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dc.creatorSoto-Urquieta,María G
dc.creatorLópez-Briones,Sergio
dc.creatorPérez-Vázquez,Victoriano
dc.creatorSaavedra-Molina,Alfredo
dc.creatorGonzález-Hernández,Gloria A
dc.creatorRamírez-Emiliano,Joel
dc.date2014-01-01
dc.date.accessioned2019-05-02T21:22:22Z
dc.date.available2019-05-02T21:22:22Z
dc.identifierhttps://scielo.conicyt.cl/scielo.php?script=sci_arttext&pid=S0716-97602014000100068
dc.identifier.urihttp://revistaschilenas.uchile.cl/handle/2250/82452
dc.descriptionBACKGROUND: Nitrosative and oxidative stress play a key role in obesity and diabetes-related mitochondrial dysfunction. The objective was to investigate the effect of curcumin treatment on state 3 and 4 oxygen consumption, nitric oxide (NO) synthesis, ATPase activity and lipid oxidation in mitochondria isolated from liver and kidneys of diabetic db/db mice. RESULTS: Hyperglycaemia increased oxygen consumption and decreased NO synthesis in liver mitochondria isolated from diabetic mice relative to the control mice. In kidney mitochondria, hyperglycaemia increased state 3 oxygen consumption and thiobarbituric acid-reactive substances (TBARS) levels in diabetic mice relative to control mice. Interestingly, treating db/db mice with curcumin improved or restored these parameters to normal levels; also curcumin increased liver mitochondrial ATPase activity in db/db mice relative to untreated db/db mice. CONCLUSIONS: These findings suggest that hyperglycaemia modifies oxygen consumption rate, NO synthesis and increases TBARS levels in mitochondria from the liver and kidneys of diabetic mice, whereas curcumin may have a protective role against these alterations.
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dc.languageen
dc.publisherSociedad de Biología de Chile
dc.relation10.1186/0717-6287-47-74
dc.rightsinfo:eu-repo/semantics/openAccess
dc.sourceBiological Research v.47 2014
dc.subjectDiabetes
dc.subjectMitochondria
dc.subjectCurcumin
dc.subjectATPase activity
dc.subjectNitric oxide synthesis
dc.subjectLipid oxidation
dc.titleCurcumin restores mitochondrial functions and decreases lipid peroxidation in liver and kidneys of diabetic db/db mice


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