El tratamiento con propionil-L-carnitina mejora el estrés oxidativo asociado a la hipertensión arterial / Treatment with propionyl-L-carnitine improves oxidative stress associated to high blood pressure

Introducción. El trabajo trata de evaluar la acción antioxidante de la propionil-L-carnitina (PLC) en el hígado y corazón de ratas hipertensas (spontaneusly hypertensive rats [SHR]) y normotensas (Wistar-Kyoto [WKY]). Además, estudiamos su acción hipolipidemiante. Material y métodos. Ratas WKY y SHR de 4 semanas se tratan con PLC (200 mg/kg de peso corporal) 8 semanas. Las ratas WKY y SHR sin tratar se usan como controles. Resultados. La actividad glutatión peroxidasa disminuyó en el hígado y corazón de ratas SHR con respecto a las ratas WKY. La PLC restituyó los valores, acercándolos a los de las ratas WKY. La glutatión reductasa aumentó en ambos tejidos de ratas SHR. La PLC no modificó estos valores. No hubo diferencias en la superóxido dismutasa entre los cuatro grupos de animales. La actividad catalasa aumentó en el hígado de las ratas SHR. La PLC aumentó aún más esta actividad, no observándose cambios en el corazón entre los cuatro grupos de ratas. Los niveles de malondialdehído, índice de la peroxidación lipídica, aumentan en las ratas SHR, disminuyendo con el tratamiento con PLC. La peroxidación lipídica disminuye en las ratas normotensas con PLC con respecto a las WKY no tratadas. El tratamiento con PLC reduce los niveles séricos de triglicéridos en ratas WKY y SHR, no modificando los niveles de colesterol total y sus fracciones. No se observaron modificaciones en las presiones arteriales diastólicas y sistólicas como consecuencia de la administración de la PLC. Discusión. La hipertensión arterial cursa con cambios en la actividad antioxidante endógena en el hígado y corazón de ratas SHR, conduciendo a un daño oxidativo. La PLC mejora el estrés oxidativo observado en las ratas hipertensas, demostrado mediante una protección peroxidativa en estos tejidos. Además, la PLC mejora el daño oxidativo en ratas normotensas, mostrando un efecto beneficioso per se con actividad antioxidante. Se muestra la capacidad hipotrigliceridimiante de la PLC tanto en ratas normotensas como hipertensas

Introduction. Assess the antioxidant action of propionyl-L-carnitine (PLC) in liver and heart of hypertensive (spontaneously hypertensive rats [SHR]) and normotensive (Wistar-Kyoto [WKY]) rats. Furthermore, we studied its lipid lowering action. Material and methods. Four week old WKY and SHR rats were treated with PLC (200 mg/kg of body weight) for eight weeks. WKY and SHR rats without treatment were used as controls. Results. Glutation peroxidase activity decreased in liver and heart of SHR rats versus WKY ones. The PLC reestablished the values, approaching them to those of the WKY. Glutation reductase increased in both tissues of SHR. PLC did not change these values. There were no differences in the superoxide dismutase among the four animal groups. Catalase activity increased in the SHR liver. PLC increased this activity even more, no changes being observed in the heart among the four rat groups. Malondialdehyde levels, a lipid peroxidation index increased in SHR, decreasing with PLC treatment. Lipid peroxidation decreased in normotensive rats with PLC in regards to untreated WKY. Treatment with PLC reduced serum levels of triglycerides in WKY and SHR rats, not modifying the total cholesterol levels and their fractions. No changes were observed in diastolic and systolic blood pressure as a consequence of PLC administration. Discussion. High blood pressure occurs with changes in endogenous antioxidant activity in the liver and heart of SHR rats, leading to oxidative damage. PLC improves oxidative stress observed in hypertensive rats, demonstrated by peroxidative protection in these tissues. Furthermore, PLC improves oxidative harm in normotensive rats, showing a beneficial effect per se with antioxidant activity. The triglyceride lowering capacity of PLC in both normotensive and hypertensive rats is demonstrated

Antioxidant enzyme activity and lipid peroxidation in liver and kidney of rats exposed to microcystin-LR administered intraperitoneally.

The effect of acute exposure of intraperitoneal injection of microcystin-LR (MCLR) on antioxidant enzymes and lipid peroxidation has been studied in liver and kidney of rats. Rats were treated with two doses, i.e. 100 and 150 microg of pure MCLR/kg body weight or saline solution. The enzyme activities of glutathione peroxidase (GSH-Px), glutathione reductase (GR), superoxide dismutase (SOD) and catalase (CAT) in the liver were significantly decreased in MCLR-treated rats. The decrease of GR activity in the liver was 60%, followed by GSH-Px, SOD and CAT. Similarly, a decrease in the antioxidant enzymes was found in the kidney of MCLR-treated rats, such as GSH-Px (27-31%), GR (22%), SOD (42%) and CAT (25-28%). Concomitantly, significant increases in lipid peroxidation levels were recorded in liver (121 and 196% for 100 and 150 microg/kg, respectively) and kidney (48 and 58% for 100 and 150 microg/kg, respectively) from MCLR-treated rats. In conclusion, acute exposure to MCLR results in a decrease in the antioxidant enzymes and an increase in lipid peroxidation in liver and kidney rats, suggesting the oxidative stress as an important role in the pathogenesis of MCLR-induced toxicity. Antioxidant enzymes were significantly consumed in the liver and a minor decrease was found in kidney, confirming the organ-specific effects of MCLR.

In vivo sugar diffusion in the ileal epithelium of spontaneously hypertensive rats.

BACKGROUND: D-glucose absorption, distinguishing between active and diffusive components, was studied in the ileum of spontaneously hypertensive rats (SHR) and their normotensive control Wistar-Kyoto (WKY) rats. Net water transport was also determined. METHODS: A perfusion system in vivo with ileum loops was used, and experiments with phlorizin, phloretin and 2,4,6-triaminopyrimidine (TAP) were performed in order to discriminate between active and diffusive components and between transcellular and paracellular routes. RESULTS: A significant decrease in total D-glucose absorption was found in SHR compared to WKY rats, this reduction being due to a lower SGLT1-mediated component. The effect was not compensated by the total diffusive component, since the phlorizin-insensitive D-glucose absorption did not significantly change between rat strains. However, the diffusive component of D-glucose transport was relatively more important in hypertensive than in normotensive rats. The use of 2,4,6-triaminopyrimidine (TAP), which blocks the transport across the paracellular route, showed that the paracellular diffusion of D-glucose was higher in SHR than in WKY rats. Intestinal net water absorption was not modified between either group of animals, though the presence of phlorizin in the perfusate decreased the ileal water absorption to a greater extent in normotensive rats. CONCLUSION: The observed reduction in D-glucose absorption in vivo in the ileum of SHR was due to a decrease in the SGLT1-active component. Despite the paracellular diffusion of D-glucose being higher in hypertensive than in normotensive rats, the total diffusion component was not high enough to compensate this alteration.