PUBLICATION
Traditional African remedies induce hemolysis in a glucose-6-phopshate dehydrogenase deficient zebrafish model
- Authors
- Arogbokun, O., Shevik, M., Slusher, T., Farouk, Z., Elfstrum, A., Weber, J., Cusick, S.E., Lund, T.
- ID
- ZDB-PUB-201120-48
- Date
- 2020
- Source
- Scientific Reports 10: 19172 (Journal)
- Registered Authors
- Lund, Troy
- Keywords
- none
- MeSH Terms
-
- Animals
- Disease Models, Animal
- Eucalyptus Oil/administration & dosage
- Eucalyptus Oil/adverse effects*
- Glucosephosphate Dehydrogenase Deficiency/blood*
- Hematologic Tests
- Hemolysis/drug effects*
- Medicine, African Traditional/adverse effects*
- Oxidative Stress/drug effects*
- Zebrafish
- PubMed
- 33154437 Full text @ Sci. Rep.
Citation
Arogbokun, O., Shevik, M., Slusher, T., Farouk, Z., Elfstrum, A., Weber, J., Cusick, S.E., Lund, T. (2020) Traditional African remedies induce hemolysis in a glucose-6-phopshate dehydrogenase deficient zebrafish model. Scientific Reports. 10:19172.
Abstract
Traditional remedies are widely used throughout Africa in routine care for infants. However, such remedies could have detrimental effects. Acute bilirubin encephalopathy (ABE) and kernicterus spectrum disorder (KSD) are common newborn health conditions in the developing world, contributing to substantial neonatal mortality and morbidity. They frequently occur in children with glucose-6-phopshate dehydrogenase (G6PD) deficiency. Using our established zebrafish model of G6PD deficiency, we tested the effects of three traditional compounds used in the care of the newborn umbilical cord: eucalyptus oil, methylated spirits, and Yoruba herbal tea. We found that eucalyptus oil induced a 13.4% increase in a hemolytic phenotype versus control, while methylated spirits showed a 39.7% increase in affected phenotype. Yoruba herbal tea exposure showed no effect. While methylated spirits are already a known pro-oxidant, these data indicate that eucalyptus oil may also be a hemolytic trigger in those with G6PD deficiency. Discovering which agents may contribute to the pathophysiology of G6PD deficiency is critical to eliminate ABE and KSD, especially in countries with a high prevalence of G6PD deficiency. The next step in elucidating the role of these agents is to determine the clinical correlation between the use of these agents and ABE/KSD.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping