Why should you eat your greens? Sulforaphane, an active compound in broccoli and other Brassica vegetables, may help prevent prostate cancer from recurring. Researchers are also investigating possible benefits to cholesterol, diabetes, skin damage, autism, and much more. Learn the latest science here.
What are Sulforaphane and Broccoli Sprouts?
For example, cutting, chewing, or otherwise disrupting the broccoli plant cells initiates the production of sulforaphane. Compared to the stable glucoraphanin, sulforaphane begins degrading soon after production .
Three-day-old sprouts of certain cruciferous vegetables contain 10 to 100 times higher concentrations of glucoraphanin than in mature plants .
Levels of glucoraphanin and sulforaphane are highest in broccoli sprouts .
Sulforaphane has antioxidant, antimicrobial, anticancer, anti-inflammatory, anti-aging, neuroprotective, and anti-diabetic properties .
Sulforaphane also protects against cardiovascular and neurodegenerative diseases .
Apart from sulforaphane, broccoli sprouts contain many other bioactive, health-promoting compounds, such as gallic, chlorogenic, ferulic, sinapinic, benzoic and salicylic acids, quercetin, kaempferol, and vitamin C .
Health Benefits of Sulforaphane
Sulforaphane supplements have not been approved by the FDA for medical use and generally lack solid clinical research. Regulations set manufacturing standards for them but don’t guarantee that they’re safe or effective. Speak with your doctor before supplementing.
Sulforaphane (in the form of broccoli sprout extract) boasts some relatively strong clinical evidence for a role in the prevention of prostate cancer and management strategies for preventing recurrence of prostate cancer.
In multiple clinical studies, men with recurrent prostate cancer who took 60 mg of sulforaphane per day had less prostate specific antigen (PSA, a marker used to measure prostate cancer progression) than those who did not take sulforaphane [6, 7].
That being said, the FDA has not approved sulforaphane for the prevention of prostate cancer recurrence. Talk to your doctor before supplementing.
Research in Other Cancers
While studies have advanced the furthest for sulforaphane in prostate cancer, it is also under investigation for possible action against other types of cancer. Sulforaphane is considered a promising compound for a few reasons; not least of these is that people who eat sulforaphane-rich Brassica vegetables are significantly less likely to develop cancer [8, 9].
Three to five servings of Brassicas per week are associated with a 30% to 40% decline in the incidence of cancer compared to people who don’t eat these vegetables .
Subjects who consumed at least one portion of cruciferous vegetables per week were less likely to develop oral cavity, pharynx, esophageal, colorectal, breast, and kidney cancers .
- SFN inhibits phase I enzymes that can activate pro-carcinogens 
- SFN induces phase II enzymes that are responsible for eliminating chemicals that damage DNA 
- SFN changes gene activation/deactivation, and causes demethylation, thereby restoring the activity of important tumor-suppressing and cell-cycle controlling genes 
- Sulforaphane induces cancer cell death 
- Sulforaphane inhibits the NF-κB pathway, thus reducing inflammation 
- Sulforaphane induces cell cycle arrest, and thereby inhibits cancer cell proliferation 
Apart from being effective in its own right, sulforaphane may also enhance the efficacy of anti-cancer drugs including cisplatin, gemcitabine, doxorubicin, and 5-fluorouracil, toward pancreatic and prostate cancer cells, while limiting their toxicity to normal cells .
Additional studies are still required before sulforaphane could be incorporated into conventional cancer therapies. Talk to your doctor before attempting to use sulforaphane and sulforaphane-rich foods for any medical purpose, let alone cancer prevention or treatment.
Potential Benefits with Insufficient Evidence
The benefits discussed in this section have been investigated in human trials, but these are not considered sufficiently large and powerful to determine whether sulforaphane is actually effective for the purpose. That is to say: sulforaphane may do these things, but more research is required.
Doctors almost universally recommend eating vegetables (broccoli, kale, brussels sprouts, etc.) that contain sulforaphane, though not necessarily because they contain sulforaphane. Eating brassica vegetables is likely to be a safer and more reliable way to achieve many of the health benefits attributed to sulforaphane.
