Carotenoids are natural pigments, which are found in bacteria, algae, fungi and plants, but which are not synthesized in animals. Animals and human beings get carotenoids through food. If we think on carotenoids, we think mostly on β-carotene, lycopene, lutein, zeaxanthin, and some others. But, meanwhile 600 to 700 carotenoids were identified. About 60 of them are components of our nutrition. Almost ten percent of all carotenoids in mammals can be metabolized to retinol, which is vitamin A, and can therefore function as vitamin A precursors. Carotenoids and retinoids act as antioxidants, influence the growth of the organism, immunological functions, the visual cycle, and modulate gene expression, too. Epidemiological data have strongly linked higher levels of carotenoid intake and increased circulating and tissue concentrations of carotenoids with reduced risk for various cancers, cardiovascular disease, and other diseases, even clinical intervention trials did not find homogeneous and significant evidence, that β-carotene alone leads to these benefits. In contrast to expectations and to the medical benefits induced by high intake of carotenoids by nutrition and via supplements in heavy smokers and asbestos workers the incidence and mortality in lung carcinoma even increased in high-dosage β-carotene supplementation. These observations initiated research projects with the aim, to find out the cause of potential toxic effects of high-dosage β-carotene supplementation. Obviously, the toxic effects can be attributed oxidative breakdown products of β-carotene and other carotenoids. The previous results argue for toxic effects only at high-dosage supplementation in heavy smokers and asbestos workers, i.e. under conditions of severe oxidative stress. From in vitro experiments was concluded, that even at very high carotenoid concentration a toxic effect towards biomolecules can be avoided if the other components of the antioxidative network are present at high levels.