Sulforaphane is a bioactive compound derived from certain cruciferous vegetables, particularly broccoli (and its sprouts) and red kale. Robust evidence from epidemiological, clinical, rodent, and in vitro studies has demonstrated that sulforaphane exhibits antioxidant and anti-inflammatory properties and may be beneficial against a wide range of chronic and acute diseases, including autism, cancer, metabolic dysfunction, and many others and may ameliorate some of the harmful effects associated with exposure to air pollution.

Sulforaphane exerts its therapeutic effects through various mechanisms, such as inhibition of phase 1 drug-metabolizing enzymes, induction of phase 2 protective enzymes, and inhibition of cell proliferation.[1] [2] [3] When used in conjunction with various anticancer treatments, sulforaphane appears to work in a synergistic fashion to potentiate the drugs' effects.[4]

This overview describes sulforaphane's chemistry and synthesis, factors that influence its bioavailability and bioactivity, sulforaphane's biological effects, and individual differences in response to sulforaphane.

Chemical structure and behavior of sulforaphane

Sulforaphane is an isothiocyanate, a non-nutrient compound derived from cruciferous vegetables. Isothiocyanates exert a wide range of beneficial health effects in humans, due to their anticancer, antidiabetic, and anti-inflammatory effects, among others.

Metabolic biotransformation

As non-nutrients, isothiocyanates such as sulforaphane experience vigorous biotransformation in the human gut and demonstrate a wide range of bioavailability. The compounds passively diffuse into gut epithelial cells, where cytochrome P450 enzymes may oxidize them to reactive intermediate compounds. Alternatively, isothiocyanates undergo spontaneous or enzyme-enhanced conjugation to glutathione (a potent endogenous antioxidant compound) and subsequent efflux via cellular transporters, particularly the multidrug resistance-associated protein 2, or MRP2, a membrane-bound cellular transporter. Consequently, isothiocyanate conjugates can be de-conjugated, re-conjugated, and shuttled in and out of cells multiple times, providing repeated exposures to cells before absorption in the gut and distribution to the body's tissues.

Eventually, isothiocyanates undergo transformation via the mercapturic acid pathway to yield cysteinylglycine, cysteine, and N-acetylcysteine conjugates, known collectively as dithiocarbamates.[5] These conjugates accumulate in urine, serving as biomarkers of isothiocyanate uptake and metabolism. Isothiocyanate elimination rates vary among individuals, however, likely due to differences in metabolism, gut microbiota population, bowel transit time, and the co-consumption of other dietary components. Urinary excretion typically peaks within eight hours of consumption.[6]

Isothiocyanate assessment in foods

Assessing isothiocyanate intake from foods is inherently challenging. Isothiocyanates are end-products, and their yield is incumbent upon the amount of available substrate, which can only be determined from the raw food. Other factors, such as cultivar, growing condition, and gut myrosinase hydrolysis, influence total intake, as well. A widely accepted assay (called cyclocondensation) measures isothiocyanate content in foods, revealing a wide range across cruciferous vegetables, from approximately 1.5 micromoles (on average) in raw cauliflower to 61 micromoles in raw mustard greens.[7]

Sulforaphane is a product of glucoraphanin and myrosinase hydrolysis


Glucoraphanin is glucosinolate, a class of defensive compounds present in many edible plants. Glucosinolates serve as deterrents or attractants to insects that lay eggs on the plants.[8] Their primary role, however, is that of potent biopesticides, participating in a dual-component chemical defense system – commonly referred to as the "mustard oil bomb" – that protects plants from environmental stressors.[9] [10]

Glucosinolate content in plants increases in response to these stressors, including temperature changes. In a study in which investigators grew the glucosinolate-rich thale cress in warm (21°C, 70°F), moderate (15°C, 59°F), and cool (9°C, 48°F) environments, the plants grown in cool temperatures produced higher levels of glucosinolates.[11]

Although glucoraphanin is distributed throughout broccoli plants, the highest amounts are present in the seeds and sprouts, with the latter containing 10 to 100 times more of the glucosinolate than mature plants.[12] These amounts vary, however, due to a host of factors, including soil and growing conditions, cultivar, harvest time, and post-harvest storage techniques.[13] [14]


Myrosinases comprise a family of enzymes that are strategically situated in vesicles present in the leaves, stems, and flowers of their host plants. Myrosinases serve as the second component in the mustard oil bomb defense system. When plants containing myrosinase and a glucosinolate sustain damage (via insect attack, herbivore consumption, or food processing techniques), the myrosinase hydrolyzes neighboring glucosinolates to yield glucose, hydrogen sulfate, and several unstable aglycones (non-sugar molecules).

These aglycones can spontaneously rearrange to form various bioactive compounds, including isothiocyanates, nitriles, and others.[15] The end products of these rearrangements vary depending on environmental conditions (such as pH and presence of iron ions) and the coexistence of proteins present in the plant. Some of these proteins promote the formation of isothiocyanates, while others promote the formation of epithionitriles, compounds that exert fewer beneficial health properties relative to isothiocyanates.[16] [17]

Myrosinases are also found in the human gut, produced by commensal bacteria that reside there. Gut bacterial myrosinases convert unhydrolyzed glucosinolates to their respective isothiocyanates, but the conversion process is highly variable and subject to differences in commensal microbiota composition, the use of antimicrobial agents, or other factors that alter or reduce the gut microbial population.[18]

Activation of myrosinases typically requires the presence of vitamin C, and in some instances, the enzymes are rendered nearly inactive in the vitamin's absence. Myrosinase activation is not dependent on vitamin C's redox capacity; rather, the vitamin helps catalyze the hydrolytic reaction.[19] Myrosinase is heat-sensitive; as such, it is readily inactivated at most cooking temperatures.[20]

Sulforaphane exploits multiple mechanisms to exert its beneficial effects.

The bulk of the health-promoting activities of sulforaphane has been attributed to the compound's inhibition of phase 1 enzymes and induction of phase 2 enzymes.

Phase 1 enzymes are xenobiotic-metabolizing proteins that subject toxic substances to oxidation, reduction, or hydrolysis to yield reactive intermediate compounds containing hydroxyl (-OH), amino (-NH2), or carboxyl (-COOH) chemical groups. These reactive compounds may be more toxic than the parent compound, and many are carcinogenic due to their capacity to form DNA adducts. These adducts damage the DNA, accelerating telomere shortening and promoting cellular dysfunction and senescence.

Phase 2 enzymes subject reactive intermediates to conjugation reactions, effectively neutralizing the reactive compounds and yielding water-soluble compounds that can be readily eliminated from the body, primarily in urine. Interestingly, phase 2 enzymes also appear to play a role in the maintenance and redox recycling of the essential vitamins A, C, and E.[21] The primary means by which sulforaphane induces phase 2 enzymes is via nuclear factor erythroid 2-related factor 2, or Nrf2.

Nrf2 regulates the expression of antioxidant and stress response proteins

Nrf2 is a cellular protein that activates the transcription of more than 200 cytoprotective proteins that protect against oxidative stress due to injury, inflammation, and normal aging processes. It is an element of the Keap1-Nrf2-ARE biological pathway, a mediator of cytoprotective responses to oxidative and electrophilic stressors.

Under normal cellular conditions, Keap1 tethers Nrf2 in the cytoplasm (the region of the cell outside the nucleus), where it can be tagged and delivered for degradation. However, following exposure to stressors, Keap1 undergoes modifications that impair its ability to bind to and target Nrf2 for degradation. As a result, Nrf2 is free to travel to the nucleus, where it binds to antioxidant response elements (AREs) of DNA.[22] AREs are sequences in the regulatory regions of genes that activate transcription of a diverse group of cytoprotective enzymes.

Isothiocyanates react with certain regions on Keap1, eliminating Keap1’s ability to target Nrf2 for degradation – effectively serving the role of stressor and stimulating Nrf2's cycling in and out of the nucleus. Typically, this cycling occurs every 129 minutes, but evidence indicates that cellular exposure to sulforaphane reduces the cycling time to as little as 80 minutes.[23] Sulforaphane is the most potent naturally occurring inducer of Nrf2 activity.[2]

Sulforaphane switches on the activity of cytoprotective enzymes

Through its induction of Nrf2, sulforaphane activates a vast array of cytoprotective proteins, including glutathione, heme oxygenase 1, and NQO1. Conversely, it inhibits the activity of nuclear factor-κB, or Nf-κB, a family of transcription factors involved in the body's inflammatory response. [24] [25] [26] Inhibition of Nf-κB impairs expression of many pro-inflammatory factors, including inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor-alpha, and various interleukin cytokines.[27]

Epidemiological data suggest that the consumption of fruits and vegetables, especially cruciferous vegetables, reduces the incidence of many chronic diseases, including cancer, cardiovascular disease, neurodegenerative disease, metabolic disorders (such as diabetes), autoimmune dysfunction, and others.[28] [29] [30] Data from clinical trials further substantiate these effects.

Despite Nrf2's clear role in the body's response to sulforaphane, evidence indicates many other mechanisms may be involved, such as inducing apoptosis,[31] [32] halting cell cycle progression,[33] [34] inhibiting angiogenesis,[35] [36] and quenching oxidative stress and inflammation,[37] thereby functioning in a synergistic fashion to potentiate sulforaphane's impact.

Sulforaphane is a potent antioxidant and anti-inflammatory compound

Prominent features in the pathogenesis of many chronic diseases are oxidative stress and inflammation. Oxidative stress is a natural repercussion of normal metabolic processes during oxidative phosphorylation (the generation of energy) in mitochondria or accompanying hypochlorite generation during immune activation. It can cause irreversible damage to DNA, lipids, proteins, mitochondria, and cells, thereby promoting chronic inflammation. Sulforaphane quenches oxidative stress and reduces inflammation.

Health effects of sulforaphane

Approximately three decades of research have elucidated numerous beneficial effects of sulforaphane on human health. This section highlights a few of these effects and directs the reader to other relevant scientific articles that provide more comprehensive overviews of the research on sulforaphane.

Sulforaphane reduces symptoms associated with autism spectrum disorder

Autism spectrum disorder, or ASD, is a neurodevelopment disorder characterized by impaired social interaction and communication, as well as restrictive, repetitive patterns of behavior. ASD affects roughly one in 68 people and is more common among males than females. Evidence from a placebo-controlled, double-blind, randomized trial suggests that sulforaphane reduces communication impairments and behavioral symptoms in young men with autism.

The trial involved 44 young men between the ages of 13 and 27 years who had been diagnosed with moderate to severe ASD. The study's authors gave 29 of the participants sulforaphane derived from broccoli sprout extracts and gave the remaining 15 participants a placebo. They received their respective treatments for 18 weeks, followed by four weeks without treatment. Sulforaphane doses ranged between 50 and 150 micromoles (~9 milligrams and 26 milligrams, respectively). The participants' parents, caregivers, and physicians provided assessments of the young men's behavior using the Aberrant Behavior Checklist, Social Responsiveness Scale, and Clinical Global Impression Improvement Scale (CGI-I).

After 18 weeks of the treatment, the participants who took the placebo experienced little change, but those who took the sulforaphane showed marked improvements in their behaviors. In particular, the CGI-I scores reflected improvements in social interaction, behavior, and verbal communication. After the sulforaphane treatment ended, the participants' scores rose toward pretreatment levels on all assessments.[38] A follow-up study reflected similar effects.[39]

Sulforaphane exerts potent anticancer effects

Sulforaphane is a potent anticancer compound that works via multiple mechanisms, including the Nrf2-Keap1-ARE pathway, phase 2 enzyme induction, antiproliferative effects (such as tumor suppression and cell cycle inhibition), histone deacetylase inhibition, and the quenching of reactive oxygen species, among others.[40]

An example of sulforaphane's anticancer effects was seen in a study in which sulforaphane reduced biochemical recurrence in men who have had prostate cancer. The double-blind, randomized, placebo-controlled study involved 75 men (average age, 69 years) who had undergone radical prostatectomy and were experiencing increased PSA levels. Approximately half of the men took a supplement providing 60 milligrams of sulforaphane for six months; the other half took a placebo. The study's authors measured the men's PSA levels before and two months after the treatment ended.

Increases in the average PSA levels were markedly lower among the men who took the sulforaphane. The PSA doubling time among men who took sulforaphane was ~29 months; doubling time among the men who took the placebo was ~16 months – an 86 percent difference. The effects of sulforaphane remained up to three months after the intervention.[41]

Other evidence demonstrates that sulforaphane may be beneficial against breast cancer, lympohoma, melanoma, and others.[42] [43] [44] [45]

Sulforaphane promotes the excretion of toxicants in air pollution

Air pollution from automobile exhaust, forest fires, and cigarette smoke contains many toxic substances, including chemicals, gases, and particulate matter. Exposure to air pollutants is associated with poor health outcomes and increased risk of both acute and chronic disease.

Robust clinical evidence has demonstrated that sulforaphane enhances the activity of endogenous detoxication pathways to protect against toxicities from airborne pollutants. In a randomized placebo-controlled trial in Qidong, China, an area known for its high levels of air pollution, participants received a broccoli sprout beverage containing 600 micromoles (approximately 263 milligrams) of glucoraphanin and approximately 40 micromoles (approximately 7 milligrams) of sulforaphane or a placebo beverage daily for 12 weeks. Urinary excretion of benzene and acrolein, known carcinogens present in air pollution, increased 61 percent and 23 percent, respectively, among the participants who took the glucoraphanin/sulforaphane beverage. The study's authors noted this effect from the first day of consuming the beverage and throughout the entire trial.[46]

A follow-up study in Qidong found that sulforaphane markedly increased the production of mercapturic acid metabolites of benzene and acrolein. These effects manifested within 24 hours of sulforaphane administration in a dose-dependent manner.[47] Moreover, the effects were sustained for several months after the intervention ended, demonstrating that sulforaphane did not exhaust the body's capacity to protect itself from environmental threats and suggesting that regular consumption of sulforaphane in foods or dietary supplements protects against future toxic exposures.

Airborne pollutants and allergens promote oxidative stress in the upper airways, triggering asthma. A placebo-controlled dose-escalation trial demonstrated that consumption of a broccoli sprout beverage had a direct effect on increasing the expression of phase 2 detoxification enzymes in the upper airway. Doses ranged from 25 to 200 grams and exhibited a clear dose-response relationship, with the largest dose having the greatest effect, robustly increasing the production of various cytoprotective enzymes, such as glutathione s-transferases, heme oxygenase-1, and NQ-O1.[48]

Sulforaphane improves blood glucose control in type 2 diabetes

Type 2 diabetes is a progressive metabolic disorder characterized by high blood glucose levels and insulin resistance. A 2017 study demonstrated that sulforaphane reduces glucose production in the liver and improves blood glucose control.

The authors of the study investigated the effects of sulforaphane in several rodent models of type 2 diabetes and found that sulforaphane ameliorated many of the hallmark characteristics of the disease. Then they assessed sulforaphane's effects in 97 people with type 2 diabetes. Sixty of the participants had well-regulated disease, but 37 had poorly regulated disease. Of those with poorly regulated disease, 17 had obesity. Nearly all of the participants took metformin, a common blood glucose-lowering drug.

Participants received either an oral placebo or glucoraphanin-rich broccoli sprout extract every day for 12 weeks. The authors of the study measured the participants' fasting blood glucose and HbA1c (a measure of long-term blood glucose control) levels and assessed their glucose tolerance prior to and after the intervention.

Sulforaphane administration improved fasting blood glucose and HbA1c levels in the obese participants who had poorly regulated type 2 diabetes. Sulforaphane mediated these effects via Nrf2 activity and subsequently reduced expression of enzymes that promote glucose production in the liver.

These findings suggest that sulforaphane ameliorates some of the hallmark characteristics of diabetes in humans. The mechanisms by which sulforaphane mediates these effects differ from those of metformin, suggesting that the two could work in a complementary manner to improve blood glucose control in obese people with type 2 diabetes.[49]

Selected publications

  1. ^ Yoxall, Victoria; Kentish, Peter; Coldham, Nick; Sauer, Maurice J.; Ioannides, Costas; Kuhnert, Nikolai (2005). Modulation Of Hepatic Cytochromes P450 And Phase II Enzymes By Dietary Doses Of Sulforaphane In Rats: Implications For Its Chemopreventive Activity International Journal Of Cancer 117, 3.
  2. ^ a b DOI: 10.1016/s0278-6915(99)00082-4
  3. ^ Juge, Nathalie; Mithen, Richard; Traka, Maria (2007). Molecular Basis For Chemoprevention By Sulforaphane: A Comprehensive Review Cellular And Molecular Life Sciences 64, 9.
  4. ^ Kamal, Mohammad M.; Akter, Sharmin; Lin, Chin-Nu; Nazzal, Sami (2020). Sulforaphane As An Anticancer Molecule: Mechanisms Of Action, Synergistic Effects, Enhancement Of Drug Safety, And Delivery Systems Archives Of Pharmacal Research 43, 4.
  5. ^ Shapiro, Theresa A.; Fahey, Jed W.; Holtzclaw, W. David; Stephenson, Katherine K.; Ye, Lingxiang; Talalay, Paul, et al. (2006). Safety, Tolerance, And Metabolism Of Broccoli Sprout Glucosinolates And Isothiocyanates: A Clinical Phase I Study Nutrition And Cancer 55, 1.
  6. ^ Shapiro TA; Fahey JW; Wade KL; Stephenson KK; Talalay P (2001). Chemoprotective glucosinolates and isothiocyanates of broccoli sprouts: metabolism and excretion in humans. Cancer Epidemiol Biomarkers Prev 10, 5.
  7. ^ Zhang Y (2012). The 1,2-benzenedithiole-based cyclocondensation assay: a valuable tool for the measurement of chemopreventive isothiocyanates. Crit Rev Food Sci Nutr 52, 6.
  8. ^ Kunert, Grit; Vassão, Daniel Giddings; Jeschke, Verena; Kearney, Emily E.; Schramm, Katharina; Shekhov, Anton, et al. (2017). How Glucosinolates Affect Generalist Lepidopteran Larvae: Growth, Development And Glucosinolate Metabolism Frontiers In Plant Science 8, .
  9. ^ DOI: 10.1016/s0015-3796(84)80059-1
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  13. ^ West, Leslie G.; Meyer, Keith A.; Balch, Barbara A.; Rossi, Frank J.; Schultz, Michael R.; Haas, George W. (2004). Glucoraphanin And 4-Hydroxyglucobrassicin Contents In Seeds Of 59 Cultivars Of Broccoli, Raab, Kohlrabi, Radish, Cauliflower, Brussels Sprouts, Kale, And Cabbage Journal Of Agricultural And Food Chemistry 52, 4.
  14. ^ DOI: 10.1016/s2095-3119(12)60185-3
  15. ^ Gershenzon, Jonathan; Halkier, Barbara Ann (2006). Biology And Biochemistry Of Glucosinolates Annual Review Of Plant Biology 57, 1.
  16. ^ Swarup, Ranjan; Juvik, John A.; Bennett, Mj; Mithen, Richard; Jeffery, Elizabeth H; Matusheski, Nathan V (2006). Epithiospecifier Protein From Broccoli (Brassica Oleracea L. Ssp. Italica) Inhibits Formation Of The Anticancer Agent Sulforaphane Journal Of Agricultural And Food Chemistry 54, 6.
  17. ^ Jeffery, Elizabeth H; Matusheski, Nathan V (2001). Comparison Of The Bioactivity Of Two Glucoraphanin Hydrolysis Products Found In Broccoli, Sulforaphane And Sulforaphane Nitrile Journal Of Agricultural And Food Chemistry 49, 12.
  18. ^ Fahey JW; Wehage SL; Holtzclaw WD; Kensler TW; Egner PA; Shapiro TA, et al. (2012). Protection of humans by plant glucosinolates: efficiency of conversion of glucosinolates to isothiocyanates by the gastrointestinal microflora. Cancer Prev Res (Phila) 5, 4.
  19. ^ Henrissat, Bernard; Cottaz, Sylvain; Burmeister, Wim Pascal; Rollin, Patrick; Vasella, Andrea (2000). High Resolution X-ray Crystallography Shows That Ascorbate Is A Cofactor For Myrosinase And Substitutes For The Function Of The Catalytic Base Journal Of Biological Chemistry 275, 50.
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  21. ^ Boddupalli, Sekhar; Mein, Jonathan R.; Lakkanna, Shantala; James, Don R. (2012). Induction Of Phase 2 Antioxidant Enzymes By Broccoli Sulforaphane: Perspectives In Maintaining The Antioxidant Activity Of Vitamins A, C, And E Frontiers In Genetics 3, .
  22. ^ Dinkova-Kostova, Albena T; Kensler, Thomas; Fahey, Jed W.; Kostov, Rumen V. (2017). KEAP1 And Done? Targeting The NRF2 Pathway With Sulforaphane Trends In Food Science & Technology 69, .
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  24. ^ Prestera, Tory; Talalay, Paul; Alam, Jawed; Ahn, Young I.; Lee, Patty J.; Choi, Augustine M. K. (1995). Parallel Induction Of Heme Oxygenase-1 And Chemoprotective Phase 2 Enzymes By Electrophiles And Antioxidants: Regulation By Upstream Antioxidant-Responsive Elements (ARE) Molecular Medicine 1, 7.
  25. ^ DOI: 10.1016/s0076-6879(04)82023-8
  26. ^ Negi, Geeta; Kumar, Ashutosh; S. Sharma, Shyam (2011). Nrf2 And NF-κB Modulation By Sulforaphane Counteracts Multiple Manifestations Of Diabetic Neuropathy In Rats And High Glucose-Induced Changes Current Neurovascular Research 8, 4.
  27. ^ Benedict, Andrea L.; Mountney, Andrea; Hurtado, Andres; Bryan, Kelley E.; Talalay, Paul; Schnaar, R L, et al. (2012). Neuroprotective Effects Of Sulforaphane After Contusive Spinal Cord Injury Journal Of Neurotrauma 29, 16.
  28. ^ Zhang, Xianglan; Shu, Xiao-Ou; Xiang, Yong-Bing; Yang, Gong; Li, Honglan; Gao, Jing, et al. (2011). Cruciferous Vegetable Consumption Is Associated With A Reduced Risk Of Total And Cardiovascular Disease Mortality The American Journal Of Clinical Nutrition 94, 1.
  29. ^ Chen, Guo-Chong; Koh, Woon-Puay; Yuan, Jian-Min; Qin, Li-Qiang; Van Dam, Rob M. (2018). Green Leafy And Cruciferous Vegetable Consumption And Risk Of Type 2 Diabetes: Results From The Singapore Chinese Health Study And Meta-Analysis JMIR Medical Informatics JMIR Medical Informatics 119, 9.
  30. ^ Kirwan, Richard; Medina-Remón, Alexander; Lamuela-Raventós, Rosa M.; Estruch, Ramón (2017). Dietary Patterns And The Risk Of Obesity, Type 2 Diabetes Mellitus, Cardiovascular Diseases, Asthma, And Neurodegenerative Diseases Critical Reviews In Food Science And Nutrition 58, 2.
  31. ^ Pledgie-Tracy, Allison; Sobolewski, Michele D.; Davidson, Nancy E. (2007). Sulforaphane Induces Cell Type–Specific Apoptosis In Human Breast Cancer Cell Lines Molecular Cancer Therapeutics 6, 3.
  32. ^ Herman-Antosiewicz, Anna; Johnson, Daniel E.; Singh, Shivendra V. (2006). Sulforaphane Causes Autophagy To Inhibit Release Of Cytochrome C And Apoptosis In Human Prostate Cancer Cells Cancer Research 66, 11.
  33. ^ Chiao, J.; Chung, F.-L.; Kancherla, R.; Ahmed, T.; Mittelman, A.; Conaway, C. (2002). Sulforaphane And Its Metabolite Mediate Growth Arrest And Apoptosis In Human Prostate Cancer Cells International Journal Of Oncology , .
  34. ^ Kim BR; Hu R; Keum YS; Hebbar V; Shen G; Nair SS, et al. (2003). Effects of glutathione on antioxidant response element-mediated gene expression and apoptosis elicited by sulforaphane. Cancer Res 63, 21.
  35. ^ Bertl, Elisabeth; Bartsch, Helmut; Gerhäuser, Clarissa (2006). Inhibition Of Angiogenesis And Endothelial Cell Functions Are Novel Sulforaphane-Mediated Mechanisms In Chemoprevention Molecular Cancer Therapeutics 5, 3.
  36. ^ Shankar, (2009). Sulforaphane Inhibits Angiogenesis Through Activation Of FOXO Transcription Factors Oncology Reports 22, 06.
  37. ^ Chhunchha, Bhavana; Kubo, Eri; Singh, Prerna; Sasaki, Hiroshi; Singh, Dhirendra P. (2017). Sulforaphane Reactivates Cellular Antioxidant Defense By Inducing Nrf2/ARE/Prdx6 Activity During Aging And Oxidative Stress Scientific Reports 7, 1.
  38. ^ Singh, Kanwaljit; Connors, Susan L.; Smith, Kirby D.; Fahey, Jed W.; Talalay, Paul; Zimmerman, Andrew W., et al. (2014). Sulforaphane Treatment Of Autism Spectrum Disorder (ASD) Proceedings Of The National Academy Of Sciences 111, 43.
  39. ^ Lynch R; Diggins EL; Connors SL; Zimmerman AW; Singh K; Liu H, et al. (2017). Sulforaphane from Broccoli Reduces Symptoms of Autism: A Follow-up Case Series from a Randomized Double-blind Study. Glob Adv Health Med 6, .
  40. ^ Yang, Fan; Wang, Faling; Liu, Yuni; Wang, Shien; Li, Xin; Xia, Yan, et al. (2018). Sulforaphane Induces Autophagy By Inhibition Of HDAC6-mediated PTEN Activation In Triple Negative Breast Cancer Cells Life Sciences 213, .
  41. ^ Cipolla, Bernard G.; Mandron, Eric; Lefort, Jean Marc; Coadou, Yves; Della Negra, Emmanuel; Corbel, Luc, et al. (2015). Effect Of Sulforaphane In Men With Biochemical Recurrence After Radical Prostatectomy Cancer Prevention Research 8, 8.
  42. ^ Jacobs, Bruce L; Singh, Shivendra V; Singh, Krishna B; Kim, Su-Hyeong; Hahm, Eun-Ryeong; Pore, Subrata K (2018). Prostate Cancer Chemoprevention By Sulforaphane In A Preclinical Mouse Model Is Associated With Inhibition Of Fatty Acid Metabolism Carcinogenesis 39, 6.
  43. ^ Fahey, Jed W; Wang, Zinian; Tu, Chengjian; Pratt, Rachel; Khoury, Thaer; Qu, Jun, et al. (2022). A Presurgical‐Window Intervention Trial Of Isothiocyanate‐Rich Broccoli Sprout Extract In Patients With Breast Cancer Molecular Nutrition & Food Research 66, 12.
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  46. ^ Egner PA; Chen JG; Zarth AT; Ng DK; Wang JB; Kensler KH, et al. (2014). Rapid and sustainable detoxication of airborne pollutants by broccoli sprout beverage: results of a randomized clinical trial in China. Cancer Prev Res (Phila) 7, 8.
  47. ^ Johnson, Jamie; Egner, Patricia; Ng, Derek; Zhu, Jian; Wang, Jin-Bing; Xue, Xue-Feng, et al. (2019). Dose-dependent Detoxication Of The Airborne Pollutant Benzene In A Randomized Trial Of Broccoli Sprout Beverage In Qidong, China The American Journal Of Clinical Nutrition 110, 3.
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  49. ^ Tang, Yunzhao; Derry, Jonathan M. J.; Mulder, Hindrik; Tubbs, Emily; Wollheim, C B; Rosengren, Anders H, et al. (2017). Sulforaphane Reduces Hepatic Glucose Production And Improves Glucose Control In Patients With Type 2 Diabetes Science Translational Medicine 9, 394.

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