As always, talk to your doctor before starting a new supplement.
In 12 healthy subjects, eating fresh broccoli sprouts (100 g/day) for 1 week decreased total and LDL cholesterol, and increased HDL cholesterol. Broccoli sprouts also improved oxidative stress markers .
Broccoli is widely recognized as one of the healthiest vegetables, and its sulforaphane content may help explain why.
Broccoli sprouts improve many parameters of diabetes. In type 2 diabetics, eating broccoli sprouts increased blood antioxidant capacity and HDL cholesterol, and decreased oxidative stress, triglycerides, insulin, insulin resistance, and CRP [20, 21, 22].
- Tissue damage
- Vascular complications
- Diabetes-induced heart dysfunction
- Thickening of the heart muscle
- Heart damage in mice
However, in rats, while SFN had positive effects on diabetes, markers of liver function and cholesterol declined after treatment .
Additional research is required on the role of sulforaphane in particular, but sulforaphane-rich greens like broccoli can and should be part of a healthy diet.
4) Skin Damage
UV radiation induces direct DNA damage and inflammation, and suppresses the immune response. Sulforaphane-rich extracts of 3-day-old broccoli sprouts increased protected against UV radiation-induced inflammation and edema in mice and reduced susceptibility to erythema (skin redness) in humans .
UVA irradiation plays a role in the premature aging of the skin by triggering oxidative stress, and inducing collagen degradation, a hallmark of photoaged skin. Pretreatment of mouse skin with sulforaphane protected against UVA-mediated collagen depletion .
Sulforaphane improved skin blistering in epidermolysis bullosa simplex .
Epidermolysis bullosa simplex (EBS) is a rare inherited condition in which the skin loses its integrity after mechanical trauma.
Direct evidence from human studies has been very limited. More clinical trials will be required to determine the role of sulforaphane in preventing and repairing skin damage.
5) Autism Symptoms
In a small clinical trial of 44 young men with autism, sulforaphane improved behavioral symptoms .
Sulforaphane may activate certain genes that protect cells against oxidative stress, inflammation, and DNA-damage, all of which are associated with autism spectrum disorder .
Larger and more robust clinical trials will be needed to determine whether sulforaphane has a role in improving the quality of life of people living with autism.
6) H. pylori Infection
These effects were temporary; values went back to their original levels 2 months after treatment was discontinued .
In another study, broccoli sprout extract did not inhibit H. pylori colonization, but nevertheless protected the stomach lining from damage .
In H. pylori-infected type 2 diabetic patients, broccoli sprout powder, in addition to standard triple therapy, considerably improved H. pylori eradication. It also improved markers of heart health in these subjects .
H. pylori increases oxidative stress, thereby causing damage to the stomach lining, slowing down damage repair, and eventually inducing gastric cancer. Sulforaphane activates Nrf2-dependent antioxidant enzyme activities, thereby protecting stomach cells from oxidative injury .
Improved stomach lining health also makes it more difficult for H. pylori to colonize the stomach, which explains the reduced rate of colonization found in some human studies .
Broccoli sprouts and other sulforaphane-rich vegetables are an important part of a healthy diet. The precise role of sulforaphane in inhibiting H. pylori infection will be clarified in larger and more robust clinical trials.
7) Liver Function
Broccoli sprouts activated detoxification and glutathione production, increasing GST while decreasing AST and ALT in rat livers .
Sulforaphane also inhibited alcohol-induced fatty liver in mice .
Human evidence is limited here, though – again – broccoli and other sulforaphane-rich vegetables are considered part of a healthy diet that can support liver function and general health.
Sulforaphane has had beneficial effects in animals with asthma and airway inflammation, but studies in humans are less conclusive .
Broccoli sprout extract suppressed airway inflammation in humans exposed to diesel exhaust particles (equivalent to daily PM exposure levels on a Los Angeles freeway) .
Sulforaphane also improved airway and lung constrictions caused by methacholine in 60% of moderate asthmatics. However, in 20% of the asthmatics, sulforaphane worsened the constrictions .
Patients with chronic obstructive pulmonary disease (COPD) have innate immune dysfunction in the lung, resulting in frequent bacterial infections. Sulforaphane restored bacteria recognition and phagocytosis in lung macrophages from COPD patients .
