Impact of intrauterine fetal resuscitation with oxygen on oxidative stress in the developing rat brain
Abstract Use of maternal oxygen for intrauterine resuscitation is contentious because of the lack of evidence for its efficacy and the possibility of fetal harm through oxidative stress. Because the developing brain is rich in lipids and low in antioxidants, it remains vulnerable to oxidative stress...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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Nature Portfolio
2021-05-01
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| Series: | Scientific Reports |
| Online Access: | https://doi.org/10.1038/s41598-021-89299-w |
| _version_ | 1818857706459496448 |
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| author | Jia Jiang Tusar Giri Nandini Raghuraman Alison G. Cahill Arvind Palanisamy |
| author_facet | Jia Jiang Tusar Giri Nandini Raghuraman Alison G. Cahill Arvind Palanisamy |
| author_sort | Jia Jiang |
| collection | DOAJ |
| description | Abstract Use of maternal oxygen for intrauterine resuscitation is contentious because of the lack of evidence for its efficacy and the possibility of fetal harm through oxidative stress. Because the developing brain is rich in lipids and low in antioxidants, it remains vulnerable to oxidative stress. Here, we tested this hypothesis in a term pregnant rat model with oxytocin-induced fetal distress followed by treatment with either room air or 100% oxygen for 6 h. Fetal brains from both sexes were subjected to assays for biomarkers of oxidative stress (4-hydroxynonenal, protein carbonyl, or 8-hydroxy-2ʹ-deoxyguanosine), expression of genes mediating oxidative stress, and mitochondrial oxidative phosphorylation. Contrary to our hypothesis, maternal hyperoxia was not associated with increased biomarkers of oxidative stress in the fetal brain. However, there was significant upregulation of the expression of select genes mediating oxidative stress, of which some were male-specific. These observations, however, were not accompanied by changes in the expression of proteins from the mitochondrial electron transport chain. In summary, maternal hyperoxia in the setting of acute uteroplacental ischemia-hypoxia does not appear to cause oxidative damage to the developing brain. |
| first_indexed | 2024-12-19T08:44:39Z |
| format | Article |
| id | doaj.art-22b0e45b5ac94c2699aa2baff9cc9913 |
| institution | Directory Open Access Journal |
| issn | 2045-2322 |
| language | English |
| last_indexed | 2024-12-19T08:44:39Z |
| publishDate | 2021-05-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Scientific Reports |
| spelling | doaj.art-22b0e45b5ac94c2699aa2baff9cc99132022-12-21T20:28:49ZengNature PortfolioScientific Reports2045-23222021-05-0111111010.1038/s41598-021-89299-wImpact of intrauterine fetal resuscitation with oxygen on oxidative stress in the developing rat brainJia Jiang0Tusar Giri1Nandini Raghuraman2Alison G. Cahill3Arvind Palanisamy4Department of Anesthesiology, Washington University School of MedicineDepartment of Anesthesiology, Washington University School of MedicineDepartment of Obstetrics and Gynecology, Washington University School of MedicineDepartment of Women’s Health, Dell Medical School, The University of Texas at AustinDepartment of Anesthesiology, Washington University School of MedicineAbstract Use of maternal oxygen for intrauterine resuscitation is contentious because of the lack of evidence for its efficacy and the possibility of fetal harm through oxidative stress. Because the developing brain is rich in lipids and low in antioxidants, it remains vulnerable to oxidative stress. Here, we tested this hypothesis in a term pregnant rat model with oxytocin-induced fetal distress followed by treatment with either room air or 100% oxygen for 6 h. Fetal brains from both sexes were subjected to assays for biomarkers of oxidative stress (4-hydroxynonenal, protein carbonyl, or 8-hydroxy-2ʹ-deoxyguanosine), expression of genes mediating oxidative stress, and mitochondrial oxidative phosphorylation. Contrary to our hypothesis, maternal hyperoxia was not associated with increased biomarkers of oxidative stress in the fetal brain. However, there was significant upregulation of the expression of select genes mediating oxidative stress, of which some were male-specific. These observations, however, were not accompanied by changes in the expression of proteins from the mitochondrial electron transport chain. In summary, maternal hyperoxia in the setting of acute uteroplacental ischemia-hypoxia does not appear to cause oxidative damage to the developing brain.https://doi.org/10.1038/s41598-021-89299-w |
| spellingShingle | Jia Jiang Tusar Giri Nandini Raghuraman Alison G. Cahill Arvind Palanisamy Impact of intrauterine fetal resuscitation with oxygen on oxidative stress in the developing rat brain Scientific Reports |
| title | Impact of intrauterine fetal resuscitation with oxygen on oxidative stress in the developing rat brain |
| title_full | Impact of intrauterine fetal resuscitation with oxygen on oxidative stress in the developing rat brain |
| title_fullStr | Impact of intrauterine fetal resuscitation with oxygen on oxidative stress in the developing rat brain |
| title_full_unstemmed | Impact of intrauterine fetal resuscitation with oxygen on oxidative stress in the developing rat brain |
| title_short | Impact of intrauterine fetal resuscitation with oxygen on oxidative stress in the developing rat brain |
| title_sort | impact of intrauterine fetal resuscitation with oxygen on oxidative stress in the developing rat brain |
| url | https://doi.org/10.1038/s41598-021-89299-w |
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