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Am J Physiol Renal Physiol (January 29, 2002). doi:10.1152/ajprenal.00302.2001
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Articles in PresS, published online ahead of print January 28, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00302.2001
Submitted on September 25, 2001
Accepted on January 24, 2002

Structural and Functional Alterations in Renal Mitochondrial Respiration in Response to the Reactive Oxaldehyde Methylglyoxal

Mariana G Rosca1, Vincent M Monnier2, Luke I Szweda3, and Miriam F Weiss4*

1 Department of Pathophysiology, University of Medicine and Pharmacy of Iasi, Iasi, Romania
2 Institute of Pathology and Department of Biochemistry, Case Western Reserve University, Cleveland, Ohio, USA
3 Department of Physiology, Case Western Reserve University, Cleveland, Ohio, USA
4 Department of Internal Medicine, Case Western Reserve University, Cleveland, Ohio, USA

Chronic hyperglycemia has been linked to alterations in mitochondrial function, suggesting an important role in the pathophysiology of the complications of diabetes mellitus. In the diabetic kidney, ultrastructural changes in mitochondria are associated with impaired tubular function. The goal of this study was to determine if methylglyoxal (MGO), a dicarbonyl compound reaching high levels in hyperglycemic conditions, has direct toxicity for renal mitochondria. Intact mitochondria isolated from the renal cortex of rats were incubated with MGO to determine (1) its effect on mitochondrial respiration, (2) the conditions under which MGO exerts these effects, and (3) the potential mitochondrial targets of MGO influence. This study demonstrates that MGO has an inhibitory effect on both the tricarboxylic acid cycle and the electron respiratory chain (ERC). The modifications appear to be specific to certain mitochondrial proteins. Alterations of these proteins lead to disturbances in mitochondria that may play an important role in renal cellular toxicity and in the development of diabetic nephropathy.




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