Stabilized sulforaphane for clinical use: Phytochemical delivery efficiency.

Scope: The isothiocyanate sulforaphane (SF) from broccoli is one of the most potent known inducers of the cytoprotective phase 2 response. Its role in a host of biochemical pathways makes it a major component of plant-based protective strategies for enhancing healthspan. Many nutritional supplements are now marketed that purport to contain SF, which in plants exists as a stable precursor, a thioglucoside hydroxysulfate.

Sulforaphane Bioavailability from Glucoraphanin-Rich Broccoli: Control by Active Endogenous Myrosinase.

Glucoraphanin from broccoli and its sprouts and seeds is a water soluble and relatively inert precursor of sulforaphane, the reactive isothiocyanate that potently inhibits neoplastic cellular processes and prevents a number of disease states. Sulforaphane is difficult to deliver in an enriched and stable form for purposes of direct human consumption. We have focused upon evaluating the bioavailability of sulforaphane, either by direct administration of glucoraphanin (a glucosinolate, or β-thioglucoside-N-hydroxysulfate), or by co-administering glucoraphanin and the enzyme myrosinase to catalyze its conversion to sulforaphane at economic, reproducible and sustainable yields.

Protection of humans by plant glucosinolates: efficiency of conversion of glucosinolates to isothiocyanates by the gastrointestinal microflora.

Plant-based diets rich in crucifers are effective in preventing cancer and other chronic diseases. Crucifers contain very high concentrations of glucosinolates (GS; β-thioglucoside-N-hydroxysulfates). Although not themselves protective, GS are converted by coexisting myrosinases to bitter isothiocyanates (ITC) which defend plants against predators.

Dietary glucoraphanin-rich broccoli sprout extracts protect against UV radiation-induced skin carcinogenesis in SKH-1 hairless mice.

Feeding broccoli sprout extracts providing daily doses of 10 micromol of glucoraphanin to SKH-1 hairless mice with prior chronic exposure to UV radiation (30 mJ cm(-2) of UVB, twice a week, for 17 weeks) inhibited the development of skin tumors during the subsequent 13 weeks; compared to the controls, tumor incidence, multiplicity, and volume were reduced by 25, 47, and 70%, respectively, in the animals that received the protective agent.

Precise determination of the erythema response of human skin to ultraviolet radiation and quantification of effects of protectors.

Background: We describe highly reproducible methods for quantifying the erythema response of precisely selected areas (spots) of human skin to graded doses of ultraviolet radiation (UVR). These methods have permitted evaluation of the efficacy of protectors, such as sulforaphane from crucifers, that defend cells through induction of cytoprotective (phase 2) genes.

Methods: Spots on the back were precisely located by opaque, adhesive, vinyl templates provided with 16 circular, 2.

Rapid body weight gain increases the risk of UV radiation-induced skin carcinogenesis in SKH-1 hairless mice.

Although it is well known that caloric restriction reduces the risk of chronic diseases including cancer, the role of weight gain in the development of UV light-induced tumors has not, to our knowledge, been investigated. In view of the increase in obesity worldwide, we asked the question whether there is any relationship between body weight gain and skin tumor development. We subjected 3 groups, each composed of 30 SKH-1 hairless female mice, to UV radiation (30 mJ/cm(2), twice weekly for 17 weeks) and observed tumor formation over the ensuing 8 to 13 weeks: group 1 received pelleted diet; group 2 received pellets during the irradiation period and was then switched to powder; and group 3 received powder exclusively.

A dicyanotriterpenoid induces cytoprotective enzymes and reduces multiplicity of skin tumors in UV-irradiated mice.

Inducible phase 2 enzymes constitute a primary line of cellular defense. The oleanane dicyanotriterpenoid 2-cyano-3,12-dioxooleana-1,9(11)-dien-28-onitrile (TP-225) is a very potent inducer of these systems. Topical application of TP-225 to SKH-1 hairless mice increases the levels of NAD(P)H-quinone acceptor oxidoreductase 1 (NQO1) and heme oxygenase 1 (HO-1) and protects against UV radiation-induced dermal thickening.

Sulforaphane mobilizes cellular defenses that protect skin against damage by UV radiation.

UV radiation (UVR) is a complete carcinogen that elicits a constellation of pathological events, including direct DNA damage, generation of reactive oxidants that peroxidize lipids and damage other cellular components, initiation of inflammation, and suppression of the immune response. Recent dramatic increases in the incidence of nonmelanoma skin cancers are largely attributable to higher exposure of an aging population to UVR. Therefore, the development of cellular strategies for intrinsic protection of the skin against the deleterious effects of UVR is imperative.

Protection against UV-light-induced skin carcinogenesis in SKH-1 high-risk mice by sulforaphane-containing broccoli sprout extracts.

Aerobic life, UV solar radiation, genetic susceptibility, and immune status contribute collectively to the development of human skin cancers. In addition to direct DNA damage, UV radiation promotes the generation of reactive oxygen intermediates that can cause oxidative damage and inflammation, and ultimately lead to tumor formation. Treatment of murine and human keratinocytes with the isothiocyanate sulforaphane elevated phase 2 enzymes and glutathione and protected against oxidant toxicity.