Sulforaphane supplement from Broccoli sprouts extract, health benefit
Food and dietary source, safety, medical benefits for cancer prevention, what is the right dosage and pill dose
March 1 2017

Sulforaphane is an isothiocyanate naturally present in widely consumed vegetables, particularly in broccoli and broccoli sprouts. Isothiocyanates are found in cruciferous vegetables such as broccoli, Brussels sprouts, cauliflower, and cabbage. This substance has been getting a lot of attention lately with articles appearing in various health related magazines.

Sulforaphane is an effective cancer protective substance in cell culture and carcinogen-induced and genetic animal cancer models. Early research focused on its “blocking activity” via Phase 2 enzyme induction, as well as inhibition of enzymes involved in carcinogen activation, but there has been growing interest in other mechanisms of action. Sulforaphane protects against tumor development during the “post-initiation” phase, including cell cycle arrest and apoptosis induction.

Availability as a supplement
There are many dietary supplement companies that sell broccoli sprouts extracts that contain sulforaphane that you can buy.

Buy Sulforaphane supplement from Broccoli Sprouts Extract 500 mg, yielding 2,000 mcg sulforaphane. 1 mg equals 1,000 mcg.

Mechanism of action
Sulforaphane can stimulate cellular adaptation to redox stressors through transcription factor Nrf2. it is an indirect antioxidant that protects animal tissues from chemical or biological insults by stimulating the expression of several NF-E2-related factor-2 regulated phase 2 enzymes.

Human studies

Bioavailability and kinetics of sulforaphane in humans after consumption of cooked versus raw broccoli.
J Agric Food Chem. 2008. TNO Quality of Life, AJ Zeist, The Netherlands.
The aim of this study was to determine the bioavailability and kinetics of sulforaphane, the hydrolysis product of glucoraphanin, from raw and cooked broccoli. Eight men consumed 200 g of crushed broccoli, raw or cooked, with a warm meal in a randomized, free-living, open cross-over trial. Higher amounts of sulforaphane were found in the blood and urine when broccoli was eaten raw (bioavailability of 37%) versus cooked (3%). Absorption of sulforaphane was delayed when cooked broccoli was consumed (peak plasma time ) 6 h) versus raw broccoli. Excretion half-lives were comparable, 2.6 and 2.4 h on average, for raw and cooked broccoli, respectively. This study shows that consumption of raw broccoli results in faster absorption, higher bioavailability, and higher peak plasma amounts of sulforaphane, compared to cooked broccoli.

Animal studies

Effect of broccoli (Brassica oleracea) and its phytochemical sulforaphane in balanced diets on the detoxification enzymes levels of tilapia (Oreochromis niloticus) exposed to a carcinogenic and mutagenic pollutant.
Chemosphere. 2009.
Tilapia fish (Oreochromis niloticus) were fed with enriched diets containing broccoli and its phytochemical sulforaphane over 30 days. The levels of cytochrome P450, superoxide dismutase, catalase, lipid peroxidation and glutathione-S-transferase activities were measured. Basal value of cytochrome P450 activity was significantly increased as consequence of the broccoli and sulforaphane enriched diets, while no statistically significant changes were found on catalase and lipid peroxidation activities. After benzo(a)pyrene exposure, the cytochrome P450 activity increased to higher levels in the fish feed with broccoli and sulforaphane when compared with the control fish. Activities of antioxidant enzymes also varied but without significant difference with the control fish. Supported by the lower concentrations of BaP metabolites in bile from fish fed with broccoli or with sulforaphane enriched diets (indicating a better xenobiotic elimination) the cytochrome P450 induction could be considered beneficial for the detoxification because this transformation is the first step for PAH elimination by the phase II system.

Rheumatoid arthritis
Inhibition of synovial hyperplasia, rheumatoid T cell activation, and experimental arthritis in mice by sulforaphane, a naturally occurring isothiocyanate.
Arthritis Rheum. 2010; Catholic University of Korea, Seoul, South Korea.
To investigate whether sulforaphane, an isothiocyanate derived from cruciferous vegetables such as broccoli, regulates synoviocyte hyperplasia and T cell activation in rheumatoid arthritis. This substance was found to inhibit synovial hyperplasia, activated T cell proliferation, and the production of IL-17 and TNFalpha by rheumatoid T cells in vitro. The antiarthritic and immune regulatory effects of this nutrient, which were confirmed in vivo, suggest that it may offer a possible treatment option for rheumatoid arthritis.

In vitro studies
Lab studies in test tubes and cell cultures show sulforaphane to have a number or beneficial properties that could lead to the protection of cancer formation and as an anti-inflammatory agent. How a sulforaphane supplement would influence the body when ingested as a supplement is difficult to know without doing actual clinical trials.

Alzheimer’s disease
Sulforaphane protects against amyloid beta cytotoxicity.

Cyclooxygenase-2 (COX-2) overexpression has been associated with the grade, prognosis and recurrence of transitional cell carcinoma of the bladder. Sulforaphane down-regulates COX-2 expression in human bladder transitional cancer T24 cells at both transcriptional- and translational levels.

Brain cells
Sulforaphane stimulates the NRF2 pathway of antioxidant gene expression in astrocytes and protects them from cell death in an in vitro model of ischemia/reperfusion.

Breast cancer
Sulforaphane is believed to be responsible along with other isothiocyanates for the cancer preventive activity of such vegetables. This substance arrests mitosis, possibly by affecting spindle microtubule function. Sulforaphane arrests proliferation and mitosis by stabilizing microtubules in a manner weaker than but similar to more powerful clinically used antimitotic anticancer drugs and strongly support the hypothesis that inhibition of mitosis by microtubule stabilization is important for chemopreventive activity of this vegetable extract.

Sulforaphane inhibits TNF-alpha-induced activation of p38 MAP kinase and VCAM-1 and MCP-1 expression in endothelial cells. Sulforaphane may be useful as a therapeutic agent for the treatment of inflammatory diseases.

The combination of curcumin and sulforaphane is more effective than used alone in preventing inflammation

Lung cancer
Sulforaphane Induces Cell-Cycle Arrest and Apoptosis in Cultured Human Lung Adenocarcinoma LTEP-A2 Cells and Retards Growth of LTEP-A2 Xenografts in Vivo.

Oral cancer
Sulforaphane acts as a potent anti-oral cancer compound by inhibiting COX-2 activity.

Parkinson’s disease
Neurotoxicology. 2013. Neuroprotective effect of sulforaphane in 6-hydroxydopamine-lesioned mouse model of Parkinson’s disease.

Prostate cancer
Oral gavage of d,l-sulforaphane, a synthetic analogue of cruciferous vegetable-derived L isomer, three times per week beginning at 6 weeks of age, significantly inhibits prostate carcinogenesis and pulmonary metastasis in TRAMP mice by reducing cell proliferation and augmenting NK cell lytic activity without causing any side effects.

Its ability to inhibit tumor growth, metastasis, and angiogenesis and to enhance the therapeutic potential of TRAIL suggests that sulforaphane alone or in combination with tumor necrosis factor-related apoptosis-inducing ligand can be used for the management of prostate cancer.

In prostate cells sulforaphane primarily induces cellular defenses and inhibits cell growth by causing G2/M phase arrest. Based on the striking similarities in the gene expression patterns induced across experiments in prostate cells, it appears to be the primary bioactive compound present in broccoli sprouts, suggesting that broccoli sprouts can serve as a suitable source for sulforaphane in intervention trials.

Salivary gland cancer
Sulforaphane has a synergistic effect with 5-fluorouracil in high and low metastasis cell lines of salivary gland adenoid cystic carcinoma.