title: Oxidative stress in urogenital tuberculosis patients: a predisposing factor for renal stone formation--amelioration by vitamin E supplementation.
abstract: BACKGROUND
  Previous studies have shown that urogenital tuberculosis (GuTb) patients treated or untreated with regular anti-Tb regimen excrete comparatively high levels of urinary stone forming constituents than normal subjects. Enhanced oxidative stress is also considered as a prime factor that accelerates urolithiasis. The present study was aimed to determine antioxidant status and lipid peroxidation of these individuals in order to assess their risk for kidney stone formation.
  
  
  METHODS
  GuTb patients and age-matched normal subjects were divided into four groups: I: normal subjects (n=60), II: GuTb patients a day before treatment (n=72), III: GuTb patients after treatment with isoniazid (300 mg), rifampicin (450 mg) and pyrazinamide (1.5 g) per day for 60 days (n=42), and IV: GuTb patients supplemented with vitamin E (200 mg/day) along with regular chemotherapy for 60 days (n=30). Blood was collected and tested for various markers of oxidative stress.
  
  
  RESULTS
  Increased levels of lipid peroxidation, protein carbonyls (PCO), advanced oxidative protein products (AOPP) and reduced antioxidant defenses by impairment in enzyme activities like superoxide dismutase, catalase, glutathione peroxidase, reduced glutathione and decreased plasma concentrations of non enzymatic antioxidants like vitamins C and E were observed in the treated and untreated GuTb patients.
  
  
  CONCLUSIONS
  These biochemical disparities may lead to membrane disintegrity, which is favorable for retention of mirolithis. Advocation of vitamin E enhanced the antioxidant status of the plasma, thereby preventing membrane injury, consequently reducing the risk of stone formation in urogenital tuberculosis patients, who were treated with their routine anti-tuberculosis drug regimen.
authors.affiliation: Department of Medical Biochemistry, Dr. A.L. Mudaliar Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani, Chennai 600 113, India.
authors.forename: S
authors.initials: S
authors.lastname: Srinivasan
authors.forename: V
authors.initials: V
authors.lastname: Pragasam
authors.forename: X
authors.initials: X
authors.lastname: Jenita
authors.forename: P
authors.initials: P
authors.lastname: Kalaiselvi
authors.forename: V
authors.initials: V
authors.lastname: Muthu
authors.forename: P
authors.initials: P
authors.lastname: Varalakshmi
mesh_terms: D000975:Antioxidants / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D005260:Female; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006801:Humans; D007669:Kidney Calculi / Q000209:etiology / Q000517:prevention & control*; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D013482:Superoxide Dismutase / Q000378:metabolism; D016896:Treatment Outcome; D014401:Tuberculosis, Urogenital / Q000150:complications* / Q000378:metabolism; D014810:Vitamin E / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D000975:Antioxidants; D014810:Vitamin E; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione; D001205:Ascorbic Acid