Send to

Choose Destination
Biomed Pharmacother. 2004 Mar;58(2):100-10.

The role of carotenoids in the prevention of human pathologies.

Author information

Université de Paris-Faculté de Pharmacie CNRS UMR 8612, 5, rue Jean Baptiste Clément, 94200 Chatenay Malabry, France.


Reactive oxygen species (ROS) and oxidative damage to biomolecules have been postulated to be involved in the causation and progression of several chronic diseases, including cancer and cardiovascular diseases, the two major causes of morbidity and mortality in Western world. Consequently dietary antioxidants, which inactivate ROS and provide protection from oxidative damage are being considered as important preventive strategic molecules. Carotenoids have been implicated as important dietary nutrients having antioxidant potential, being involved in the scavenging of two of the ROS, singlet molecular oxygen (1O2) and peroxyl radicals generated in the process of lipid peroxidation. Carotenoids are lipophilic molecules which tend to accumulate in lipophilic compartments like membranes or lipoproteins. Chronic ethanol consumption significantly increases hydrogen peroxide and decreases mitochondrial glutathione (GSH) in cells overexpressing CYP2E1. The depletion of mitochondrial GSH and the rise of hydrogen peroxide are responsible for the ethanol-induced apoptosis. Increased intake of lycopene, a major carotenoid in tomatoes, consumed as the all-trans-isomer attenuates alcohol induced apoptosis in 2E1 cells and reduces risk of prostate, lung and digestive cancers. Cancer-preventive activities of carotenoids have been associated as well as with their antioxidant properties and the induction and stimulation of intercellular communication via gap junctions which play a role in the regulation of cell growth, differentiation and apoptosis. Gap junctional communication between cells which may be a basis for protection against cancer development is independent of the antioxidant property.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center