RGD Reference Report - Preconditioning with physiological levels of ethanol protect kidney against ischemia/reperfusion injury by modulating oxidative stress. - Rat Genome Database

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Preconditioning with physiological levels of ethanol protect kidney against ischemia/reperfusion injury by modulating oxidative stress.

Authors: Yuan, Q  Hong, S  Han, S  Zeng, L  Liu, F  Ding, G  Kang, Y  Mao, J  Cai, M  Zhu, Y  Wang, QX 
Citation: Yuan Q, etal., PLoS One. 2011;6(10):e25811. doi: 10.1371/journal.pone.0025811. Epub 2011 Oct 12.
RGD ID: 7241603
Pubmed: PMID:22022451   (View Abstract at PubMed)
PMCID: PMC3192120   (View Article at PubMed Central)
DOI: DOI:10.1371/journal.pone.0025811   (Journal Full-text)

BACKGROUND: Oxidative stress due to excessive production of reactive oxygen species (ROS) and subsequent lipid peroxidation plays a critical role in renal ischemia/reperfusion (IR) injury. The purpose of current study is to demonstrate the effect of antecedent ethanol exposure on IR-induced renal injury by modulation of oxidative stress. MATERIALS AND METHODS: Bilateral renal warm IR was induced in male C57BL/6 mice after ethanol or saline administration. Blood ethanol concentration, kidney function, histological damage, inflammatory infiltration, cytokine production, oxidative stress, antioxidant capacity and Aldehyde dehydrogenase (ALDH) enzymatic activity were assessed to evaluate the impact of antecedent ethanol exposure on IR-induced renal injury. RESULTS: After bilateral kidney ischemia, mice preconditioned with physiological levels of ethanol displayed significantly preserved renal function along with less histological tubular damage as manifested by the reduced inflammatory infiltration and cytokine production. Mechanistic studies revealed that precondition of mice with physiological levels of ethanol 3 h before IR induction enhanced antioxidant capacity characterized by significantly higher superoxidase dismutase (SOD) activities. Our studies further demonstrated that ethanol pretreatment specifically increased ALDH2 activity, which then suppressed lipid peroxidation by promoting the detoxification of Malondialdehyde (MDA) and 4-hydroxynonenal (HNE). CONCLUSIONS: Our results provide first line of evidence indicating that antecedent ethanol exposure can provide protection for kidneys against IR-induced injury by enhancing antioxidant capacity and preventing lipid peroxidation. Therefore, ethanol precondition and ectopic ALDH2 activation could be potential therapeutic approaches to prevent renal IR injury relevant to various clinical conditions.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Kidney Reperfusion Injury  ISOAldh2 (Mus musculus)7241603; 7241603 RGD 
Kidney Reperfusion Injury  IMP 7241603 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Aldh2  (aldehyde dehydrogenase 2 family member)

Genes (Mus musculus)
Aldh2  (aldehyde dehydrogenase 2, mitochondrial)

Genes (Homo sapiens)
ALDH2  (aldehyde dehydrogenase 2 family member)


Additional Information