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Objective:To better investigate the protective role of branched-chain amino acids (BCAAs) and Cymbopogon schoenanthus (CS) extract against the potassium dichromate (PDC)-induced oxido-nitrosative nephrotoxic insult in the experimental rat model.Methods:Thirty male rats were randomly divided into five equal groups: The 1st group served as control; the 2Results:The PDC-induced nephrotoxic effect caused a depletion of renal oxidative scavengers glutathione, superoxide dismutase with consequent lipo-oxidative cellular membrane deterioration manifested by a rise in malonaldehyde, oxidized glutathione, myeloperoxidase and the concomitant increase in inflammatory response elements tumor necrosis factor α, nitric oxide, and interleukin 1 β. Moreover, the comet assay and increased 8-hydroxy-2-deoxyguanosine proved an accelerated apoptotic DNA fragmentation. These local renal changes were met with global altered blood biochemistry. The BCAAs and CS or their compiled administration showed an ameliorative effect against PDC-induced nephrotoxic in a synergistic pattern.Conclusions:Both BCAAs and CS or their combined administration afford potential competitors against renal insult induced by polyvalent anion pollutants in experimentally studied animals model. As a route for novel drug discovery, further investigation should be attempted to optimize their augmenting reno-protecting potential.
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OBJECTIVE@#To compare the degree of ameliorative effects of Melatonin (MEL), Ursodeoxycholic acid (UDCA) and Balanites aegyptiaca (BA) against hepatotoxicity induced by MTX for one month.@*METHODS@#Eighty adult male rats (Sprague Dawely) weighing (190 ± 10 g), were randomly divided into eight equal groups: Control, MTX, MEL, BA, UDCA, MTX + MEL, MTX + BA, MTX + UDCA. Liver function biomarker enzymes, liver tissue oxidative stress parameters, together with total antioxidant capacity and tumor necrosis factor (TNF-α) were determined. Histopathological and immunohistochemistry examinations for TNF-α were also done.@*RESULTS@#MTX showed significant increase in alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT), total and direct bilirubin, as well as TNF-α levels, oxidized glutathione (GSSG), malodialdehyde (MDA) and nitric oxide (NO). Whereas total protein, albumin, total antioxidant capacity, reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT) levels were significantly decreased in MTX treated group. These alterations were improved by MEL and BA treatment, whereas no improvement was noticed in UDCA treatment.@*CONCLUSIONS@#BA may be as promising as MEL in the hepatoprotection against MTX toxicity through their antioxidant and radical scavenging activities. In addition, it is not recommended to co-administer UDCA with MTX as it enhanced inflammation and damage to the liver.
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Objective To compare the degree of ameliorative effects of Melatonin (MEL), Ursodeoxycholic acid (UDCA) and Balanites aegyptiaca (BA) against hepatotoxicity induced by MTX for one month. Methods Eighty adult male rats (Sprague Dawely) weighing (190 ± 10 g), were randomly divided into eight equal groups: Control, MTX, MEL, BA, UDCA, MTX + MEL, MTX + BA, MTX + UDCA. Liver function biomarker enzymes, liver tissue oxidative stress parameters, together with total antioxidant capacity and tumor necrosis factor (TNF-α) were determined. Histopathological and immunohistochemistry examinations for TNF-α were also done. Results MTX showed significant increase in alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT), total and direct bilirubin, as well as TNF-α levels, oxidized glutathione (GSSG), malodialdehyde (MDA) and nitric oxide (NO). Whereas total protein, albumin, total antioxidant capacity, reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT) levels were significantly decreased in MTX treated group. These alterations were improved by MEL and BA treatment, whereas no improvement was noticed in UDCA treatment. Conclusions BA may be as promising as MEL in the hepatoprotection against MTX toxicity through their antioxidant and radical scavenging activities. In addition, it is not recommended to co-administer UDCA with MTX as it enhanced inflammation and damage to the liver.