearic and palmitic acids concentration decreased. Phosphatidylcholine showed a global decrease in its fatty acid content, except for oleic which is increased. Phosphatidylserine showed an increase over the two-days cholestasis fatty acids values. Phosphatidylinositol decreased in most fatty acids except in docosahexaenoic acid that recovered normal values. It was concluded that cholestasis produced significative changes in the fatty acid composition of the major phospholipids constituents of the microsomal membranes.

Cholestasis as a liver protective factor in paracetamol acute overdose.

1. The effect of paracetamol overdoses on its disposition was investigated in cholestatic rats. 2. Paracetamol plasma concentration and hepatic accumulation decrease about 70-80% in cholestatic rats. 3. Cholestatic rats intoxicated with paracetamol showed less hepatic damage as concluded from biochemical and histological findings. These data are correlated with liver and plasmatic paracetamol. 4. These results indicate a decrease in paracetamol toxicity related to stagnant bile.

Aumento de la capacidad de conjugación del acetaminofene en colestasis experimental / [Increase of acetaminophen conjugation ability in experimental cholestasis]

Acetaminophen glucuronidation ability and its relationship to hepatic microsomal phospholipid changes were studied during experimental extrahepatic cholestasis. This study included two groups of Wistar rats: 1) normal rats and 2) cholestatic rats. UDP-Glucuronyltransferase activity (UDP-GT) towards acetaminophen resulted increased in 38

(p < 0.05) in the cholestatic group when compared to normal rats. We also found important changes in hepatocyte microsomal phospholipid profile. When phosphatidylcholine fatty acid composition was analysed, all of them resulted diminished except for an increment on oleic acid content (36

). This fatty acid increase in the main membrane phospholipid had a parallel behaviour with acetaminophen glucuronidation activity. This fact could support an activation role for oleic acid over this enzymic system.

Violencia sexual: un nuevo enfoque institucional / Sexual violence: a new institutional approach

Introducción: la violencia por motivos de género es una cuestión social que cobra un enorme precio en materia de salud mental y física. Es posible que la mitad de todas las mujeres estén sujetas en algún momento de su vida actos de violencia por motivos de género. Cada año, dos millones de niñas y mujeres corren riesgo de mutilación genital. La violencia puede ser evidente, como en el caso de los castigos físicos o las agresiones sexuales, o encubierta, como en el abandono o en maltrato emocional. Objetivo: Contribuir a la concientización del cuerpo profesional, a fin de hacerlo perceptivo a las necesidades de las víctimas de violaciones, pudiendo así lograr el desarrollo de un programa asistencial integral de las mismas. Material y método: Se realizó una revisión de los conceptos de definición y diagnósticos diferenciales de violación y abuso sexual. Se realizó el estudio comparativo entre distintos Códigos Penales (Españo, Argentino y su modificatoria del año 1999) de los principales artículos que reglamentan este tema. Se selecionaron las principales normativas vigentes que reglamentan los derechos humanos, la eliminación de las formas de discriminación de la mujer y los principios fundamentales de justicia para las víctimas de delitos. Resultados: Se conceptualizaron premisas profesionales, éticas y humanas que creemos fundamentales en el abordaje de esta problemática. Se plantea como necesidad una definición más abarcativa de violación de nuestro Código Penal, que permita instaurar una forma inequívoca la fellatio in ore como delito de violación. Se reseñan los principales indicadores específicos y de sospecha, así como los estudios infectológicos y la profilaxis a instaurar en caso de violación y abuso sexual. Conclusiones: No actuar para asegurar los derechos de la mujer es ponerse del lado del abuso y la violencia. Al ser indiferentes, resultaremos destructivos