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Free radical scavenging enzymes in fetal dysmorphogenesis among offspring of diabetic rats.
Teratology. 1997 Dec; 56(6):343-9.T

Abstract

Recent studies have suggested that the fetal dysmorphogenesis in diabetic pregnancies is associated with an increase in embryonic oxygen-free radicals. This excess of oxygen-free radicals may result from either overproduction or decreased clearance by the enzymatic scavenging mechanism. However, there are no in vivo data on the activity of embryonic oxygen-free radical scavenging enzymes. The purpose of the current study is to investigate whether this increase in embryonic oxygen-free radicals is the result of a change in the activity of the fetal oxygen-free radical scavenging/antioxidant enzymes during pregnancy complicated by maternal diabetes in an in vivo rat model. Thirty-six Sprague-Dawley rats were randomly assigned to one of two study groups: nondiabetic control and an untreated diabetic group. On day 12, fetuses were examined for crown-rump lengths, somite numbers, and external anomalies. The activity of fetal oxygen-free radical scavenging enzymes, including superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT), were determined. The untreated diabetic group of rats had a significantly higher mean blood glucose level than that of the nondiabetic controls and also a significantly lower weight gain, higher resorption rate, smaller embryonic size with lower total protein content, and a approximately 6-fold increase in the rate of fetal neural tube defects compared to the nondiabetic controls. Superoxide dismutase activity was significantly reduced in the embryos with neural tube defects regardless of maternal diabetic status (2.25 +/- 0.83 vs. 1.17 +/- 0.04 u/mg protein; P < 0.05). Glutathione peroxidase and catalase activity were significantly reduced in malformed versus normal-formed embryos of nondiabetic mothers (GPX-2.68 +/- 1.15 vs. 4.46 +/- 1.12 mu/mg protein, CAT -1.67 +/- 0.53 vs 2.49 +/- 0.61 u/mg protein respectively; P < 0.01). However, overall catalase activity was increased in embryos of diabetic mothers as compared to controls. Two-way analysis of variance identified fetal malformations as the variance associated with reduced fetal SOD activity, whereas maternal diabetes was associated with the increase in fetal catalase activity. Neither neural tube defect nor maternal diabetes was found to be the variable affecting fetal GPX activity, Fetal oxygen-free radical scavenging enzymes respond differently to the adverse environment created by maternal diabetes during pregnancy. Defects in embryonic SOD and catalase activity, regardless of maternal diabetic status, may reduce the ability of the fetus to clear free oxygen radicals, thereby exposing it to an increased oxidative load that may cause fetal dysmorphogenesis. The diabetic state of the mothers did not decrease embryonic activity of any of the scavenging enzymes. Therefore, although excess oxidative load, as observed in diabetes, may cause tissue injury and embryopathy, the mechanism does not appear to be a diabetes-induced reduction in the action of the scavenging enzymes.

Authors+Show Affiliations

Department of Obstetrics, Gynecology and Reproductive Sciences, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

9485543

Citation

Sivan, E, et al. "Free Radical Scavenging Enzymes in Fetal Dysmorphogenesis Among Offspring of Diabetic Rats." Teratology, vol. 56, no. 6, 1997, pp. 343-9.
Sivan E, Lee YC, Wu YK, et al. Free radical scavenging enzymes in fetal dysmorphogenesis among offspring of diabetic rats. Teratology. 1997;56(6):343-9.
Sivan, E., Lee, Y. C., Wu, Y. K., & Reece, E. A. (1997). Free radical scavenging enzymes in fetal dysmorphogenesis among offspring of diabetic rats. Teratology, 56(6), 343-9.
Sivan E, et al. Free Radical Scavenging Enzymes in Fetal Dysmorphogenesis Among Offspring of Diabetic Rats. Teratology. 1997;56(6):343-9. PubMed PMID: 9485543.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Free radical scavenging enzymes in fetal dysmorphogenesis among offspring of diabetic rats. AU - Sivan,E, AU - Lee,Y C, AU - Wu,Y K, AU - Reece,E A, PY - 1998/3/5/pubmed PY - 2000/6/20/medline PY - 1998/3/5/entrez SP - 343 EP - 9 JF - Teratology JO - Teratology VL - 56 IS - 6 N2 - Recent studies have suggested that the fetal dysmorphogenesis in diabetic pregnancies is associated with an increase in embryonic oxygen-free radicals. This excess of oxygen-free radicals may result from either overproduction or decreased clearance by the enzymatic scavenging mechanism. However, there are no in vivo data on the activity of embryonic oxygen-free radical scavenging enzymes. The purpose of the current study is to investigate whether this increase in embryonic oxygen-free radicals is the result of a change in the activity of the fetal oxygen-free radical scavenging/antioxidant enzymes during pregnancy complicated by maternal diabetes in an in vivo rat model. Thirty-six Sprague-Dawley rats were randomly assigned to one of two study groups: nondiabetic control and an untreated diabetic group. On day 12, fetuses were examined for crown-rump lengths, somite numbers, and external anomalies. The activity of fetal oxygen-free radical scavenging enzymes, including superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT), were determined. The untreated diabetic group of rats had a significantly higher mean blood glucose level than that of the nondiabetic controls and also a significantly lower weight gain, higher resorption rate, smaller embryonic size with lower total protein content, and a approximately 6-fold increase in the rate of fetal neural tube defects compared to the nondiabetic controls. Superoxide dismutase activity was significantly reduced in the embryos with neural tube defects regardless of maternal diabetic status (2.25 +/- 0.83 vs. 1.17 +/- 0.04 u/mg protein; P < 0.05). Glutathione peroxidase and catalase activity were significantly reduced in malformed versus normal-formed embryos of nondiabetic mothers (GPX-2.68 +/- 1.15 vs. 4.46 +/- 1.12 mu/mg protein, CAT -1.67 +/- 0.53 vs 2.49 +/- 0.61 u/mg protein respectively; P < 0.01). However, overall catalase activity was increased in embryos of diabetic mothers as compared to controls. Two-way analysis of variance identified fetal malformations as the variance associated with reduced fetal SOD activity, whereas maternal diabetes was associated with the increase in fetal catalase activity. Neither neural tube defect nor maternal diabetes was found to be the variable affecting fetal GPX activity, Fetal oxygen-free radical scavenging enzymes respond differently to the adverse environment created by maternal diabetes during pregnancy. Defects in embryonic SOD and catalase activity, regardless of maternal diabetic status, may reduce the ability of the fetus to clear free oxygen radicals, thereby exposing it to an increased oxidative load that may cause fetal dysmorphogenesis. The diabetic state of the mothers did not decrease embryonic activity of any of the scavenging enzymes. Therefore, although excess oxidative load, as observed in diabetes, may cause tissue injury and embryopathy, the mechanism does not appear to be a diabetes-induced reduction in the action of the scavenging enzymes. SN - 0040-3709 UR - https://www.unboundmedicine.com/medline/citation/9485543/Free_radical_scavenging_enzymes_in_fetal_dysmorphogenesis_among_offspring_of_diabetic_rats_ L2 - https://doi.org/10.1002/(SICI)1096-9926(199712)56:6&lt;343::AID-TERA1&gt;3.0.CO;2-X DB - PRIME DP - Unbound Medicine ER -