Abstract：
:Ischemia-reperfusion is a common cause for acute kidney injury and can lead to distant organ dysfunction. Glutathione is a major endogenous antioxidant and its depletion directly correlates to ischemia-reperfusion injury. The liver has high capacity for producing glutathione and is a key organ in modulating local and systemic redox balance. In the present study, we investigated the mechanism by which kidney ischemia-reperfusion led to glutathione depletion and oxidative stress. The left kidney of Sprague-Dawley rats was subjected to 45 min ischemia followed by 6 h reperfusion. Ischemia-reperfusion impaired kidney and liver function. This was accompanied by a decrease in glutathione levels in the liver and plasma and increased hepatic lipid peroxidation and plasma homocysteine levels. Ischemia-reperfusion caused a significant decrease in mRNA and protein levels of hepatic glutamate-cysteine ligase mediated through the inhibition of transcription factor Nrf2. Ischemia-reperfusion inhibited hepatic expression of cystathionine γ-lyase, an enzyme responsible for producing cysteine (an essential precursor for glutathione synthesis) through the transsulfuration pathway. These results suggest that inhibition of glutamate-cysteine ligase expression and downregulation of the transsulfuration pathway lead to reduced hepatic glutathione biosynthesis and elevation of plasma homocysteine levels, which, in turn, may contribute to oxidative stress and distant organ injury during renal ischemia-reperfusion.
journal_name
Oxid Med Cell Longevjournal_title
Oxidative medicine and cellular longevityauthors
Shang Y,Siow YL,Isaak CK,O Kdoi
10.1155/2016/9707292subject
Has Abstractpub_date
2016-01-01 00:00:00pages
9707292eissn
1942-0900issn
1942-0994journal_volume
2016pub_type
杂志文章abstract：:Oxidative stress reflects an imbalance between oxidants and antioxidants in favor of the oxidants capable of evoking tissue damage. Like hydrogen sulfide (H2S) and nitric oxide (NO), carbon monoxide (CO) is an endogenous gaseous mediator recently implicated in the physiology of the gastrointestinal (GI) tract. CO is p...
journal_title：Oxidative medicine and cellular longevity
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journal_title：Oxidative medicine and cellular longevity
pub_type： 杂志文章,评审
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journal_title：Oxidative medicine and cellular longevity
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abstract：:There is accumulating evidence that blood pressure (BP) control significantly reduces the risk of future cardiovascular events in patients with essential hypertension. However, strict BP control is often difficult to maintain, and half of hypertensive patients fail to attain BP goals on single-drug therapy. Therefore,...
journal_title：Oxidative medicine and cellular longevity
pub_type： 杂志文章
doi：10.4161/oxim.3.5.13199
更新日期：2010-09-01 00:00:00
abstract：:Oxidative stress is crucially involved in the pathogenesis of neurological diseases such as stroke and degenerative diseases. We previously demonstrated that platelet-derived growth factors (PDGFs) protected neurons from H2O2-induced oxidative stress and indicated the involvement of PI3K-Akt and MAP kinases as an unde...
journal_title：Oxidative medicine and cellular longevity
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