JOURNAL ARTICLE
The role of dietary vitamin A in mechanisms of cataract development in the teleost lumpfish (Cyclopterus lumpus L).
Published In: Journal of Fish Diseases, 2024, v. 47, n. 3. P. 1 1 of 3
Database: Academic Search Ultimate 2 of 3
Authored By: Deering, Margret J.; Paradis, Hélène; Ahmad, Raahyma; Al‐Mehiawi, Adil S.; Gendron, Robert L. 3 of 3
Abstract
Lumpfish (Cyclopterus lumpus L) are highly prone to cataract development in the wild and in culture. There is evidence that cataract in farmed fish is related to nutrition. However, both the nutrients and the mechanisms involved in cataract development in lumpfish are not clear. Here we investigated the mechanisms involved and the role of dietary vitamin A in cataract development in a cultured lumpfish population. Cultured lumpfish were fed three diets differing only in vitamin A supplementation level (5000, 15,000 and 120,000 IU/kg) over an 18‐month period, and fish weight, cataract frequencies and severities were determined. Western blotting and immunohistochemistry were performed on lens tissue to measure the levels of oxidative stress, and apoptosis. The lowest levels of vitamin A significantly reduced cataract frequencies in adult lumpfish and resulted in less severe cataract and increased weight in males. Oxidative stress levels in the lens were positively correlated with vitamin A intake. Apoptosis was observed at high levels in lenses with severe cataract. Oxidative stress and apoptosis levels were the highest in regions of the lens with severe, advanced cataract pathology when compared to regions with no visible pathology. These results suggest that higher vitamin A intake contributes to cataract development through an oxidative stress pathway, and that both oxidative stress and apoptosis are involved in advanced stages of cataract in lumpfish. [ABSTRACT FROM AUTHOR]
Additional Information
- Source:Journal of Fish Diseases. 2024/03, Vol. 47, Issue 3, p1
- Document Type:Article
- Subject Area:Nutrition and Dietetics
- Publication Date:2024
- ISSN:0140-7775
- DOI:10.1111/jfd.13899
- Accession Number:175328019
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