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Renal Oxidative Stress Induced by Long-Term Hyperuricemia Alters Mitochondrial Function and Maintains Systemic Hypertension
المؤلفون المشاركون
Zazueta, Cecilia
Johnson, Richard J.
García-Arroyo, Fernando Enrique
Cristóbal-García, Magdalena
Sánchez-Lozada, Laura Gabriela
Madero, Magdalena
Rodríguez-Iturbe, Bernardo
Correa, Francisco
Tapia, Edilia
Pedraza-Chaverri, José
Arellano, Abraham
Osorio, Horacio
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2015، العدد 2015 (31 ديسمبر/كانون الأول 2015)، ص ص. 1-8، 8ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2015-03-31
دولة النشر
مصر
عدد الصفحات
8
التخصصات الرئيسية
الملخص EN
We addressed if oxidative stress in the renal cortex plays a role in the induction of hypertension and mitochondrial alterations in hyperuricemia.
A second objective was to evaluate whether the long-term treatment with the antioxidant Tempol prevents renal oxidative stress, mitochondrial alterations, and systemic hypertension in this model.
Long-term (11-12 weeks) and short-term (3 weeks) effects of oxonic acid induced hyperuricemia were studied in rats (OA, 750 mg/kg BW), OA+Allopurinol (AP, 150 mg/L drinking water), OA+Tempol (T, 15 mg/kg BW), or vehicle.
Systolic blood pressure, renal blood flow, and vascular resistance were measured.
Tubular damage (urine N-acetyl-β-D-glucosaminidase) and oxidative stress markers (lipid and protein oxidation) along with ATP levels were determined in kidney tissue.
Oxygen consumption, aconitase activity, and uric acid were evaluated in isolated mitochondria from renal cortex.
Short-term hyperuricemia resulted in hypertension without demonstrable renal oxidative stress or mitochondrial dysfunction.
Long-term hyperuricemia induced hypertension, renal vasoconstriction, tubular damage, renal cortex oxidative stress, and mitochondrial dysfunction and decreased ATP levels.
Treatments with Tempol and allopurinol prevented these alterations.
Renal oxidative stress induced by hyperuricemia promoted mitochondrial functional disturbances and decreased ATP content, which represent an additional pathogenic mechanism induced by chronic hyperuricemia.
Hyperuricemia-related hypertension occurs before these changes are evident.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Cristóbal-García, Magdalena& García-Arroyo, Fernando Enrique& Tapia, Edilia& Osorio, Horacio& Arellano, Abraham& Madero, Magdalena…[et al.]. 2015. Renal Oxidative Stress Induced by Long-Term Hyperuricemia Alters Mitochondrial Function and Maintains Systemic Hypertension. Oxidative Medicine and Cellular Longevity،Vol. 2015, no. 2015, pp.1-8.
https://search.emarefa.net/detail/BIM-1075685
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Cristóbal-García, Magdalena…[et al.]. Renal Oxidative Stress Induced by Long-Term Hyperuricemia Alters Mitochondrial Function and Maintains Systemic Hypertension. Oxidative Medicine and Cellular Longevity No. 2015 (2015), pp.1-8.
https://search.emarefa.net/detail/BIM-1075685
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Cristóbal-García, Magdalena& García-Arroyo, Fernando Enrique& Tapia, Edilia& Osorio, Horacio& Arellano, Abraham& Madero, Magdalena…[et al.]. Renal Oxidative Stress Induced by Long-Term Hyperuricemia Alters Mitochondrial Function and Maintains Systemic Hypertension. Oxidative Medicine and Cellular Longevity. 2015. Vol. 2015, no. 2015, pp.1-8.
https://search.emarefa.net/detail/BIM-1075685
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1075685
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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