Antioxidant effect
The antioxidant effect of beta-carotene is based on the inactivation (quenching) of reactive oxygen compounds. These include, for example, peroxyl radicals, superoxide radical ions, singlet oxygen, hydrogen peroxide, and hydroxyl and nitrosyl radicals, which are produced by aerobic metabolic processes, photobiological effects, endogenous defense processes, and exogenous noxious agents. As free radicals, they can react with lipids, especially polyunsaturated fatty acids and cholesterol, proteins, nucleic acids, and carbohydrates, modifying or destroying them. In lipid peroxidation, a chain reaction occurs whereby, as a result of a radical attack, membrane lipids become lipid radicals by splitting off a hydrogen atom. The latter react with oxygen and are converted to peroxyl radicals. Subsequently, the peroxyl radicals remove a hydrogen atom from further fatty acids, which in turn radicalize them. The end products of lipid peroxidation include malondialdehyde or 4-hydroxynonenal, which exhibit strong cytotoxic effects and can alter DNA. Oxidative DNA damage can lead to strand breaks, base modifications, or deoxyribose fragmentation. When free radicals react with proteins, changes in primary, secondary, and tertiary structure and amino acid side chains can result. These structural modifications are often associated with a loss of function of the corresponding protein molecules.
Interaction with peroxyl radicals
Beta-carotene exerts its effects in the lipid phase. As an electron acceptor, it has the ability to bind peroxyl radicals and thus interrupt the chain reaction in lipid peroxidation. In this way, the carotenoid inhibits the formation of free radicals in the function of a “free radical scavenger”. In addition, by aborting lipid peroxidation, beta-carotene prevents the destruction of polyunsaturated fatty acids – omega-3 fatty acids (such as alpha-linolenic acid, EPA and DHA) and omega-6 fatty acids (such as linoleic acid, gamma-linolenic acid and arachidonic acid) – in tissues, cells, cell organelles and artificial systems, protecting membrane lipids, lipoproteins and depot lipids. By preserving essential fatty acids from peroxidation as a chain-breaking antioxidant, beta-carotene complements the actions of other endogenous – for example, superoxide dismutases (zinc-, manganese– and copper-dependent enzymes), catalases (iron-dependent enzymes) and glutathione peroxidases (selenium-dependent enzymes) – or exogenous – for example vitamins A, C, E (tocopherol), coenzyme Q10, glutathione, lipoic acid and polyphenols such as flavonoids – antioxidant systems. Inactivation of peroxyl radicals depends on oxygen partial pressure. At low oxygen concentrations, beta-carotene can effectively exert its antioxidant properties. In contrast, under high oxygen concentrations, it has a prooxidant effect. During the quenching process, beta-carotene undergoes auto-oxidation, which means it is destroyed. In contrast to vitamin E, no mechanisms for regeneration are yet known for beta-carotene.
Interaction with singlet oxygen
Singlet oxygen is one of the most aggressive radicals, the formation of which occurs in a light-dependent reaction. Tissues exposed to light, such as skin and eyes, are therefore particularly susceptible to oxidative damage. In the deactivation of singlet oxygen, beta-carotene acts as an intermediate carrier of energy. When exposure to light results in the formation of singlet oxygen, the carotenoid intercepts this highly reactive form. It extracts the energy from the radical in the reaction sequence and becomes an excited carotenoid that releases the energy in interaction with its environment in the form of heat – “physical quenching.” Thus, beta-carotene renders oxygen free radicals harmless and protects cell structures from oxidative damage. The quenching ability of a carotenoid depends on the number of double bonds. Accordingly, beta-carotene with its 11 conjugated double bonds exhibits the strongest quenching activity together with lycopene. A deficiency of antioxidant substances leads to a shift in the balance of antioxidants and prooxidants (reactive oxygen compounds) to the side of the prooxidants. This imbalance is called oxidative stress, which is due either to an increased occurrence of free radicals or to a weakening of the antioxidant protection system.Both a high number of free radicals and a deficiency of antioxidants increase susceptibility to stress and thus to disease.
Effect on the immune system
Beta-carotene contributes to the stimulation of the immune system. The carotenoid increases the proliferation of T and B cells, the number of T helper cells, and the activity of natural killer cells. Intervention studies indicated that beta-carotene at a dose up to 25 mg/day increased natural killer cell activity in men over 65 years of age. In 51- to 64-year-old men, adhesion molecule expression and exvivo secretion of tumor necrosis factor-alpha (TNF-α) were increased.
Intercellular communication
Beta-carotene may stimulate communication between cells via gap junctions. Gap junctions are channel-like connections between neighboring cells that are composed of a protein called connexin. They are essential for the exchange of low molecular weight signaling, nutrients and vital substances. Furthermore, gap junctions are essential for the regulation of growth and development processes. In contrast to normal cells, which are in constant contact with neighboring cells through gap junctions, tumor cells generally exhibit little intercellular communication. This is due to tumor promoters, which impair intercellular communication via gap junctions. In contrast, carotenoids promote intercellular contact by increasing the expression of mRNA for connexin. By improving intercellular communication via gap junctions, uncontrolled growth of degenerate cells can be suppressed. Accordingly, beta-carotene contributes to tumor prevention. A deficiency of beta-carotene worsens the signal transmission via gap junctions. As a result, the important function of gap junctions to regulate growth and development processes is diminished. Eventually, this leads to uncontrolled development of degenerate cells, increasing the risk of tumor disease.
Skin Protection
Beta-carotene intake leads to an increase in skin carotenoid levels, with the provitamin accumulating primarily in the epidermis as well as the subcutis of the skin. Due to its antioxidant properties, beta-carotene can actively protect against the negative effects of UVA and UVB rays. The carotenoid binds free radicals, which are increasingly formed in the skin due to the aggressive ultraviolet radiation. Subsequently, beta-carotene prevents their accumulation by interrupting radical chain reactions. As a result of neutralizing free radicals, beta-carotene can therefore help prevent cell damage and significantly reduce skin redness – erythema formation. Studies in which beta-carotene was used as an oral sunscreen showed that a clear reduction in UV light-induced erythema formation was achieved when > 20 mg beta-carotene/day was administered for 12 weeks compared to the control group. Overall, beta-carotene can increase the basic protection of the skin. The provitamin also counteracts pigment disorders – patchy lightening (hypopigmentation, for example acral vitiligo) or darkening of the skin (hyperpigmentation, for example chloasma (melasma)) due to local shifts in pigmentation. It brings about pigment balancing, as beta-carotene leads to color equalization in weakly pigmented areas – especially after sunlight – and effectively protects hyperpigmented areas from sunlight.
Eye Protection
UVA and UVB rays can damage the lens of the eye through oxidation processes, which can lead to clouding of the lens and eventually cataract. Beta-carotene in combination with other antioxidant protective substances can prevent the oxidation processes and thus significantly reduce the risk of cataract. According to large multicenter intervention studies in China, carotenoids together with vitamin E and selenium can reduce cataract incidence by up to 40%.