Ischemia-reperfusion injury: Biochemical alterations in peroxisomes of rat kidney
References (51)
Am. J. Emerg. Med
(1983)- et al.
J. Lipid Res
(1985) - et al.
J. Biol. Chem
(1973) - et al.
J. Biol. Chem
(1951) Anal. Biochem
(1976)J. Biol. Chem
(1974)- et al.
Biochim. Biophys. Acta
(1988) - et al.
Exp. Mol. Pathol
(1977) - et al.
J. Biol. Chem
(1978) - et al.
Biochim. Biophys. Acta
(1960)
J. Mol. Cell. Cardiol
FEBS Lett
Clin. Chim. Acta
Am. J. Pathol
Biochem. J
Ann. Emerg. Med
Neurochem. Res
J. Clin. Invest
J. Clin. Invest
Am. J. Physiol
Eur. J. Cell Biol
Biochem. J
J. Cell Biol
Biochem. J
Cited by (59)
White shrimp Litopenaeus vannamei catalase: Gene structure, expression and activity under hypoxia and reoxygenation
2013, Comparative Biochemistry and Physiology Part - B: Biochemistry and Molecular BiologyCitation Excerpt :Anoxia and reoxygenation showed a specific behavior in catalase activity and other antioxidant enzymes in Carassius auratus; in liver, reoxygenation (14 h) after anoxia (8 h) induced catalase activity, while in kidney and muscle, the opposite occurred (Lushchak et al., 2001). In contrast to our results, in low oxygen availability, peroxisomes density and catalase activity decreased (43% less than control) and furthermore, the activity decreased even more after reperfusion in rat liver (Gulati et al., 1992), this might give insight about different responses of antioxidant systems to oxygen variability in vertebrates or terrestrial animals and crustaceans. In summary, the shrimp catalase gene is interrupted by four introns, is a very conserved protein with different responses in expression and activity in gills and hepatopancreas under hypoxic and reoxygenation conditions.
Kidney-specific overexpression of Sirt1 protects against acute kidney injury by retaining peroxisome function
2010, Journal of Biological ChemistryCitation Excerpt :Furthermore, Sirt1 has been reported to preserve mitochondria function by inducing PGC-1α, which increases mitochondrial number (10). Because both peroxisome and mitochondrial functions are compromised by pathophysiological conditions, including cisplatin-induced (11, 12) and ischemic/reperfusion (I/R)-induced acute kidney injury (AKI) (13, 14), it is anticipated that Sirt1 is capable of alleviating renal injury by modulating peroxisome and mitochondrial function. To examine the role of Sirt1 in renal tubules, we produced TG mice overexpressing Sirt1 specifically in proximal tubules.
A role of liver fatty acid-binding protein in cisplatin-induced acute renal failure
2007, Kidney InternationalCitation Excerpt :In this study, we demonstrate that CP causes a significant reduction in the peroxisome population of the proximal tubule determined by reduced protein expression of PMP70, and by quantification of peroxisomes using quantum dot technique. Our findings in the CP model of ARF are in agreement with findings described in the ischemia–reperfusion model of ARF, where a significant loss of catalase and fatty acid β-oxidation enzymes were accompanied by reduced number of peroxisomes in kidney tissue.26 The mechanisms responsible for the degradation of peroxisomal proteins during ARF are unclear, but could involve autophagy, a global process by which intracellular components including soluble proteins and organelles, are degraded in lysosomes.27-29
Peroxisomes and oxidative stress
2006, Biochimica et Biophysica Acta - Molecular Cell ResearchEnergy metabolism and cytotoxicity
2003, Seminars in NephrologyThe biochemistry and medical significance of the flavonoids
2002, Pharmacology and TherapeuticsCitation Excerpt :SOD is a relatively small enzyme that can be injected into the blood stream without much danger of immunological complications. It is used to scavenge free radicals in the reperfusion phase after ischemic heart stop, e.g., during heart transplantation (Gulati et al., 1992; Fritz-Niggli, 1968). Another molecule, which is used for the same purpose, is ubiquinone, coenzyme Q.