Increased nitrotyrosine in the diabetic placenta: Evidence for oxidative stress

Fiona Lyall, Janice L. Glbson, Ian A. Greer, Diane E. Brockman, Annie L W Eis, Leslie Myatt

Research output: Contribution to journalArticle

91 Citations (Scopus)

Abstract

Original languageEnglish
Pages (from-to)1753-1758
Number of pages6
JournalDiabetes Care
Volume21
Issue number10
DOIs
StatePublished - 1998
Externally publishedYes

Fingerprint

Placenta
Oxidative Stress
Nitric Oxide Synthase Type III
Superoxide Dismutase
Vascular Endothelium
Nitric Oxide Synthase Type II
Superoxides
Blood Vessels
Pregnancy in Diabetics
Pregnancy
Peroxynitrous Acid
Trophoblasts
Type 1 Diabetes Mellitus
Endothelium
3-nitrotyrosine
Nitric Oxide
Research Design
Staining and Labeling
Antibodies

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

Lyall, F., Glbson, J. L., Greer, I. A., Brockman, D. E., Eis, A. L. W., & Myatt, L. (1998). Increased nitrotyrosine in the diabetic placenta: Evidence for oxidative stress. Diabetes Care, 21(10), 1753-1758. https://doi.org/10.2337/diacare.21.10.1753

Increased nitrotyrosine in the diabetic placenta : Evidence for oxidative stress. / Lyall, Fiona; Glbson, Janice L.; Greer, Ian A.; Brockman, Diane E.; Eis, Annie L W; Myatt, Leslie.

In: Diabetes Care, Vol. 21, No. 10, 1998, p. 1753-1758.

Research output: Contribution to journalArticle

Lyall, F, Glbson, JL, Greer, IA, Brockman, DE, Eis, ALW & Myatt, L 1998, 'Increased nitrotyrosine in the diabetic placenta: Evidence for oxidative stress', Diabetes Care, vol. 21, no. 10, pp. 1753-1758. https://doi.org/10.2337/diacare.21.10.1753
Lyall, Fiona ; Glbson, Janice L. ; Greer, Ian A. ; Brockman, Diane E. ; Eis, Annie L W ; Myatt, Leslie. / Increased nitrotyrosine in the diabetic placenta : Evidence for oxidative stress. In: Diabetes Care. 1998 ; Vol. 21, No. 10. pp. 1753-1758.
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title = "Increased nitrotyrosine in the diabetic placenta: Evidence for oxidative stress",
abstract = "OBJECTIVE - To evaluate the presence of nitrotyrosine (NT) residues in placental villous tissue of diabetic pregnancies as an index of vascular damage linked to oxidative stress. RESEARCH DESIGN AND METHODS - Villous tissue was collected and flash frozen after delivery from 10 class C and D IDDM patients (37.9 ± 3.2 weeks) and 10 normotensive pregnant individuals (37.5 ± 3.8 weeks). Serial sections of tissue were immunostained with specific antibodies to NT, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), and manganese superoxide dismutase (MnSOD). Sections were scored for intensity of immunostaining (0-3) by three observes blinded to the identity of tissue. RESULTS - All tissues demonstrated immunostaining for eNOS in both syncytiotrophoblast and stem villous vascular endothelium with no apparent differences between groups. Immunostaining for iNOS was seen in the villous stroma, but again was no different between the two groups. Significantly more intense NT staining was apparent in vascular endothelium and villous stroma (both P < 0.02) of diabetic placentas. The endothelium of large villous vessels of diabetic tissues also showed more intense immunostaining for MnSOD (P < 0.01). CONCLUSIONS - In these diabetic pregnancies, we were unable to show increased eNOS, unlike previous findings in preeclamptic pregnancies. The presence of NT may indicate vascular damage in the diabetic placenta due to peroxynitrite action formed from increased synthesis/interaction of nitric oxide and superoxide. The apparently paradoxical increase in MnSOD expression may be an adaptive response to increased superoxide generation.",
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T1 - Increased nitrotyrosine in the diabetic placenta

T2 - Evidence for oxidative stress

AU - Lyall, Fiona

AU - Glbson, Janice L.

AU - Greer, Ian A.

AU - Brockman, Diane E.

AU - Eis, Annie L W

AU - Myatt, Leslie

PY - 1998

Y1 - 1998

N2 - OBJECTIVE - To evaluate the presence of nitrotyrosine (NT) residues in placental villous tissue of diabetic pregnancies as an index of vascular damage linked to oxidative stress. RESEARCH DESIGN AND METHODS - Villous tissue was collected and flash frozen after delivery from 10 class C and D IDDM patients (37.9 ± 3.2 weeks) and 10 normotensive pregnant individuals (37.5 ± 3.8 weeks). Serial sections of tissue were immunostained with specific antibodies to NT, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), and manganese superoxide dismutase (MnSOD). Sections were scored for intensity of immunostaining (0-3) by three observes blinded to the identity of tissue. RESULTS - All tissues demonstrated immunostaining for eNOS in both syncytiotrophoblast and stem villous vascular endothelium with no apparent differences between groups. Immunostaining for iNOS was seen in the villous stroma, but again was no different between the two groups. Significantly more intense NT staining was apparent in vascular endothelium and villous stroma (both P < 0.02) of diabetic placentas. The endothelium of large villous vessels of diabetic tissues also showed more intense immunostaining for MnSOD (P < 0.01). CONCLUSIONS - In these diabetic pregnancies, we were unable to show increased eNOS, unlike previous findings in preeclamptic pregnancies. The presence of NT may indicate vascular damage in the diabetic placenta due to peroxynitrite action formed from increased synthesis/interaction of nitric oxide and superoxide. The apparently paradoxical increase in MnSOD expression may be an adaptive response to increased superoxide generation.

AB - OBJECTIVE - To evaluate the presence of nitrotyrosine (NT) residues in placental villous tissue of diabetic pregnancies as an index of vascular damage linked to oxidative stress. RESEARCH DESIGN AND METHODS - Villous tissue was collected and flash frozen after delivery from 10 class C and D IDDM patients (37.9 ± 3.2 weeks) and 10 normotensive pregnant individuals (37.5 ± 3.8 weeks). Serial sections of tissue were immunostained with specific antibodies to NT, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), and manganese superoxide dismutase (MnSOD). Sections were scored for intensity of immunostaining (0-3) by three observes blinded to the identity of tissue. RESULTS - All tissues demonstrated immunostaining for eNOS in both syncytiotrophoblast and stem villous vascular endothelium with no apparent differences between groups. Immunostaining for iNOS was seen in the villous stroma, but again was no different between the two groups. Significantly more intense NT staining was apparent in vascular endothelium and villous stroma (both P < 0.02) of diabetic placentas. The endothelium of large villous vessels of diabetic tissues also showed more intense immunostaining for MnSOD (P < 0.01). CONCLUSIONS - In these diabetic pregnancies, we were unable to show increased eNOS, unlike previous findings in preeclamptic pregnancies. The presence of NT may indicate vascular damage in the diabetic placenta due to peroxynitrite action formed from increased synthesis/interaction of nitric oxide and superoxide. The apparently paradoxical increase in MnSOD expression may be an adaptive response to increased superoxide generation.

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