TABLE 8-1 Concentrations of Selected Carotenoids in Human Serum and Tissues

Carotenoid

Serum (µmol/L)

Liver (µmol/g)

α-Carotene

0.02–0.47

0.075–10.8

 

(1.0–25.3 µg/dL)

(0.04–5.8 µg/g)

β-Carotene

0.04–2.26

0.39–19.4

 

(2.2–122.7 µg/dL)

(0.21–6.3 µg/g)

β-Cryptoxanthin

0.03–0.70

0.037–20.0

 

(1.4–38.2 µg/dL)

(0.05–11.0 µg/g)

Lutein

0.10–1.23

0.10–3.0

 

(5.8–69.8 µg/dL)

(0.06–6.9 µg/g)

Lycopene

0.05–1.05

0.20–17.2

 

(2.7–54.6 µg/dL)

(0.11–11.1 µg/g)

SOURCE: Data from Schmitz et al. (1991) and Kaplan et al. (1990) for tissues and Iowa State University Department of Statistics (1999) for serum.

were decreased deoxyribonucleic acid strand breaks observed when 22 mg/day of β-carotene was administered as carrot juice (Pool-Zobel et al., 1997) and lowered copper-induced oxidation of low-density lipoprotein when 12 or 24 mg/day of β-carotene was given along with vitamins C and E (Mosca et al., 1997). As shown in Table 8-2, feeding β-carotene in amounts greater than 25 mg/day generally resulted in inconsistent responses of the biological markers monitored. Administration of β-carotene to subjects with increased oxidative stress (e.g., smoking, cystic fibrosis) was associated with more consistent evidence of decreased lipid peroxidation compared to studies in which subjects without known additional oxidative stress were given β-carotene. In studies that involved depletion followed by repletion of body stores of β-carotene, as indicated by plasma concentrations, the biological markers that were negatively altered as a result of depleted body stores of β-carotene were restored to baseline values as a consequence of repletion (Table 8-2).

In summary, results from some studies show improvement of measures of antioxidant activity due to intake of relatively high levels of β-carotene, while studies that investigated low to modest levels of β-carotene show no or inconsistent changes in the same activities.



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