The responses of HT22 cells to the blockade of mitochondrial complexes and potential protective effect of selenium supplementation

<p>Mitochondria are the major reactive oxygen species (ROS) &#8211; generating sites in mammalian cells. Blockade of complexes in the electron transport chain (ETC) increases the leakage of single electrons to O<sub>2</sub> and therefore increases ROS levels. Complexes I and II...

Full description

Bibliographic Details
Main Author: Jun Panee, Wanyu Liu, Kyoko Nakamura, Marla J. Berry
Format: Article
Language:English
Published: Ivyspring International Publisher 2007-01-01
Series:International Journal of Biological Sciences
Online Access:http://www.biolsci.org/v03p0335.htm
_version_ 1819117844252590080
author Jun Panee, Wanyu Liu, Kyoko Nakamura, Marla J. Berry
author_facet Jun Panee, Wanyu Liu, Kyoko Nakamura, Marla J. Berry
author_sort Jun Panee, Wanyu Liu, Kyoko Nakamura, Marla J. Berry
collection DOAJ
description <p>Mitochondria are the major reactive oxygen species (ROS) &#8211; generating sites in mammalian cells. Blockade of complexes in the electron transport chain (ETC) increases the leakage of single electrons to O<sub>2</sub> and therefore increases ROS levels. Complexes I and III have been reported to be the major ROS-generating sites in mitochondria. In this study, using mouse hippocampal HT22 cells as in vitro model, we monitored the change of intracellular ROS level in response to the blockade of ETC at different complex, and measured changes of gene expression of antioxidant enzymes and phase II enzymes, also evaluated potential protective effect of selenium (Se) supplementation to the cells under this oxidative stress. In summary, our results showed that complex I was the major ROS-generating site in HT22 cells. Complex I blockade upregulated the mRNA levels of glutamylcysteine synthetase heavy and light chains, glutathione-S-transferases omega1 and alpha 2, hemoxygenase 1, thioredoxin reductase 1, and selenoprotein H. Unexpectedly, the expression of the enzymes that directly scavenge ROS decreased, including superoxide dismutases 1 and 2, glutathione peroxidase 1, and catalase. Se supplementation increased glutathione levels and glutathione peroxidase activity, indicating a potential protective role in oxidative stress caused by ETC blockade.</p>
first_indexed 2024-12-22T05:39:26Z
format Article
id doaj.art-3ebbe5e986f54c31811ef7cccda81465
institution Directory Open Access Journal
issn 1449-2288
language English
last_indexed 2024-12-22T05:39:26Z
publishDate 2007-01-01
publisher Ivyspring International Publisher
record_format Article
series International Journal of Biological Sciences
spelling doaj.art-3ebbe5e986f54c31811ef7cccda814652022-12-21T18:37:14ZengIvyspring International PublisherInternational Journal of Biological Sciences1449-22882007-01-0135335341The responses of HT22 cells to the blockade of mitochondrial complexes and potential protective effect of selenium supplementationJun Panee, Wanyu Liu, Kyoko Nakamura, Marla J. Berry<p>Mitochondria are the major reactive oxygen species (ROS) &#8211; generating sites in mammalian cells. Blockade of complexes in the electron transport chain (ETC) increases the leakage of single electrons to O<sub>2</sub> and therefore increases ROS levels. Complexes I and III have been reported to be the major ROS-generating sites in mitochondria. In this study, using mouse hippocampal HT22 cells as in vitro model, we monitored the change of intracellular ROS level in response to the blockade of ETC at different complex, and measured changes of gene expression of antioxidant enzymes and phase II enzymes, also evaluated potential protective effect of selenium (Se) supplementation to the cells under this oxidative stress. In summary, our results showed that complex I was the major ROS-generating site in HT22 cells. Complex I blockade upregulated the mRNA levels of glutamylcysteine synthetase heavy and light chains, glutathione-S-transferases omega1 and alpha 2, hemoxygenase 1, thioredoxin reductase 1, and selenoprotein H. Unexpectedly, the expression of the enzymes that directly scavenge ROS decreased, including superoxide dismutases 1 and 2, glutathione peroxidase 1, and catalase. Se supplementation increased glutathione levels and glutathione peroxidase activity, indicating a potential protective role in oxidative stress caused by ETC blockade.</p>http://www.biolsci.org/v03p0335.htm
spellingShingle Jun Panee, Wanyu Liu, Kyoko Nakamura, Marla J. Berry
The responses of HT22 cells to the blockade of mitochondrial complexes and potential protective effect of selenium supplementation
International Journal of Biological Sciences
title The responses of HT22 cells to the blockade of mitochondrial complexes and potential protective effect of selenium supplementation
title_full The responses of HT22 cells to the blockade of mitochondrial complexes and potential protective effect of selenium supplementation
title_fullStr The responses of HT22 cells to the blockade of mitochondrial complexes and potential protective effect of selenium supplementation
title_full_unstemmed The responses of HT22 cells to the blockade of mitochondrial complexes and potential protective effect of selenium supplementation
title_short The responses of HT22 cells to the blockade of mitochondrial complexes and potential protective effect of selenium supplementation
title_sort responses of ht22 cells to the blockade of mitochondrial complexes and potential protective effect of selenium supplementation
url http://www.biolsci.org/v03p0335.htm
work_keys_str_mv AT junpaneewanyuliukyokonakamuramarlajberry theresponsesofht22cellstotheblockadeofmitochondrialcomplexesandpotentialprotectiveeffectofseleniumsupplementation
AT junpaneewanyuliukyokonakamuramarlajberry responsesofht22cellstotheblockadeofmitochondrialcomplexesandpotentialprotectiveeffectofseleniumsupplementation