Methylglyoxal, the foe and friend of glyoxalase and Trx/TrxR systems in HT22 nerve cells
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- 作者：A.L. Dafrea ; alcir.dafre@ufsc.br" class="auth_mail" title="E-mail the corresponding author ; J. Goldbergb ; T. Wangc ; D.A. Spiegelc ; P. Maherb
- 关键词：AGE ; advanced glycation end products ; ARE ; antioxidant response element ; BSA ; bovine serum albumin ; DMEM ; high-glucose Dulbecco&rsquo ; s modified Eagle medium ; DTNB ; 5 ; 5-dithiobis(2-nitrobenzoic acid) ; EDTA ; ethylenediaminetetraacetic acid ; FCS ; fetal calf serum ; GCL ; glutamate cysteine ligase ; GLO ; glyoxalase ; GSH ; glutathione ; HBSS ; Hank's balanced salt solution ; Hepes ; N-(2-hydroxyethyl)-piperazine-N-(2-ethanesulfonic acid) ; HO1 ; heme oxygenase 1 ; MBo ; methyl diaminobenzene-BODIPY ; MGO ; methyl
- 刊名：Free Radical Biology and Medicine
- 出版年：2015
- 出版时间：December 2015
- 年：2015
- 卷：89
- 期：Complete
- 页码：8-19
- 全文大小：2248 K
文摘
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Methylglyoxal (MGO) metabolism decreases GSH and system xc– activity in HT22 cells.
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MGO induces Nrf2, its target genes (HO1 and GCL), GSH and system xc– activity.
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The cytosolic Trx/TrxR system is impaired while the mitochondrial system is induced by MGO.
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GLO1 is inhibited and GLO2 depleted or induced, depending on the MGO concentration.