Lutein is one of the predominant carotenoids that accumulates in both the lens and retinal macula ⁽²⁴⁾. It scavenges reactive oxygen species, preventing damage to DNA and protein molecules ^(19) (25). As an oxycarotenoid, its structure is less hydrophobic than beta-carotene and lycopene. This enables lutein to react with free radicals in a membrane’s aqueous phase, resulting in increased membrane integrity, which may in turn affect tissue permeability to oxygen and other molecules ⁽¹⁹⁾. It may also protect against ocular damage by reducing the amount of blue light that reaches photoreceptors ⁽²⁵⁾.

As a nonprovitamin A carotenoid, lutein does not have any vitamin A activity, but does have antioxidant, anti-inflammatory, and immune-enhancing properties. In an obese rat model, lutein independently reduced superoxide dismutase activity, and also raised glutathione peroxidase activity in lean rats when combined with ascorbic acid ⁽²⁶⁾. In vitro and atherosclerotic mouse models demonstrate the ability of lutein to inhibit monocyte inflammatory responses to low-density lipoprotein (LDL) in the artery wall and reduce monocyte migration ⁽⁷⁾. In humans, lutein supplementation decreases lipid peroxidation and inflammatory response ⁽⁵⁾.

Carotenoids including lutein inhibit mutagenesis and transformation, and premalignant lesions ⁽¹⁾. In murine mammary cancer models, dietary lutein selectively modulated apoptosis and inhibited angiogenesis by increasing p53 and Bax proapoptotic gene expression, while decreasing Bcl-2 antiapoptotic gene expression with a subsequent increase in Bax:Bcl-2 ratio in tumors ⁽²⁷⁾. Lutein-mediated AP-1 suppression and anti-inflammatory effects are due to its antioxidative and p38/c-Jun-N-terminal kinase inhibitory activities ⁽³⁾. In a hepatocellular carcinoma animal model, lutein reduced γ-glutamyl transpeptidase activity, a marker of cellular proliferation ⁽²⁾.