Epigallocatechin-3-gallate enhances key enzymatic activities of hepatic thioredoxin and glutathione systems in selenium-optimal mice but activates hepatic Nrf2 responses in selenium-deficient mice
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- 作者：Ruixia Donga ; c ; Dongxu Wanga ; d ; Xiaoxiao Wanga ; Ke Zhanga ; Pingping Chena ; Chung S. Yangb ; d ; Jinsong Zhanga ; d ; zjs@ahau.edu.cn" class="auth_mail" title="E-mail the corresponding author
- 关键词：ALT ; alanine aminotransferase ; AST ; aspartate aminotransferase ; BSO ; buthionine sulfoximine ; CDNB ; 1-chloro-2 ; 4-dinitrobenzene ; ECL ; enhanced chemiluminescense ; EDTA ; ethylene diamine tetraacetic acid ; EGCG ; epigallocatechin-3-gallate ; FoxO ; Forkhead box class O ; GAPDH ; glyceraldehyde 3-phosphate dehydrogenase ; GPx ; glutathione peroxidase ; GR ; glutathione reductase ; Grx ; glutaredoxin ; GSH ; glutathione ; GSSG ; oxidized glutathione ; GST ; glutathione S-transferase ; γ-H2AX ; phosphorylated histone 2A
- 刊名：Redox Biology
- 出版年：2016
- 出版时间：December 2016
- 年：2016
- 卷：10
- 期：Complete
- 页码：221-232
- 全文大小：1380 K
文摘
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EGCG increases hepatic activities of TrxR, GR and Grx in selenium-optimal mice.
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EGCG fails to manipulate the above-mentioned enzymes in selenium-deficient mice.
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EGCG in turn activates hepatic Nrf2 response in selenium-deficient mice.
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Selenium deficiency does not increase EGCG toxicity due to potent Nrf2 response.