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• Male C57BL/6J mice were fed a 0.2 % fucoxanthin-containing diet for one week. • Total lipids in the tissues were analyzed to identify carotenoid fatty acid esters. • Fucoxanthinol-3-fatty acid esters abundantly accumulated in the liver. • Epididymal white adipose tissue was rich in amarouciaxanthin A-3-fatty acid esters. • Fucoxanthinol and amaroucixanthin A can be acylated in fucoxanthin-fed mice tissues. Administered carotenoid fatty acid esters are thought to be hydrolyzed to their free forms and absorbed into the body, and information on the tissue distribution of carotenoid fatty acid esters has been limited. Fucoxanthin, a marine carotenoid, exhibits various health benefits, including anti-diabetic and anti-obesity effects. However, fucoxanthin metabolism in mammals remains unclear. Herein, we investigated the fatty acid esters of fucoxanthin metabolites, fucoxanthinol and amarouciaxanthin A, in the tissues of male C57BL/6J mice fed a fucoxanthin-containing diet for one week. Fucoxanthinol and amarouciaxanthin A-3-esters accumulated abundantly in the liver and epididymal white adipose tissue, respectively. These esters were less detectable in the serum and other tissues. Therefore, it is suggested that fucoxanthinol and amarouciaxanthin A are partially acylated in the liver and epididymal white adipose tissue after being transported through the body as their free forms. This study presents a novel carotenoid metabolic pathway in mammals. [ABSTRACT FROM AUTHOR]

[Display omitted] • Melatonin treatment maintained the sensory quality of postharvest broccoli florets. • Melatonin induced the enrichment of endogenous melatonin in broccoli florets. • Melatonin down-regulated expression of carotenoid metabolism-related genes. • Melatonin inhibited contents of β-carotene, β-cryptoxanthin, zeaxanthin and lutein. The effect of melatonin treatment on the carotenoid metabolism in broccoli florets during storage was explored. The results indicated that 100 µmol/L of melatonin maintained the sensory quality of broccoli florets, which retarded the increase of the L* value and the decrease of the H value. Melatonin treatment increased the activities of tryptophan decarboxylase (TDC), tryptamine 5-hydroxylase (T5H), serotonin N -acetyltransferase (SNAT) and N -acetylserotonin methyltransferase (ASMT), leading to the enrichment of endogenous melatonin content in broccoli florets. Meanwhile, the treatment inhibited the concentrations of β-carotene, β-cryptoxanthin, zeaxanthin and lutein, which was beneficial in delaying the yellowing of broccoli. In addition, a series of carotenoid biosynthetic genes such as BoPSY, BoPDS, BoZDS, BoLCYβ and BoZEP was also suppressed by melatonin. Further analysis revealed that the lower carotenoid content and the down-regulated BoNCED expression in treated broccoli resulted in less accumulation of abscisic acid precursors, inhibiting abscisic acid production during the yellowing process. [ABSTRACT FROM AUTHOR]