Fetal and neonatal bilirubin metabolism
Human fetal and neonatal bilirubin metabolism is centered on 4Z,15Z-bilirubin IXα (BR) due to the extremely low BR conjugating capacity of the liver. BR is a unique, highly lipophilic substance with physiological and toxic effects in the cell membranes of organs and body tissues. The fetus excretes...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2023-02-01
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| Series: | Frontiers in Pediatrics |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fped.2022.1002408/full |
| _version_ | 1811170444355567616 |
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| author | Susumu Itoh Hitoshi Okada Kosuke Koyano Shinji Nakamura Yukihiko Konishi Takashi Iwase Takashi Kusaka |
| author_facet | Susumu Itoh Hitoshi Okada Kosuke Koyano Shinji Nakamura Yukihiko Konishi Takashi Iwase Takashi Kusaka |
| author_sort | Susumu Itoh |
| collection | DOAJ |
| description | Human fetal and neonatal bilirubin metabolism is centered on 4Z,15Z-bilirubin IXα (BR) due to the extremely low BR conjugating capacity of the liver. BR is a unique, highly lipophilic substance with physiological and toxic effects in the cell membranes of organs and body tissues. The fetus excretes BR through the placenta to the maternal circulation. After birth, BR is thought to act as an antioxidant against the increase in reactive oxygen species caused by the rapid increase in oxygen concentration during the adaptation process from in amniotic fluid to in air. However, bilirubin encephalopathy is a toxic effect of bilirubin. Due to the lipophilic nature of BR, it must be bound to a carrier to be distributed to various parts of the body by hydrophilic blood. This carrier of BR is human serum albumin (HSA). In humans, BR can be excreted efficiently after undergoing photochemical reactions upon high affinity binding to HSA. HSA also plays an important role in the prevention of bilirubin encephalopathy. This review focuses on the developmental and physiological role of bilirubin metabolism during the fetal and neonatal periods. |
| first_indexed | 2024-04-10T16:56:53Z |
| format | Article |
| id | doaj.art-e5109605a1104be0b7e930a96ef05f0d |
| institution | Directory Open Access Journal |
| issn | 2296-2360 |
| language | English |
| last_indexed | 2024-04-10T16:56:53Z |
| publishDate | 2023-02-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Pediatrics |
| spelling | doaj.art-e5109605a1104be0b7e930a96ef05f0d2023-02-07T05:57:08ZengFrontiers Media S.A.Frontiers in Pediatrics2296-23602023-02-011010.3389/fped.2022.10024081002408Fetal and neonatal bilirubin metabolismSusumu Itoh0Hitoshi Okada1Kosuke Koyano2Shinji Nakamura3Yukihiko Konishi4Takashi Iwase5Takashi Kusaka6Department of Pediatrics, Faculty of Medicine, Kagawa University, Kagawa, JapanDivision of Analytical Technology, Department of Medical Technology, Kagawa Prefectural University of Health Sciences, Kagawa, JapanMaternal Perinatal Center, Faculty of Medicine, Kagawa University, Kagawa, JapanDepartment of Pediatrics, Faculty of Medicine, Kagawa University, Kagawa, JapanDepartment of Pediatrics, Faculty of Medicine, Kagawa University, Kagawa, JapanDepartment of Pediatrics, Faculty of Medicine, Kagawa University, Kagawa, JapanDepartment of Pediatrics, Faculty of Medicine, Kagawa University, Kagawa, JapanHuman fetal and neonatal bilirubin metabolism is centered on 4Z,15Z-bilirubin IXα (BR) due to the extremely low BR conjugating capacity of the liver. BR is a unique, highly lipophilic substance with physiological and toxic effects in the cell membranes of organs and body tissues. The fetus excretes BR through the placenta to the maternal circulation. After birth, BR is thought to act as an antioxidant against the increase in reactive oxygen species caused by the rapid increase in oxygen concentration during the adaptation process from in amniotic fluid to in air. However, bilirubin encephalopathy is a toxic effect of bilirubin. Due to the lipophilic nature of BR, it must be bound to a carrier to be distributed to various parts of the body by hydrophilic blood. This carrier of BR is human serum albumin (HSA). In humans, BR can be excreted efficiently after undergoing photochemical reactions upon high affinity binding to HSA. HSA also plays an important role in the prevention of bilirubin encephalopathy. This review focuses on the developmental and physiological role of bilirubin metabolism during the fetal and neonatal periods.https://www.frontiersin.org/articles/10.3389/fped.2022.1002408/fullbilirubin photoisomersbreast milk jaundicehuman serum albuminneonatal jaundicephysiological effectsreactive oxygen species |
| spellingShingle | Susumu Itoh Hitoshi Okada Kosuke Koyano Shinji Nakamura Yukihiko Konishi Takashi Iwase Takashi Kusaka Fetal and neonatal bilirubin metabolism Frontiers in Pediatrics bilirubin photoisomers breast milk jaundice human serum albumin neonatal jaundice physiological effects reactive oxygen species |
| title | Fetal and neonatal bilirubin metabolism |
| title_full | Fetal and neonatal bilirubin metabolism |
| title_fullStr | Fetal and neonatal bilirubin metabolism |
| title_full_unstemmed | Fetal and neonatal bilirubin metabolism |
| title_short | Fetal and neonatal bilirubin metabolism |
| title_sort | fetal and neonatal bilirubin metabolism |
| topic | bilirubin photoisomers breast milk jaundice human serum albumin neonatal jaundice physiological effects reactive oxygen species |
| url | https://www.frontiersin.org/articles/10.3389/fped.2022.1002408/full |
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