Carotenoids

Carotenoids are compounds found in photosynthetic organisms, commonly used as pigments or dyes. Most humans and animals cannot synthesize carotenoids endogenously and must obtain them by eating fruits and vegetables. Structurally, carotenoids consist of isoprene units, which confer effective free radical scavenging capabilities. As antioxidants, carotenoids exhibit various bioactivities and health benefits, including reduced risk of breast, prostate, and stomach cancers.

Figure 1. Chemical structure of β-carotene

β-Carotene (C110501, C425668, C110502) is a red-orange pigment found in sweet potatoes, carrots, pumpkins, and spinach. It serves as a precursor to vitamin A, capable of being cleaved into two molecules of vitamin A. Its intake is associated with a reduced risk of amyotrophic lateral sclerosis (ALS), potentially due to alleviation of oxidative stress. High dietary consumption is also linked to lowered risks of breast and stomach cancers. Administration of β-carotene inhibits invasion of liver cancer cells, and in breast cancer animal models, intake within a high-fat diet reduces tumor incidence and growth.

Figure 2. Chemical structure of lycopene

Lycopene (L465063) is another bioactive red pigment widely found in red fruits and vegetables such as tomatoes, melons, and grapefruits, possessing antioxidant properties. Its intake helps protect against ultraviolet-induced skin damage by increasing procollagen I levels and decreasing MMP-1 levels, a biomarker of UV-induced erythema. In liver cancer animal models, lycopene alleviates diethylnitrosamine-induced reductions in antioxidant enzyme activity, inflammation, and activation of mTOR and NF-κB pathways, thereby reducing the incidence, number, and size of liver nodules.

Figure 3. Chemical structure of capsaicin

Capsaicin (C107693, C107692, C107691, C423851) is also widely used in research. It reduces the expression of IL-6, TNF-α, and MCP-1, thereby inhibiting adipocyte inflammation induced by obesity. Additionally, capsaicin suppresses the cell cycle and induces apoptosis in leukemia cells, potentially through upregulation of PPARγ.

References

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