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      Metabolic Rates of 4-Hydroxynonenal in Tubular and Mesangial Cells of the Kidney

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          The degradation of the lipid peroxidation product 4-hydroxynonenal (HNE) in primary cultures of kidney tubular and mesangial cells was determined. Using various initial concentrations of the aldehyde a decline of cellular viability was found. Mesangial cells were more susceptible to the toxic effects of HNE. In consumption studies of HNE the decline of the exogenously added aldehyde was comparable in both cell types after addition of 10 and 1 µmol HNE/l. After addition of 100 µmol/l aldehyde a drastically lower HNE degrading capacity was found in mesangial cells as compared to tubular cells. The loss in the HNE degrading capacity was accompanied by an increased formation of HNE-protein aggregates as demonstrated by immunoblots. Therefore, we concluded that the low ability of mesangial cells to degrade HNE may be a factor of the toxicity of free radicals on the kidney.

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          Most cited references 3

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          Identification of metabolic pathways of the lipid peroxidation product 4-hydroxynonenal by mitochondria isolated from rat kidney cortex.

           O Ullrich,  T Grune,  W Henke (1994)
          The cytosolic lipid peroxidation product 4-hydroxynonenal (HNE) is rapidly metabolized in mitochondria isolated from rat kidney cortex. About 80% of HNE was degraded within 3 min of incubation. Main products of HNE which were identified in mitochondria were the hydroxynonenoic acid, the 1,4-dihydroxynonene and the glutathione-HNE-conjugate. Furthermore, formation of metabolites of the tricarboxylic acid cycle from HNE is suggested. The quantitative share of HNE binding to proteins was high with about 8% of total HNE consumption after 3 min of incubation. Therefore, rapid degradation of HNE by mitochondria might be involved in an intracellular antioxidative defense system.
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            The role of oxygen free radicals in the development of chronic renal failure

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              Prostaglandin synthesis is increased in selenium supplemented human mesangial cells despite suppression of phospholipase A2 - activity


                Author and article information

                Nephron Exp Nephrol
                Cardiorenal Medicine
                S. Karger AG
                February 1999
                14 January 1999
                : 7
                : 1
                : 59-62
                aClinics of Physical Medicine and Rehabilitation, Medical Faculty (Charité), Humboldt University, Berlin; bHerzog-Julius Hospital for Rheumatology and Orthopaedics, Bad Harzburg; cClinics of Urology, Medical Faculty (Charité), Humboldt University, Berlin, and dClinics of Nephrology, Medical Academy, Hannover, Germany
                20585 Exp Nephrol 1999;7:59–62
                © 1999 S. Karger AG, Basel

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                Figures: 4, Tables: 1, References: 28, Pages: 4
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