Fatty acid metabolism in renal ischemia

Ruidera, E; Irazú, Carlos E.; Rajagopalan, P. R.; Orak, John K.; Fitts, Charles T.; Singh, Inderjit

doi:10.1007/bf02536209

Cited by 32 publications

(27 citation statements)

References 28 publications

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“…Excessive parenchymal accumulation of FFAs stimulates their oxidation to lipid peroxides. Tissue levels of lipid peroxides in kidneys explanted from rats subjected to renal ischemia are about 2.5-fold higher than in control animals (89).…”

Section: Ischemic Akimentioning

confidence: 73%

“…Ruidera et al showed that renal ischemia impairs FAO in both organelles, mitochondria and peroxisomes. The study demonstrated a comparable loss of FAO activity for short-, long-, and very long-chain fatty acids and an equal degree of mitochondrial and peroxisomal FAO dysfunction (89). Sixty minutes of renal ischemia reduces the activity of FAO almost by 70 percent.…”

Section: Ischemic Akimentioning

confidence: 75%

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Peroxisomes and Kidney Injury

Vasko

2016

Antioxidants & Redox Signaling

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Significance: Peroxisomes are organelles present in most eukaryotic cells. The organs with the highest density of peroxisomes are the liver and kidneys. Peroxisomes possess more than fifty enzymes and fulfill a multitude of biological tasks. They actively participate in apoptosis, innate immunity, and inflammation. In recent years, a considerable amount of evidence has been collected to support the involvement of peroxisomes in the pathogenesis of kidney injury. Recent Advances: The nature of the two most important peroxisomal tasks, betaoxidation of fatty acids and hydrogen peroxide turnover, functionally relates peroxisomes to mitochondria. Further support for their communication and cooperation is furnished by the evidence that both organelles share the components of their division machinery. Until recently, the majority of studies on the molecular mechanisms of kidney injury focused primarily on mitochondria and neglected peroxisomes. Critical Issues: The aim of this concise review is to introduce the reader to the field of peroxisome biology and to provide an overview of the evidence about the contribution of peroxisomes to the development and progression of kidney injury. The topics of renal ischemia-reperfusion injury, endotoxin-induced kidney injury, diabetic nephropathy, and tubulointerstitial fibrosis, as well as the potential therapeutic implications of peroxisome activation, are addressed in this review. Future Directions: Despite recent progress, further studies are needed to elucidate the molecular mechanisms induced by dysfunctional peroxisomes and the role of the dysregulated mitochondria-peroxisome axis in the pathogenesis of renal injury. Antioxid. Redox Signal. 25, 217-231.

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Section: Ischemic Akimentioning

confidence: 73%

Section: Ischemic Akimentioning

confidence: 75%

Peroxisomes and Kidney Injury

Vasko

2016

Antioxidants & Redox Signaling

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“…Additionally, in our laboratory we have recently identified glutathione peroxidase and Mn SOD in peroxisomal fractions [22]. We have previously shown that ischemia-reperfusion injury has significant effects on the structure of peroxisomes and the ensuing oxidative damage leads to loss of peroxisomal function [24,25]. In this study we evaluated the effect of a sublethal dose of endotoxin on peroxisomal antioxidant enzyme function (the enzymatic activities of catalase, superoxide dismutase, and glutathione peroxidase), in the absence of any additional oxidative insult.…”

Section: Introductionmentioning

confidence: 97%

Peroxisomal participation in the cellular response to the oxidative stress of endotoxin

1993

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Exposure to a sublethal dose of endotoxin offers protection against subsequent oxidative stresses. The cellular mechanisms involved in generating this effect are not well understood. We evaluated the effect of endotoxin on antioxidant enzymes in liver peroxisomes. Peroxisomes have recently been shown to contain superoxide dismutase (SOD) and glutathione peroxidase (GPX) in addition to catalase. Peroxisomes were isolated from liver homogenates by differential and density gradient centrifugations. Endotoxin treatment increased the specific activity of SOD and GPX in peroxisomes to 208% and 175% of control activity, respectively. These findings correlated with increases in peroxisomal SOD and GPX proteins observed by immunoblot. Although the quantity of catalase protein was increased when assessed by immunoblot analysis, the specific activity of catalase was decreased to 68% of control activity. Activation of catalase with ethanol only restored catalase activity to control levels suggesting that catalase had undergone irreversible inactivation. The observed increase in GPX activity may represent a compensatory mechanism triggered by accumulating H2O2. The data presented here suggest for the first time that mammalian peroxisomal antioxidant enzymes are altered during the oxidative injury of endotoxin treatment.

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“…In general, the cellular free PUFA levels in normal tissues are low and almost undetectable. However, in inflamed tissues, such as alcoholic fatty liver and during renal ischemia, the free fatty acids level can be highly elevated (Mavrelis et al, 1983;Ruidera et al, 1988). In certain situations, the AA level can go up to 100 μM (Brash, 2001).…”

Section: Introductionmentioning

confidence: 98%