Alterations in renal mitochondrial respiration in response to the reactive oxoaldehyde methylglyoxal

Mariana G. Rosca, Vincent M. Monnier, Luke I. Szweda, Miriam F. Weiss

Research output: Contribution to journalArticle

86 Scopus citations

Abstract

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. 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.

Original languageEnglish (US)
Pages (from-to)F52-F59
JournalAmerican Journal of Physiology - Renal Physiology
Volume283
Issue number1 52-1
DOIs
StatePublished - 2002

Keywords

  • Diabetic nephropathy
  • Dicarbonyl
  • Mitochondria

ASJC Scopus subject areas

  • Physiology
  • Urology

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