The capacity for quenching of singlet oxygen has been mentioned above; the exceptionally high rate constant, K = 3.1 x 1010mol-1 s , renders it one of the most efficient of known quenchers of this powerful oxidant. In the plant, it probably protects chlorophyll, which produces singlet oxygen as a by-product of photosynthesis. In experiments with lymphoid cells, lycopene provided better protection against singlet oxygen damage than several other carotenoids tested. In skin exposed to UV light, lycopene disappears much more rapidly than ^-carotene. Lycopene is also able, in model systems, to inhibit the peroxidation of polyunsaturated lipids and the oxidation of DNA bases to products such as 8-hydroxydeoxyguanosine (8-OHdG). It can react directly with hydrogen peroxide and nitrogen dioxide.
Several studies in cell culture have shown a reduction in the formation of oxidation damage products such as malondialdehyde, and have found less injury to cells exposed to oxidants such as carbon tetrachloride, if lycopene (or other carotenoids) are present.
Another characteristic of lycopene and other caro-tenoids that may be relevant to inhibition of cancer cell growth is the modulation of gap junction cell-cell communication processes. In particular, carotenoids including lycopene have been shown to enhance the efficacy of the protein, connexin43, which helps to ensure the maintenance of the differentiated state of cells and to reduce the probability of unregulated cell division, and which is deficient in many tumors. They may also interact with and enhance the synthesis of binding proteins that downregulate the receptor for the growth-promoting hormone insulin-like growth factor-1 (IGF-1).
In certain circumstances, lycopene can reduce LDL-cholesterol levels, possibly by inhibiting hydroxymethylglutaryl CoA reductase (HMGCoA reductase), the rate-limiting enzyme for cholesterol synthesis (see below). Lycopene was shown to have modest hypocholesterolemic properties in one small clinical trial.
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