Astaxanthin is a carotenoid that is present in high quantities in the meat of fish like salmon and the shells of shrimp and crab. It exhibits free radical scavenging antioxidant activity when consumed dietarily. Astaxanthin is absorbed by the small intestine before exerting its antioxidant effect; however, a portion of dietary intake remains unabsorbed in the digestive tract and reaches the large intestines. We hypothesized that astaxanthin may exert its antioxidant action in the large intestine to influence the gut microbiota. In this review we introduce the results of two studies of astaxanthin. Firstly, a clinical trial targeting post-menopausal women screened for high oxidative stress burden. Astaxanthin was administered orally for eight weeks in order to examine its effects and safety, and subjects were surveyed for any changes in subjective symptoms. Secondly, in a mouse model, real time PCR (polymerase chain reaction) was used to examine the ability of astaxanthin to prevent changes in the enteric flora induced by a high-fat diet. When fat intake increases due to changes in diet, the equilibrium between the various species that constitute the intestinal flora is altered. As a result, degenerative changes in lifestyle-related disease and aging of the host are promoted. Here we find that the intake of astaxanthin was able to inhibit these changes in the gut microbiota of mice induced by a high-fat diet. Even in humans, it is highly probably that the unabsorbed astaxanthin that remains in the intestinal tract exerts a positive effect against disturbance of the intestinal flora caused by a high-fat diet.

Staphylococcus aureus is a Gram-positive bacterium that plays a role in the pathogenesis of skin lesions in diabetes mellitus, atopic dermatitis, and psoriasis, all of which are associated with elevated non-enzymatic glycation biomarkers. The production of biofilm protects resident bacteria from host immune defenses and antibiotic interventions, prolonging pathogen survival, and risking recurrence after treatment. Glycated proteins formed from keratin and glucose induce biofilm formation in S. aureus, promoting dysbiosis and increasing pathogenicity. In this study, several glycation-inhibiting and advanced glycation endproduct (AGE) crosslink-breaking compounds were assayed for their ability to inhibit glycated keratin-induced biofilm formation as preliminary screening for clinical testing candidates. Ascorbic acid, astaxanthin, clove extract, n-phenacylthiazolium bromide, and rosemary extract were examined in an in vitro static biofilm model with S. aureus strain ATCC 12600. Near complete biofilm inhibition was achieved with astaxanthin (ED50 = 0.060 mg/mL), clove extract (ED50 = 0.0087 mg/mL), n-phenacylthiazolium bromide (ED50 = 5.3 mg/mL), and rosemary extract (ED50 = 1.5 mg/mL). The dosage necessary for biofilm inhibition was not significantly correlated with growth inhibition (R2 = 0.055. p = 0.49). Anti-glycation and AGE breaking compounds with biofilm inhibitory activity are ideal candidates for treatment of S. aureus dysbiosis and skin infection that is associated with elevated skin glycation.