Effect of Alpha lipoic acid on cadmium induced oxidative damage on heart, brain, kidney, liver and lung of rats

En el presente estudio se investigó el efecto protector del ácido alfa lipoico (ALA) sobre el daño oxidativo inducido por el cadmio en ratas. El cadmio (100 ppm) suministrado a ratas normales dio lugar a un aumento significativo de los niveles de transaminasa glutámico-oxalacética sérica (SGOT), transaminasa glutámico-pirúvica sérica (SGPT) y fosfatasa alcalina (ALP). En los animales expuestos al cadmio se observó igualmente un aumento significativo del nivel de peroxidación lipídica (LPO) y una disminución de los niveles de glutatión reducido (GSH), superóxido dismutasa (SOD), catalasa (CAT) y ATPasas de la membrana (Na+K+-ATPasa, Ca2+-ATPasa y Mg2+-ATPasa) en cerebro, pulmón, riñón, hígado y corazón en comparación con el grupo de control. La administración conjunta de ALA (25mg/kg/día, i.p.) y cadmio durante treinta días dio lugar a una disminución significativa de los niveles de SGOT, SGPT y fosfatasa alcalina en suero hasta niveles cercanos a los normales. El uso de ALA también supuso una reducción del nivel de MDA y un aumento de los niveles de SOD, CAT, GSH y ATPasas unidas a la membrana en todos los órganos de los animales tratados con cadmio hasta niveles cercanos a los normales. El presente estudio demuestra el daño inducido por radicales libres derivados de la administración de cadmio sobre distintos órganos y el efecto antioxidante del ALA que protege a los órganos frente a este daño cuando se administra conjuntamente con cadmio.This study investigated the protective effect of alpha lipoic acid (ALA) on cadmium induced oxidative damage in rats. Cadmium (100ppm) fed to normal rats resulted in signifi cant increase in the level of serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT) and Alkaline Phosphatase (ALP). Animals exposed to cadmium also showed a signifi cant increase in level of lipid peroxidation (LPO) and decreased levels of reduced glutathione (GSH), superoxide dismutase (SOD) , catalase (CAT) and membrane bound ATPases (Na+K+ATPase, Ca2+ATPase and Mg2+ATPase) in brain, lung, kidney, liver and heart as compared to control group. Coadministration of ALA (25mg/kg/day, i.p.) along with cadmium for thirty days significantly decreased the levels of SGOT, SGPT and Alkaline Phosphatase in the serum to near normal levels. ALA also reduced the level of MDA and increased the levels of SOD, CAT, GSH and membrane bound ATPases in all the organs of the animals treated with cadmium to near normal levels. This study demonstrates the free radical damage caused by administration of cadmium on different organs and the antioxidant effect of ALA which protects the organs from this damage when it is given along with cadmium

Efecto del ácido alfa lipoico sobre el daño oxidativo inducido por cadmio en corazón, cerebro, riñón, hígado y pulmón de ratas

This study investigated the protective effect of alpha lipoic acid (ALA) on cadmium induced oxidative damage in rats.Cadmium (100ppm) fed to normal rats resulted in signifi cant increase in the level of serum glutamate oxaloacetatetransaminase (SGOT), serum glutamate pyruvate transaminase (SGPT) and Alkaline Phosphatase (ALP). Animalsexposed to cadmium also showed a signifi cant increase in level of lipid peroxidation (LPO) and decreased levels of reducedglutathione (GSH), superoxide dismutase (SOD) , catalase (CAT) and membrane bound ATPases (Na+K+ATPase,Ca2+ATPase and Mg2+ATPase) in brain, lung, kidney, liver and heart as compared to control group. Co administrationof ALA (25mg/kg/day, i.p.) along with cadmium for thirty days signifi cantly decreased the levels of SGOT, SGPT andAlkaline Phosphatase in the serum to near normal levels. ALA also reduced the level of MDA and increased the levels ofSOD, CAT, GSH and membrane bound ATPases in all the organs of the animals treated with cadmium to near normallevels. This study demonstrates the free radical damage caused by administration of cadmium on different organs andthe antioxidant effect of ALA which protects the organs from this damage when it is given along with cadmium.En el presente estudio se investigó el efecto protector del ácido alfa lipoico (ALA) sobre el daño oxidativo inducidopor el cadmio en ratas. El cadmio (100 ppm) suministrado a ratas normales dio lugar a un aumento signifi cativode los niveles de transaminasa glutámico-oxalacética sérica (SGOT), transaminasa glutámico-pirúvica sérica (SGPT)y fosfatasa alcalina (ALP). En los animales expuestos al cadmio se observó igualmente un aumento signifi cativodel nivel de peroxidación lipídica (LPO) y una disminución de los niveles de glutatión reducido (GSH), superóxidodismutasa (SOD), catalasa (CAT) y ATPasas de la membrana (Na+K+-ATPasa, Ca2+-ATPasa y Mg2+-ATPasa) encerebro, pulmón, riñón, hígado y corazón en comparación con el grupo de control. La administración conjunta deALA (25mg/kg/día, i.p.) y cadmio durante treinta días dio lugar a una disminución signifi cativa de los niveles deSGOT, SGPT y fosfatasa alcalina en suero hasta niveles cercanos a los normales. El uso de ALA también supusouna reducción del nivel de MDA y un aumento de los niveles de SOD, CAT, GSH y ATPasas unidas a la membranaen todos los órganos de los animales tratados con cadmio hasta niveles cercanos a los normales. El presente estudiodemuestra el daño inducido por radicales libres derivados de la administración de cadmio sobre distintos órganosy el efecto antioxidante del ALA que protege a los órganos frente a este daño cuando se administra conjuntamentecon cadmio

