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Glutathione metabolism and oxidative stress in neonatal rat tissues from streptozotocin‐induced diabetic mothers
Author(s) -
Raza Haider,
John Annie
Publication year - 2004
Publication title -
diabetes/metabolism research and reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.307
H-Index - 110
eISSN - 1520-7560
pISSN - 1520-7552
DOI - 10.1002/dmrr.422
Subject(s) - glutathione , oxidative stress , endocrinology , medicine , diabetes mellitus , streptozotocin , fetus , pancreas , pregnancy , kidney , offspring , reactive oxygen species , antioxidant , chemistry , biology , biochemistry , enzyme , genetics
Abstract Background Diabetes in pregnancy has been reported to cause congenital malformations in the offspring. Hyperglycemia‐induced teratogenecity is related to the increased oxidative stress and depletion of glutathione (GSH) in fetal tissues. Methods In the present study, we have examined the levels of reactive oxygen species (ROS) and peroxide production in the tissues of neonatal rats and in the pancreas of diabetic mother rats. Diabetes was induced one day after pregnancy by a single injection of streptozotocin (60 mg/kg body weight). Different tissues from one‐day‐old neonates and the pancreas from the mothers were collected to study the level of oxidative stress and GSH metabolism. Results An increase in ROS and peroxide production was observed in the pancreas of diabetic rats and in the liver, kidney, brain and skin of the neonates of the diabetic mothers. The catalytic activity of cytochrome P450 2E1 (CYP2E1) was also increased in these tissues from diabetic rats. With the exception of the kidney, the GSH concentration was significantly lower in the tissues of neonates and in the pancreas of diabetic mothers. Conclusion This reduction in GSH concentration was presumably associated with its increased utilization, due to increased production of peroxides and also due to its reduced regeneration. The study may have an implication in understanding the pathology of diabetic complications in pregnancy and sensitivity toward antioxidant therapy during pregnancy. Copyright © 2004 John Wiley & Sons, Ltd.