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Article: Decrease in myocardial antioxidant capacity and cardiac function precedes oxidative stress-mediated lipid peroxidation damage in early stage diabetic rats

TitleDecrease in myocardial antioxidant capacity and cardiac function precedes oxidative stress-mediated lipid peroxidation damage in early stage diabetic rats
Authors
KeywordsAntioxidant Capacity
Cardiac Function
Diabetic Rats
Lipid Peroxidation
Issue Date2010
Citation
Medical Journal Of Wuhan University, 2010, v. 31 n. 1, p. 16-18+99 How to Cite?
AbstractObjective: To investigate the changes of myocardial antioxidant capacity and its relationship with cardiac function and reactive oxygen species mediated lipid peroxidation production in rats with early stage diabetes. Methods: Sixteen Wistar rats were randomly assigned to non-diabetic control group (n=8) and diabetic group. Diabetes were induced by a single intravenous injection of streptozotocin (60 mg/kg). Four weeks after the establishment of diabetes, cardiac function, myocardial antioxidant capacity and lipid peroxidation product 15-2t-Isoprostane as well as plasma total antioxidant concentration were assessed. Results: As compared to the control group, plasma and cardiac level of 15-F2t-Isoprostane did not increase in the 4 week diabetic rats. However, my-ocardial antioxidant capacity was decreased in the diabetic rats, which was reflected by the increased production of TBARS (thiobartituric acid reactive substances) when heart tissue was subjected to in vitro challenge to the oxidant t-butylhydroperoxide (P<0. 05), accompanied with reduced cardiac ejection fraction (P<0.05 vs control). Conclusion: Decrease in myocardial antioxidant capacity and cardiac function precedes oxidative stress-mediated lipid peroxidation damage in early stage diabetes in rats.
Persistent Identifierhttp://hdl.handle.net/10722/147273
ISSN
2023 SCImago Journal Rankings: 0.111
References

 

DC FieldValueLanguage
dc.contributor.authorXu, Ben_US
dc.contributor.authorLei, Sen_US
dc.contributor.authorLiu, Hen_US
dc.contributor.authorXu, Jen_US
dc.contributor.authorXia, Zen_US
dc.contributor.authorXia, Zen_US
dc.date.accessioned2012-05-29T06:01:10Z-
dc.date.available2012-05-29T06:01:10Z-
dc.date.issued2010en_US
dc.identifier.citationMedical Journal Of Wuhan University, 2010, v. 31 n. 1, p. 16-18+99en_US
dc.identifier.issn1671-8852en_US
dc.identifier.urihttp://hdl.handle.net/10722/147273-
dc.description.abstractObjective: To investigate the changes of myocardial antioxidant capacity and its relationship with cardiac function and reactive oxygen species mediated lipid peroxidation production in rats with early stage diabetes. Methods: Sixteen Wistar rats were randomly assigned to non-diabetic control group (n=8) and diabetic group. Diabetes were induced by a single intravenous injection of streptozotocin (60 mg/kg). Four weeks after the establishment of diabetes, cardiac function, myocardial antioxidant capacity and lipid peroxidation product 15-2t-Isoprostane as well as plasma total antioxidant concentration were assessed. Results: As compared to the control group, plasma and cardiac level of 15-F2t-Isoprostane did not increase in the 4 week diabetic rats. However, my-ocardial antioxidant capacity was decreased in the diabetic rats, which was reflected by the increased production of TBARS (thiobartituric acid reactive substances) when heart tissue was subjected to in vitro challenge to the oxidant t-butylhydroperoxide (P<0. 05), accompanied with reduced cardiac ejection fraction (P<0.05 vs control). Conclusion: Decrease in myocardial antioxidant capacity and cardiac function precedes oxidative stress-mediated lipid peroxidation damage in early stage diabetes in rats.en_US
dc.languageengen_US
dc.relation.ispartofMedical Journal of Wuhan Universityen_US
dc.subjectAntioxidant Capacityen_US
dc.subjectCardiac Functionen_US
dc.subjectDiabetic Ratsen_US
dc.subjectLipid Peroxidationen_US
dc.titleDecrease in myocardial antioxidant capacity and cardiac function precedes oxidative stress-mediated lipid peroxidation damage in early stage diabetic ratsen_US
dc.typeArticleen_US
dc.identifier.emailXia, Z:zyxia@hkucc.hku.hken_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.scopuseid_2-s2.0-77950152616en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77950152616&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume31en_US
dc.identifier.issue1en_US
dc.identifier.spage16en_US
dc.identifier.epage18+99en_US
dc.identifier.issnl1671-8852-

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