PUBLICATION
Sexual dimorphism in the reaction of zebrafish (Brachydanio rerio) to ascorbic acid deficiency: Induction of steatosis in hepatocytes of male fish
- Authors
- Phromkunthong, W., Storch, V., Braunbeck, T.
- ID
- ZDB-PUB-160311-11
- Date
- 1994
- Source
- Zeitschrift fur angewandte Ichthyologie = Journal of applied ichthyology 10(2-3): 146-153 (Journal)
- Registered Authors
- Braunbeck, Thomas
- Keywords
- none
- MeSH Terms
- none
- PubMed
- none Full text @ Zeitschrift Angew. Ichthyol. (J. Appl. Ichtyol.)
Citation
Phromkunthong, W., Storch, V., Braunbeck, T. (1994) Sexual dimorphism in the reaction of zebrafish (Brachydanio rerio) to ascorbic acid deficiency: Induction of steatosis in hepatocytes of male fish. Zeitschrift fur angewandte Ichthyologie = Journal of applied ichthyology. 10(2-3):146-153.
Abstract
Zebrafish (Brachydanio rerio) fed diets free of ascorbic acid (vitamin C) or suplemented with 200 mg/kg ascorbic acid for 12 weeks were compared with respect to macroscopically detectable symptoms of pathology and cytoloical alterations of hepatocytes. Fish fed the ascorbic acid-free diet displayed symptoms of scurvy including hemorrhages, fin erosion, and darker pigmentation. Hepatocytes of male zebrafish developed steatosis, whereas liver cells of female zebrafish were free of microvesicular lipid accumulation within the endoplasmic reticulum cisternae, indicating the presence of sex-dependent protection mechanisms against ascorbic acid depletion. Female fish showed a reduction of hepatocellular size and a less regular arrangement of the rough endoplasmic reticulum; hepatocellular glycogen depletion as well as induction of smooth endoplasmic reticulum were characterstic of hepatocytes in either sex. Since zebrafish fed the diet supplemented with ascorbic acid were free of pathological alterations in both external appearance and hepatocellular ultrastructure, results indicate that ascorbic acid not only plays a key role in collagen biosynthesis, but also fulfills central functions in the maintenance of a well-equilibrated lipid metabolism in fish. Accumulation of oxidative reagents represents one possible mechanism leading to hepatocellular steatosis in fish.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping