Product Details: Sulforaphane+
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DISCUSSION: Sulforaphane + TM contains sgsTM and wasabia japonica extract. sgsTM is a patented broccoli seed concentrate rich in glucoraphanin, which is converted into the isothiocyanate sulforaphane. Wasabia japonica contains similar isothiocyanates such as 6-MITC. Sulforaphane and 6-MITC have been documented to induce the Phase-2 detoxification enzyme system. | ||||
| 30 Vegi-Caps 380 mg AOR04144 SUPPLEMENT FACTS: Serving Size: 1 Capsule
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Non-medicinal ingredients: none. Capsule: hypromellose, sorbitol, silicon dioxide, water. Product produced under Canadian patent 2,232,488 licensed from Brassica Protection Products LLC. sgsTM is a trademark of Brassica Protection Products LLC. AOR guarantees that no ingredients not listed on the label have been added to the product. Contains no corn, wheat, gluten, nuts, dairy, soy, eggs, fish or shellfish. Suggested Use Take 1 capsule daily with/without food, or as directed by a qualified health practitioner. Do not use if pregnant or breastfeeding. Main Applications • Liver detoxification • Normal cellular growth and differentiation • Immune support Source Broccoli sprouts Wasabi Pregnancy / Nursing None. Cautions None. *These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. The information and product descriptions appearing on this website are for information purposes only, and are not intended to provide medical advice to individuals. Consult with your physician if you have any health concerns, and before initiating any new diet, exercise, supplement, or other lifestyle changes. Any reproduction in whole or part and in print or electronic form without express permission is strictly forbidden. Permission to reproduce selected material may be granted by contacting AOR Inc. Copyright © 2005, Advanced Orthomolecular Research |
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Imagine a cell that never dies and replicates without end - such cells exist; an eternal cell that replicates uncontrollably is a cancer cell. Cancer develops when the machinery that induces the cellular death of abnormal cells (apoptosis), is inactivated. The answer to the treatment of cancer is to reactivate cellular apoptosis or to improve the function of the immune system so that it can target and destroy abnormal cells.
Several nutrients found in our diet have been shown to possess anticarcinogenic properties. For example, cruciferous vegetables contain indoles and isothiocyanates, and high intakes of cruciferous vegetables have been associated with lower |
| risk of lung and colorectal cancer in epidemiological studies. Other nutrients can prevent the development of cancer, support our immune system and improve the cellular processes that lead to apoptosis. Researchers have determined that in the 22-year span from 1981 to 2002, 62% of new cancer treatments were of natural origin. Natural ingredients can and have played an important role in the prevention and treatment of cancer. Two nutrients that have attracted considerable scientific interest with regards to abnormal cellular differentiation and growth are broccoli sprouts and wasabi extracts. The anticarcinogenic properties of both plants come from their isothiocyanate content: Sulforaphane and 6-methylsulfinylhexyl isothiocyanate (6-HITC) - respectively. 6-HITC is also a sulforaphane analogue. Sulforaphane is the most characterized isothiocyanate.
Sulforaphane is a natural compound found in broccoli sprouts that has been shown to inhibit tumor formation. Sulforaphane extracts have several benefits for cancer patients. These include: • Protecting DNA from mutagens Sulforaphane induces several cellular signals that lead to apoptosis in cancer cells. Animal studies also demonstrate that sulforaphane improves the immune response. Sulforaphane also increases the production of immune cells in the bone marrow and leads to higher levels of circulating antibodies. Furthermore, sulforaphane improves macrophage and natural killer cell activity. The latest research confirms that sulforaphane is a promising agent to prevent, treat and reverse cancer. Sulforaphane acts against a variety of cancer types and is helpful at early, intermediate or late stages of the disease. New research suggests that sulforaphane also protects the heart. In a rat model of ischemia (oxygen shortage), rats that were fed broccoli extracts had significantly improved ventricular function and reduced myocardial infarct size. The extracts also prevented the cell death of heart muscle cells and preserved and increased levels of the thioredoxin family of proteins, which play an important protective role in a number of degenerative diseases including cardiovascular disease. These results are attributable to sulforaphane's beneficial impacts on cellular pathways. Recent in vitro studies have shown that Sulforaphane also has the potential of reducing the risk of vascular disease in people with diabetes. It was found that Sulforaphane was able to activate an important transcription factor called NF-E2-related factor-2 (nrf2), which is responsible for stimulating the production of numerous protective enzymes that are able to reverse certain negative effects caused by hyperglycemia, that are responsible for an increased risk of vascular disease among diabetics. Sulforaphane's beneficial impact on this cellular pathway results in a reduction of epithelial cell dysfunction, a 73% decrease in reactive oxygen species, and reduced oxidative stress. Wasabi (Wasabia japonica syn. Eutrema japonica) or Japanese horse radish, is a highly valued plant in Japanese cuisine and is a member of the brassicacea family which includes over 3000 species. These include Brussels sprouts, broccoli, mustard, cabbages and many others. Wasabi is a condiment traditionally served with raw fish (sushi and sashimi) and noodle (soba) dishes in Japan. The ground root-like rhizome pungently flavours many other foods in Japanese cuisine and its bright green colour provides for a palliative colour contrast, something for which Japanese dishes are famous. In the last twenty years, because of the low supply of fresh wasabi rhizomes, substitutes made of mixtures of horseradish, mustard and food colouring have often taken the place of freshly prepared wasabi. However, true wasabi plant extract (as contained in Sulforaphane +TM) has been shown to combat carcinogenesis by inhibiting cellular proliferation, scavenging free radicals and inducing apoptosis. Like many plants in the mustard family, wasabi contains compounds known as glucosinolates. When the plant cells are chewed or ground up, these compounds are converted into isothiocyanates (ITCs) which are associated with inducing Phase one and Phase II detoxification enzymes and have a fantastic array of biomedical qualities. First of all, ITCs work very rapidly and in low doses to counter inflammation. This happens when a compound called 6-MITC inhibits lipoxygenase, cyclooxygenase and cAMP phosphodiesterase, all of which contribute to inflammation. By blocking these, wasabi may provide a way to control allergies, asthma, and eczema. In addition, wasabi is an effective scavenger of reactive oxygen species (ROS), an important point to consider since most chronic diseases are thought to be associated with ROS to some degree or another. The isothiocyanates within the wasabi plant, particularly 6-HITC, are considered to be up to 40 times more potent than more common isothiocyanates found in such sources as cabbage, Brussels sprouts, and mustard seeds. Wasabi may have antibiotic-like potential, since the vapors of ITC inhibit the growth of many types of bacteria, yeast and mold. For instance, 6-MITC can be toxic towards Staphylococcus aureus and Escherichia Coli. ITCs can help fight off Streptococcus mutans which causes dental cavities, and Helicobacter pylori, which causes gastric ulcers and stomach cancer. 6-MITC can also block inappropriate platelet aggregation, for instance during heart attacks and strokes. Still more promising, wasabi appears to be useful in cancer treatment and prevention. The ITCs block certain enzymes that may potentiate carcinogenesis, while inducing the action of detoxifying enzymes. ITCs can prevent cancer cells from metastasizing, thereby preventing the spread of the disease. They can also cause cancer cells to commit cell suicide by the process known as apoptosis. Wasabia extracts have been shown to be effective against a variety of cancer cell types, including leukemia, breast cancer, lung cancer and colorectoral cancer. However, they do all this without any harm to healthy cells, which means that no side effects have been encountered. Finally, wasabi seems to be helpful in many other ways, from protecting kidney function in diabetics to protecting cardiovascular function to reducing diarrhea. An extract from its leaf stalk has even been shown to stimulate bone calcification. The research on isothiocyanates from wasabi and broccoli has shown that they are ideal for those whose cellular function has gone unchecked and for those whose immune system has been unable to keep up with the inner turmoil engendered by the development of cancer. Indeed, as concluded in one study on sulforaphane, the nutrient can "prevent, delay, or reverse preneoplastic lesions, as well as to act on cancer cells as a therapeutic agent." Broccoli: A unique vegetable that protects mammalian hearts through the redox cycling of the thioredoxin superfamily. Mukherjee S, Gangopadhyay H and Das DK. Journal of Agriculture and Food Chemistry. 2008;56:609-617. Fimognari C, Hrelia P. Sulforaphane as a promising molecule for fighting cancer. Review. Mutat Res. 2007 May-Jun; 635(2-3): 90-104. Nagel G, Oates B. A phytomedical overview: Wasabia Japonica. Naturopathic Doctor News and Review. 2007 Aug: 3(8): 8-9. Jin, CY et al. Sulforaphane sensitizes tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis through downregulation of ERK and Akt in lung adenocarcinoma A549 cells. Carcinogenesis. 2007 May;28(5):1058-66. Fuke Y et al. Preventive effect of oral administration of 6-(methylsulfinyl)hexyl isothiocyanate derived from wasabi (Wasabia japonica Matsum) against pulmonary metastasis of B16-BL6 mouse melanoma cells. Cancer Detect Prev. 2006: 30:174-179. Yu R et al. The effect of 6-methylthiohexyl isothiocyanate isolated from Wasabia japonica (wasabi) on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-inducing lung tumorigenesis in mice. Cancer Lett. 2000: 155:115-120. Hashimoto T et al. 6-methylsulfinylhexyl isothiocyanate inhibits cell cycle progression in mouse epidermal JB6 cells. Dietary Factors and Cancer Prevention. 2004: 9. Hasegawa, N et-al. Comparison of effects of Wasabi japonica and allyl isothiocyanate on the growth of four strains of Vibrio parahaemolyticus in lean and fatty tuna meat suspension. Int. J. Food. Micro. 1999:49;27-34. Das, S et-al. Cancer modulation by glucosinolates: A review. Curr. Science. 2000:79;1665-1671. Kinae,N et-al. Functional properties of wasabi and horseradish. Biofactors.2000:13;265-269. Depree JA et al. Flavour and pharmaceutical properties of the volatile sulphur compounds of Wasabi (Wasabia japonica). Food Res Intern. 1998: 31:329-337. Kumagai H et al. Analysis of volatile components in essential oil of upland Wasabi and their inhibitory effects on platelet aggregation. Bioscience Biotechnology and Biochemistry. 1994: 58:2131-2135. The information and product descriptions appearing on this website are for information purposes only, and are not intended to provide medical advice to individuals. Consult with your physician if you have any health concerns, and before initiating any new diet, exercise, supplement, or other lifestyle changes. Any reproduction in whole or part and in print or electronic form without express permission is strictly forbidden. Permission to reproduce selected material may be granted by contacting AOR Inc. Copyright © 2005, Advanced Orthomolecular Research |
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| Activation of NF-E2-related factor-2 reverses biochemical dysfunction of endothelial cells induced by hyperglycemia linked to vascular disease. Diabetes. August 2008. Early Online Publication Xue M, Qian Q, Antonysunil A, Rabbani N, Babei-Jadidi R, Thornalley PJ OBJECTIVE - Sulforaphane (SFN) is an activator of transcription factor NF-E2-related factor-2 (nrf2) that regulates gene expression through the promoter antioxidant response element (ARE). Nrf2 regulates the transcription of a battery of protective and metabolic enzymes. The aim of this study was to assess if activation of nrf2 by SFN in human microvascular endothelial cells prevents metabolic dysfunction in hyperglycemia. RESEARCH DESIGN AND METHODS - Human microvascular HMEC-1 endothelial cells were incubated in low and high glucose concentrations (5 and 30 mM) and activation of nrf2 assessed by nuclear translocation. The effect of SFN on multiple pathways of biochemical dysfunction, increased reactive oxygen species (ROS) formation, hexosamine pathway, protein kinase C pathway and increased formation of methylglyoxal, was assessed. RESULTS - Activation of nrf2 by SFN induced nuclear translocation of nrf2 and increased ARE-linked gene expression. For example, 3 - 5 fold increased expression of transketolase and glutathione reductase. Hyperglycemia increased the formation of ROS - an effect linked to mitochondrial dysfunction and prevented by SFN. ROS formation was increased further by knockdown of nrf2 and transketolase expression. This also abolished the counteracting effect of SFN, suggesting mediation by nrf2 and related increase of transketolase expression. SFN also prevented hyperglycemia-induced activation of the hexosamine and protein kinase C pathways, and prevented increased cellular accumulation and excretion of the glycating agent, methylglyoxal. CONCLUSION - We conclude that activation of nrf2 may prevent biochemical dysfunction and related functional responses of endothelial cells induced by hyperglycemia in which increased expression of transketolase has a pivotal role. Broccoli: A Unique Vegetable That Protects Mammalian Hearts through the Redox Cycling of the Thioredoxin Superfamily. J Agric Food Chem. 2008 Jan 23;56(2):609-17. Mukherjee S, Gangopadhyay H, Das DK. Epidemiological evidence indicates several health benefits of the consumption of broccoli, especially related to chemoprevention. Because broccoli contains high amounts of selenium and glucosinolates (particularly glucoraphanin and isothiocyanate sulforaphane), which can produce redox-regulated cardioprotective protein thioredoxin (Trx), it was reasoned that consumption of broccoli could be beneficial to the heart. To test this hypothesis, a group of rats were fed broccoli (slurry made with water) through gavaging; control animals were gavaged water only. After 30 days, the rats were sacrificed; isolated hearts perfused via working mode were made ischemic for 30 min followed by 2 h of reperfusion. The results demonstrated significant cardioprotection with broccoli as evidenced by improved postischemic ventricular function, reduced myocardial infarct size, and decreased cardiomyocyte apoptosis accompanied by reduced cytochrome c release and increased pro-caspase 3 activities. Ischemia/reperfusion reduced both RNA transcripts and protein levels of the thioredoxin superfamily including Trx1, Trx2, glutaredoxin Grx1, Grx2, and peroxiredoxin (Prdx), which were either restored or enhanced with broccoli. Broccoli enhanced the expression of Nrf2, a cytosolic suppressor of Keap1, suggesting a role of antioxidant response element (ARE) in the induction of Trx. Additionally, broccoli induced the expression of another cardioprotective protein, heme oxygenase (HO)-1, which could be transactivated during the activation of Trx. Examination of the survival signal revealed that broccoli caused the phosphorylation of Akt and the induction of Bcl2 in concert with the activation of redox-sensitive transcription factor NFkappaB and Src kinase, indicating a role of Akt, Bcl2, and cSrc in the generation of survival signal. Taken together, the results of the present study indicate that the consumption of broccoli triggers cardioprotection by generating a survival signal through the activation of several survival proteins and by redox cycling of thioredoxins. Enhancing expression of Nrf2-driven genes protects the blood brain barrier after brain injury. J Neurosci. 2007 Sep 19;27(38):10240-8. Zhao J, Moore AN, Redell JB, Dash PK. The integrity of the blood-brain barrier (BBB) is critical for normal brain function, and its compromise contributes to the pathophysiology of a number of CNS diseases and injuries. Using a rodent model of brain injury, the present study examines the pathophysiology of BBB disruption. Western blot and immunohistochemical analyses indicate that brain injury causes a loss of capillary endothelial cells and tight junction proteins, two critical components of the BBB. Activation of the transcription factor NF-E2-related factor-2 (Nrf2) by sulforaphane, a naturally occurring compound present in high levels in cruciferous vegetables, significantly increased the expression of endogenous cytoprotective genes in brain tissue and microvessels as indicated by real-time PCR analysis. Postinjury administration of sulforaphane reduced the loss of endothelial cell markers and tight junction proteins and preserved BBB function. These protective effects were dependent on the activity of Nrf2. Injured rats pretreated with decoy oligonucleotides containing the binding site of Nrf2, and mice lacking the nrf2 gene, did not benefit from sulforaphane administration. These findings indicate a potential therapeutic usefulness for Nrf2-activating molecules to improve the function of the neurovascular unit after injury. Sulforaphane induces cell cycle arrest and apoptosis in murine osteosarcoma cells in vitro and inhibits tumor growth in vivo. Oncol Rep. 2007 Nov;18(5):1263-8. Matsui TA, Murata H, Sakabe T, Sowa Y, Horie N, Nakanishi R, Sakai T, Kubo T. Sulforaphane (SFN), a naturally occurring isothiocyanate, is an attractive agent due to its potent anticancer effects. SFN suppresses the proliferation of various cancer cells in vitro and in vivo. In this study, we report that SFN inhibited the proliferation of cultured murine osteosarcoma LM8 cells. Twenty micromolar SFN completely inhibited the growth of LM8 cells and caused G2/M-phase arrest. SFN induced the expression of p21(WAF1/CIP1) protein causing the cell cycle arrest in a dose-dependent manner. SFN induced apoptosis which was characterized by the appearance of cells with sub-G1 DNA content and the cleavage and activation of caspase-3. We showed that SFN induced the growth arrest and up-regulated the expression of p21(WAF1/CIP1) protein in a p53-independent manner in human osteosarcoma MG63 cells. We found that intraperitoneal administration of SFN (1 or 2 mg, 5 times/week) significantly inhibited the growth of LM8 xenografts to <30% of the controls in a preclinical animal model without causing any toxicity. In osteosarcoma cells, our findings provide in vivo evidence for the efficacy of SFN against the advanced growth of tumor. We showed that SFN induces cell cycle arrest and apoptosis in osteosarcoma cells and inhibits tumor xenograft growth. Furthermore, SFN is a potent inducer of p21(WAF1/CIP1) in osteosarcoma cells. These results raise the possibility that SFN may be a promising candidate for molecular-targeting chemotherapy against osteosarcoma. Preventive effect of oral administration of 6-(methylsulfinyl)hexyl isothiocyanate derived from wasabi (Wasabia japonica Matsum) against pulmonary metastasis of B16-BL6 mouse melanoma cells. Cancer Detect Prev. 2006;30(2):174-9. Epub 2006 Apr 27. Fuke Y, Shinoda S, Nagata I, Sawaki S, Murata M, Ryoyama K, Koizumi K, Saiki I, Nomura T. AIM: Effect of oral administration of 6-(methylsulfinyl)hexyl isothiocyanate (6-MITC) or a 6-MITC-containing T-wasabi fraction from wasabi root (Wasabia japonica Matsum) to inhibit the macroscopic pulmonary metastasis was studied with a murine B16-BL6 melanoma model. METHOD: Two administration routes, subcutaneous or intravenous, and two administration times, prior to or concomitant with tumor inoculation, of 6-MITC or T-wasabi against the metastatic foci formation in C57BL/6J mouse lungs were compared. RESULTS: The number of metastasized foci per lung in either subcutaneous or intravenous injection was significantly reduced by intake of 6-MITC or a T-wasabi fraction. The maximum reduction by a T-wasabi fraction reached to 82%. Fifty-six percent of foci formation was inhibited by a 2 week-prior administration of 6-MITC (200 microM), whereas only 27% inhibition was obtained by a concomitant administration with tumor inoculation. Neither 6-MITC nor T-wasabi at tested concentrations showed any toxic effects. DISCUSSION: Together with our previous results, a component of the Japanese pungent spice, wasabi appears to inhibit not only tumor cell growth but also tumor metastasis. Therefore, 6-MITC from wasabi is apparently a useful dietary candidate for controlling tumor progression. The information and product descriptions appearing on this website are for information purposes only, and are not intended to provide medical advice to individuals. Consult with your physician if you have any health concerns, and before initiating any new diet, exercise, supplement, or other lifestyle changes. Any reproduction in whole or part and in print or electronic form without express permission is strictly forbidden. Permission to reproduce selected material may be granted by contacting AOR Inc. Copyright © 2005, Advanced Orthomolecular Research |
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