Carotenoids and apo‐carotenoids in human plasma after continued consumption of high β‐carotene or high lycopene tomato juice

Many studies have found associations between diets rich in carotenoids and a decreased risk for chronic diseases. Recent work has suggested that putative carotenoid metabolites resulting from the cleavage of β‐carotene (β‐C) and lycopene (LYC) by β‐C 15,15′‐oxygenase or β‐C 9,10‐oxygenase may be responsible for bioactivity attributed to the parent carotenoids. As a result, significant efforts have attempted to quantify these elusive carotenoid metabolites in vivo , with limited success. The objective of our study was to quantify both carotenoids and apo‐carotenoids in the blood of individuals consuming β‐C and LYC derived from whole foods. Healthy non‐smokers (n=35) consumed a low carotenoid diet for two weeks, and then consumed the same basal diet for 4 weeks with one of three juices: high β‐C tomato juice (360 mL, 30 mg β‐C, 35 μg apo‐carotenoids/day) or high LYC tomato juice (360 mL, 43 mg LYC, 120 μg apo‐lycopenoids/day) or a calorie matched cucumber juice control (360 mL, no detectable carotenoids). Targeted HPLC‐MS/MS methods were developed to quantitate apo‐carotenoids (apo‐8′, 10′, 12′, 14′, 15′‐carotenals, 13‐carotenone) and apo‐lycopenoids (apo‐6′, 8′, 10′, 12′, 14′, 15′‐lycopenals, 13‐lycopenone) in blood plasma with a limit of quantitation (LOQ) of ~50 pM. Plasma carotenoids were determined by HPLC. After four weeks, plasma β‐C levels reached 0.36, 0.62 and 3.18 μM in groups fed control diet, high‐LYC and high β‐C tomato juice, respectively, significantly increasing in the high‐β‐C group (P<0.001). Plasma lycopene reached 0.25, 1.40 and 0.58 μM in the control, high‐LYC and high β‐C groups, respectively, significantly increasing in the high‐LYC group (P<0.001). Plasma retinol was unchanged during this intervention, and not different among groups. Apo‐10‐ and 12‐carotenal were the only carotenals detected in plasma but not above our LOQ. Apo‐6′‐lycopenal was the only lycopenoid detected. Apo‐13‐carotenone was quantifiable in all subjects, measuring 0.46 ± 0.11 nM in control and 0.53 ± 0.12 in high‐LYC groups but higher ( P <0.05) in those on the high β‐C juice at 1.01 ±0.27 nM at the end of study. These data suggest blood apo‐13‐carotenone increases with supplemental β‐C intake, but its occurrence is not dependent on it. New data also suggests that apo‐13‐carotenone can be derived from vitamin A. Support or Funding Information This study was supported by NCI‐USDA‐IAA #ACN15005‐001‐00000. Carotenoid and apocarotenoid analyses were conducted within the Nutrient and Phytochemical Analytical Shared Resource (NPASR) at the OSU Comprehensive Cancer Center (NIH P30 CA016058).