Abstract
BackgroundGalactosamine (GalN), an established experimental toxin, mainly causes liver injury via the generation of free radicals and depletion of UTP nucleotides. Renal failure is often associated with end stage liver damage. GalN intoxication also induces renal dysfunction in connection with hepatic disorders. Present study was designed to find out the effect of a protein isolated from the leaves of the herb Cajanus indicus against GalN induced renal damage.MethodsBoth preventive as well as curative effect of the protein was investigated in the study. GalN was administered intraperitoneally at a dose of 800 mg/kg body weight for 3 days pre and post to protein treatment at an intraperitoneal dose of 2 mg/kg body weight for 4 days. The activities of antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR) and glutathione-S-transferase (GST), levels of cellular metabolites, reduced glutathione (GSH), total thiols, oxidized glutathione (GSSG) and lipid peroxidation end products were determined to estimate the status of the antioxidative defense system. In addition, serum creatinine and urea nitrogen (UN) levels were also measured as a marker of nephrotoxicity.ResultsResults showed that GalN treatment significantly increased the serum creatinine and UN levels compared to the normal group of mice. The extent of lipid peroxidation and the level of GSSG were also enhanced by the GalN intoxication whereas the activities of antioxidant enzymes SOD, CAT, GR and GST as well as the levels of total thiols and GSH were decreased in the kidney tissue homogenates. Protein treatment both prior and post to the toxin administration successfully altered the effects in the experimental mice.ConclusionOur study revealed that GalN caused a severe oxidative insult in the kidney. Protein treatment both pre and post to the GalN intoxication could protect the kidney tissue against GalN induced oxidative stress. As GalN induced severe hepatotoxicity followed by renal failure, the protective role of the protein against GalN induced renal damages is likely to be an indirect effect. Since the protein possess hepatoprotective activity, it may first ameliorate GalN-induced liver damage and consequently the renal disorders are reduced. To the best of our knowledge, this is probably the first report describing GalN-induced oxidative stress in renal damages and the protective role of a plant protein molecule against it.
Highlights
Galactosamine (GalN), an established experimental toxin, mainly causes liver injury via the generation of free radicals and depletion of UTP nucleotides
Effect on nephrotoxicity markers Creatinine levels The creatinine levels in serum obtained from the normal control mice, toxin control mice, mice treated separately with protein, vitamin E and Bovine serum albumin (BSA) followed by GalN intoxication, mice treated separately with protein, vitamin E after GalN intoxication and mice kept for normal recovery after GalN administration are shown in figure 1
It has been observed that patient suffering with liver disease have a decrease in renal blood flow, indicating renal vasoconstriction and this effect is more prominent in those people affected with hepatorenal syndrome (HRS) [49]
Summary
Galactosamine (GalN), an established experimental toxin, mainly causes liver injury via the generation of free radicals and depletion of UTP nucleotides. Renal failure is often associated with end stage liver damage. Javle et al reported that GalN-induced liver injury is associated with the development of renal failure [6]. A very recent report of Anand et al revealed that renal failure appeared with acute liver damage where the histological status of the kidney was normal but the renal blood flow was decreased [8]. Oxidative stress has been reported as one of the major causes in GalN induced liver damages [9,10,11], it is not, clear whether GalN-induced renal disorders occur via the generation of reactive oxygen species followed by oxidative stress in the kidney or not
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