Prevention of hepatorenal toxicity with Sonchus asper in gentamicin treated rats

<p>Abstract</p> <p>Background</p> <p><it>Sonchus asper </it>possesses antioxidant capacity and is used in liver and kidney disorders. We have investigated the preventive effect of methanolic extract of <it>Sonchus asper </it>(SAME) on the gentamicin induced alterations in biochemical and morphological parameters in liver and kidneys of Sprague-Dawley male rat.</p> <p>Methods</p> <p>Acute oral toxicity studies were performed for selecting the therapeutic dose of SAME. 30 Sprague-Dawley male rats were equally divided into five groups with 06 animals in each. Group I received saline (0.5 ml/kg bw; 0.9% NaCl) while Group II administered with gentamicin 0.5 ml (100 mg/kg bw; i.p.) for ten days. Animals of Group III and Group IV received gentamicin and SAME 0.5 ml at a dose of 100 mg/kg bw and 200 mg/kg bw, respectively while Group V received only SAME at a dose of 200 mg/kg bw. Biochemical parameters including aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), γ-glutamyltransferase (γ-GT), total cholesterol, triglycerides, total protein, albumin, creatinine, blood urea nitrogen (BUN), total bilirubin and direct bilirubin were determined in serum collected from various groups. Urinary out puts were measured in each group and also assessed for the level of protein and glucose. Lipid peroxides (TBARS), glutathione (GSH), DNA injuries and activities of antioxidant enzymes; catalase (CAT), peroxidase (POD) and superoxide dismutase (SOD) were determined in liver and renal samples. Histopathological studies of liver and kidneys were also carried out.</p> <p>Results</p> <p>On the basis of acute oral toxicity studies, 2000 mg/kg bw did not induce any toxicity in rats, 1/10^thof the dose was selected for preventive treatment. Gentamicin increased the level of serum biomarkers; AST, ALT, ALP, LDH, γ-GT, total cholesterol, triglycerides, total protein, albumin, creatinine, BUN, total and direct bilirubin; as were the urinary level of protein, glucose, and urinary output. Lipid peroxidation (TBARS) and DNA injuries increased while GSH contents and activities of antioxidant enzymes; CAT, POD, SOD decreased with gentamicin in liver and kidney samples. SAME administration, dose dependently, prevented the alteration in biochemical parameters and were supported by low level of tubular and glomerular injuries induced with gentamicin.</p> <p>Conclusion</p> <p>These results suggested the preventive role of SAME for gentamicin induced toxicity that could be attributed by phytochemicals having antioxidant and free radical scavenging properties.</p

Protective effect of coenzyme Q10 in simvastatin and gemfibrozil induced rhabdomyolysis in rats

845-848Administration of simvastatin (80 mg/kg, po. evening dose) and gemfibrozil (600 mg/kg, po twice) for 30 days produced significant decrease in the level of reduced glutathione, superoxide dismutase, catalase and increase in the level of lipid peroxidation and various serum parameters (creatine phosphokinase, lactate dehydrogenase, serum glutamate oxaloacetate transaminase, creatinine, urea and blood urea nitrogen). This suggested involvement of oxidative stress in rhabdomyolysis. Increase in the level of reduced glutathione, superoxide dismutase, catalase and decrease in the level of lipid peroxidation and serum parameters after administration of antioxidant CoQ10 (10 mg/kg.ip) proved the protective effect of CoQ 10 in rhabdomyolysis

Prevention of Insulin Resistance by Silymarin.

Objective The aim of this study was to evaluate the effect of silymarin on the dexamethasone and fructose – induced insulin resistance since its effect potential protective effects have been addressed in other models of cell damage induced by drugs. Methods Insulin resistance was induced by administration of either dexamethasone or fructose. In both model effect of concomitant administration of silymarinÂ&nbsp; in two divided doses 100 and 200 mg/kg continued till end of the experiment were studied group 3-5, dexamethasone was administered to the overnight-fasted rats and continued till the end of the experiment along with silymarin 100 or 200 mg/kg p.o. At the end of the experimental period i.e. on day 11 in dexamethasone insulin resistance model, the serum glucose triglyceride and body weight was determined. Subsequently, insulin secretion in vitro from isolated perfused pancreas were determinedÂ&nbsp; On day 21 in fructose induced insulin resistance model the estimation of serum glucose, cholesterol triglyceride and insulin were done. Then the animals were sacrificed, a piece of liver was dissected out for determination of glycogen as per the method described by Montgomery. Results Silymarin 200 mg/kg treatment with Dexamethasone significantly inhibited the dexamethasone induced increase in serum glucose, triglyceride level, insulin secretion and reduction in body weight. After 21 days increase in serum glucose and insulin levels in fructose feeding rats was significantly decreased in group treated with Silymarin 200 mg/kg. Silymarin treatment to fructose fed rats increases glycogen levels of tissue compared to fructose control group Conclusion Silymarin might improve insulin resistance through enhanced insulin sensitivity in peripheral tissues. The results obtained in the present investigation indicate that silyamarin may have considerable therapeutic potential in the treatment of insulin resistance in NIDDM and its complications. Keywords: Dexamethasone, Silymarin, Insulin resistance, fructose , Diabetes mellitus Â&nbsp

Amyotrophic lateral sclerosis

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