title: Abrogation of maternal and fetal oxidative stress in the streptozotocin-induced diabetic rat by dietary supplements of Tinospora cordifolia.
abstract: OBJECTIVE
  Diabetes during pregnancy increases the incidences of congenital anomalies, morbidity, and mortality in the mother and her fetus/newborn. Oxidative stress (OS) has been implicated to be responsible because various antioxidants have been demonstrated to be beneficial in diabetic embryopathy. In this study, we examined the propensity of Tinospora cordifolia (TC) to attenuate embryopathy and OS in pregnant diabetic rats.
  
  
  METHODS
  Pregnant rats were rendered diabetic with streptozotocin (45 mg/kg of body weight, on gestation day 4) and fed a normal or a TC-supplemented (1% or 2%) diet. After monitoring diet intake, body weight gain, and urine output, dams were sacrificed on gestation day 20 and the markers of OS were determined in the maternal liver and the fetal brain and liver.
  
  
  RESULTS
  Although streptozotocin induced a significant (40%) increase in embryopathy, the dietary supplements offered significant protection (63%). Interestingly, TC significantly offset the diabetes-associated OS in the maternal liver as evidenced by the lower levels of malondialdehyde (25%) and reactive oxygen species (72%) and the higher levels of glutathione (53%) and total thiols (45%). The protective effects of TC could be observed even in the fetal milieu, with higher levels of antioxidant molecules and enzymes.
  
  
  CONCLUSIONS
  These data suggest that TC during pregnancy may provide significant protection against diabetes-induced OS and thus serve as an effective therapeutic supplement.
authors.affiliation: Department of Biochemistry and Nutrition, Central Food Technological Research Institute, Mysore, Karnataka, India. shivanm@ccf.org
authors.forename: Mahesh Mysore
authors.initials: MM
authors.lastname: Shivananjappa
authors.lastname: Muralidhara
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001786:Blood Glucose / Q000187:drug effects; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000188:drug therapy* / Q000503:physiopathology; D004032:Diet; D019587:Dietary Supplements; D005260:Female; D005315:Fetal Diseases / Q000188:drug therapy / Q000517:prevention & control; D005978:Glutathione / Q000097:blood; D005979:Glutathione Peroxidase / Q000097:blood; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D018384:Oxidative Stress / Q000187:drug effects*; D010936:Plant Extracts / Q000494:pharmacology*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000139:chemically induced / Q000188:drug therapy* / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D013482:Superoxide Dismutase / Q000097:blood; D031610:Tinospora / Q000737:chemistry*
chemical_list: D000975:Antioxidants; D001786:Blood Glucose; D010936:Plant Extracts; D017382:Reactive Oxygen Species; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione