title: Therapeutic potential of different commercially available synbiotic on acetaminophen-induced uremic rats.
abstract: BACKGROUND
  Currently kidney disease appears a foremost problem across the world. Acetaminophen is a commonly used antipyretic agent, which in high doses, causes uremia and used for experimentally induction of kidney disease. Bacteriotherapy affords a promising approach to mitigate uremic toxins by ingestion of urease positive bacteria, probiotics and symbiotic able to catabolize uremic solutes within the gut. The present study evaluates the effect of seven commercial symbiotic on kidney disease.
  
  
  METHODS
  Fifty-four albino male rats were randomly divided into nine groups. Control group (Group-I) received distilled water interperitoneally for 7 days. Positive control group (Group-II) received 500 mg/kg acetaminophen interperitoneally for 7 days. Commercially available seven symbiotic combinations at a dose of 10(9)cells/day for 3 weeks was administered to the tested groups (Group III-IX) after receiving 500 mg/kg/day acetaminophen interperitoneally for 7 days. Blood, kidney, liver and stool samples were collected after scarification for biochemical tests and DNA fragmentation assay of kidney tissue, kidney histological studies. Limited fecal analysis was conducted.
  
  
  RESULTS
  Blood urea nitrogen and toxicity indicators were increased, and antioxidant enzymes were decreased in Group-II. Blood urea nitrogen, toxicity indicators, glomerular necrosis, DNA damage of kidney tissue were reduced, and antioxidant enzymes were increased significantly in the treated Groups IV and IX (p < 0.05) in response to Group-II. Number of pathogenic bacteria decreased in synbiotic treated groups than Group I and II.
  
  
  CONCLUSIONS
  The study demonstrated that some of commercial symbiotic combination can reduce the sever effect of kidney disease.
authors.affiliation: Department of Microbiology, Nutrition, and Human Physiology, Raja N L Khans Women's College, Midnapore, 721102, West Bengal, India.
authors.forename: Arpita
authors.initials: A
authors.lastname: Mandal
authors.forename: Arpita
authors.initials: A
authors.lastname: Patra
authors.forename: Shreya
authors.initials: S
authors.lastname: Mandal
authors.forename: Suchismita
authors.initials: S
authors.lastname: Roy
authors.forename: Shreya Das
authors.initials: SD
authors.lastname: Mahapatra
authors.forename: Tapasi Das
authors.initials: TD
authors.lastname: Mahapatra
authors.forename: Tanmay
authors.initials: T
authors.lastname: Paul
authors.forename: Koushik
authors.initials: K
authors.lastname: Das
authors.forename: Keshab Chandra
authors.initials: KC
authors.lastname: Mondal
authors.forename: Dilip Kumar
authors.initials: DK
authors.lastname: Nandi
mesh_terms: D000082:Acetaminophen; D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D001806:Blood Urea Nitrogen; D002374:Catalase / Q000378:metabolism; D003404:Creatinine / Q000097:blood; D053938:DNA Fragmentation; D005243:Feces / Q000382:microbiology*; D005978:Glutathione / Q000378:metabolism; D007678:Kidney Glomerulus / Q000378:metabolism / Q000473:pathology*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009336:Necrosis / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D058616:Synbiotics / Q000008:administration & dosage*; D014508:Urea / Q000097:blood; D014511:Uremia / Q000097:blood / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology*
chemical_list: D000082:Acetaminophen; D008315:Malondialdehyde; D014508:Urea; D003404:Creatinine; D002374:Catalase; D013482:Superoxide Dismutase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D005978:Glutathione
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