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2023-03-14
Requirement of glutathione
for Sod1 activation during lifespan
extension; PY2011; Brazil
(巴西);_IR95_V001R01_
Source or References (資訊來源或是參考的資訊):
https://pubmed.ncbi.nlm.nih.gov/20737429/
Info cited on 2023-03-14-WD2 (資訊引用於 中華民國112年西元2023年3月14日) by 湯偉晉 (WeiJin Tang)
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Requirement of glutathione for Sod1 activation
during lifespan extension
January 2011Yeast 28(1):19-25
DOI:10.1002/yea.1817
SourcePubMed
Authors:
Sérgio C Mannarino
Leonardo Vilela
Universidade Federal de Lavras (UFLA)
Aline Araújo Brasil
Instituto D’Or de Pesquisa e Ensino
Juliana N Aranha
Abstract
It has been shown that the activation of cytosolic superoxide dismutase (Sod1) in Saccharomyces
cerevisiae is only dependent on Ccs1, which is responsible for insertion of copper into the enzyme catalytic center, and that glutathione (GSH) is not necessary for this
process. In this work, we addressed an important role of GSH in Sod1 activation by a
Ccs1-dependent mechanism during
oxidative stress and its role in yeast lifespan. Exponential cells of
Saccharomyces cerevisiae, treated or not with 0.5 mM menadione for 1 h, were
used for evaluation of the effect of a mild oxidative stress pre-treatment on
chronological lifespan. The results showed that menadione induced a lifespan
extension in the wild-type (WT) strain but this adaptive response was repressed
in gsh1 and in sod1 strains. Interestingly, menadione treatment increased SOD1
and CCS1 gene expression in both WT and gsh1 strains. However, while these
strains showed the same Sod1 activity before treatment, only the WT presented
an increase of Sod1 activity after menadione exposure. Glutathionylation seems to be essential for Sod1 activation since no
increase in activity was observed after menadione treatment in grx1 and
grx2 null mutants. Our results
suggest that GSH and glutathionylation are fundamental to protect Sod1 sulfhydryl residues under mild oxidative
stress, enabling Sod1 activation and lifespan extension.
Begin_電腦自動翻譯的內容_Y2023M03D14H15M26Rn5692_
(請注意：電腦自動翻譯的內容，可能會夾雜一些錯誤！)
已經表明，釀酒酵母中胞質超氧化物歧化酶 (Sod1) 的激活僅依賴於 Ccs1，後者負責將銅插入酶催化中心，而穀胱甘肽 (GSH) 對於該過程不是必需的。 在這項工作中，我們探討了 GSH 在氧化應激期間通過 Ccs1 依賴性機制激活 Sod1 的重要作用及其在酵母壽命中的作用。 釀酒酵母的指數細胞，用或不用 0.5 mM 甲萘醌處理 1 小時，用於評估輕度氧化應激預處理對時間壽命的影響。 結果表明甲萘醌誘導野生型 (WT) 菌株的壽命延長，但這種適應性反應在 gsh1 和 sod1 菌株中受到抑制。 有趣的是，甲萘醌處理增加了 WT 和 gsh1 菌株中的 SOD1 和 CCS1 基因表達。 然而，雖然這些菌株在治療前表現出相同的 Sod1 活性，但只有 WT 在甲萘醌暴露後表現出 Sod1 活性的增加。 穀胱甘肽化似乎對 Sod1 激活至關重要，因為在 grx1 和 grx2 無效突變體中甲萘醌處理後未觀察到活性增加。 我們的研究結果表明，GSH 和穀胱甘肽化是在輕度氧化應激下保護 Sod1 巰基殘基的基礎，能夠激活 Sod1 並延長壽命。
End_電腦自動翻譯的內容_Y2023M03D14H15M26Rn5692_
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