Bioaccessibility and intestinal cell uptake of astaxanthin from salmon and commercial supplements

- Astaxanthin content from wild salmon flesh was greater than aquacultured salmon flesh.
- Common styles of home cooking markedly decreased astaxanthin content in wild and aquacultured salmon.
- Astaxanthin bioaccessibility after in vitro digestion of wild salmon was greater than that of digested aquacultured salmon.
- The relative bioaccessibility of astaxanthin in soft-gel capsules was greater than that in acquacultured salmon.
- Phospholipid-rich krill oil enhanced the uptake and basolateral secretion of Ast by Caco-2 human intestinal cells.

Although the keto-carotenoid astaxanthin (Ast) is not typically present in human plasma due to its relative scarcity in the typical diet, global consumption of salmon, the primary source of Ast in food, and Ast supplements continues to increase. The first objective of the present study was to investigate the bioaccessibility of Ast from uncooked and cooked fillets of wild and aquacultured salmon, Ast-supplements and krill oil, during simulated gastric and small intestinal digestion. Uptake of E-Ast from micelles generated during digestion of wild salmon by monolayers of Caco-2 was also monitored. Both wild and aquacultured salmon flesh contained E-Ast and Z-isomers of unesterified Ast, whereas Ast esters were the predominant form of the carotenoid in commercial supplements and krill oil. Flesh from wild salmon contained approximately 10 times more Ast than aquacultured salmon. Common styles of cooking flesh from wild and aquacultured salmon decreased Ast content by 48-57% and 35-47%, respectively. Ast in salmon flesh, supplements and krill oil was relatively stable (> 80% recovery) during in vitro digestion. The efficiency of transfer of Ast into mixed micelles during digestion of uncooked wild salmon was 43%, but only 12% for uncooked acquacultured salmon. Cooking wild salmon significantly decreased Ast bioaccessibility. The relative bioaccessibility of Ast (41-67%) after digestion of oil vehicle in commercial supplements was inversely proportional to carotenoid content (3-10 mg/capsule), whereas bioaccessibility of endogenous Ast in phospholipid-rich krill oil supplement was 68%. > 95% of Ast in mixed micelles generated during digestion of supplements and krill oil was unesterified. Caco-2 intestinal cells accumulated 11-14% of E-Ast delivered in mixed micelles generated from digested wild salmon. Apical uptake and basolateral secretion of E-Ast by Caco-2 cells grown on inserts were greater after digestion of Ast-enriched krill oil compared to uncooked wild salmon. These data suggest that the bioacessibility of Ast in wild salmon and soft-gel capsules is greater than that in aquacultured salmon, and that uptake and basolateral secretion of the carotenoid by enterocyte-like cells is enhanced by the digestion products of phospholipid-rich krill oil.