Sulforaphane enhanced bacterial clearance by lung macrophages and reduced inflammation in mice exposed to cigarette smoke for 6 months .
Very little human evidence is available about sulforaphane for this purpose. Future clinical trials will clarify whether sulforaphane and sulforaphane-rich vegetables could play a role in managing asthma.
Early Research & Areas of Future Study
Sulforaphane is currently being investigated for many other potential health benefits, but these have only been studied in animal or cell studies. That is to say, there is not enough evidence to say whether sulforaphane can benefit human health in this way. Until such time as clinical trials address them, there are better-studied ways to improve these aspects of health.
As we said earlier, doctors do recommend eating sulforaphane-rich vegetables like broccoli, kale, and brussels sprouts.
Sulforaphane has demonstrated antiviral activity when infected cells are exposed directly; however, there is currently not enough evidence to support its use in an animal or human with a viral infection.
In people with the flu, eating broccoli sprouts reduced influenza viral load .
Eating broccoli sprouts also seemed to enhance the antiviral response of immune cells in humans .
Researchers are currently using cell studies to try to flesh out the mechanism by which sulforaphane might boost the immune system and fight viral infection.
- SFN exhibited significant antiviral activity against influenza (the flu), HIV, Epstein-Barr virus, and the hepatitis C virus .
- SFN blocked HIV infection in macrophages. Macrophages play a critical role in HIV infection, forming long-lived viral reservoirs and distributing the virus in the body .
- On the other hand, SFN may exacerbate infections by viruses that hijack Nrf2, such as the Marburg virus, the Kaposi’s sarcoma-associated herpesvirus (KSHV), and Dengue virus .
10) Bacterial and Fungal Infections
Sulforaphane has antimicrobial activity on direct contact. However, it is unclear whether it could be useful in fighting infection in animal or human models. The potential demonstrated in cell studies has yet to be repeated in a living animal.
In one study, 23 out of 28 tested bacterial and fungal species were inhibited by sulforaphane when directly exposed in a dish .
Mycobacterium abscessus is frequently found in patients with cystic fibrosis and in immunosuppressed patients. Pretreatment of macrophages with sulforaphane significantly decreased bacterial burden, but this has not been repeated in animals or humans .
Human β-defensin-2 (HBD-2) plays an important role against bacterial invasion. Sulforaphane may be able to increase antimicrobial peptides such as HBD-2 .
Sulforaphane is an indirect antioxidant. It boosts the antioxidant capacity of cells by at least 2 mechanisms :
- Inducing phase 2 detoxification enzymes – Sulforaphane is the most potent inducer of phase 2 enzymes identified to date. It acts by activating Nrf2 and ARE, and increasing glutathione S-transferase activity [4, 2, 57, 58]
- Increasing cellular glutathione levels
Damage from Pollution
Sulforaphane may help the body detoxify airborne pollutants, pesticides, and heavy metals by activating detoxification systems, mainly the phase II enzymes. These potential benefits have only been studied in animals or cells so far; these studies may or may not translate to human trials.
In a farming community exposed to airborne pollutants with a high risk of hepatocellular carcinoma, eating broccoli sprouts enhanced the detoxification of airborne pollutants and reduced the risk of cancer .
Sulforaphane induced phase II enzymes in the upper airway of human subjects .
In mice, sulforaphane reduced the pro-inflammatory and pro-allergic effects typically caused by exposure to diesel exhaust particles .
Aflatoxin binds DNA and causes liver cancer. Sulforaphane reduced the binding of aflatoxin to DNA in rats .
Sulforaphane inhibited the mutagenicity caused by heterocyclic amines (cooked food mutagens) .
Sulforaphane lessened liver damage caused by cadmium selenide in mice .
Exposure to arsenic increases the risk of lung disease. Sulforaphane blocked DNA damage and mild lung damage caused by a 2-week exposure of mice to arsenic-containing dust .
12) Cardiovascular Health
A diet rich in Brassica vegetables decreases the risk of cardiovascular disease. The role of sulforaphane in this benefit is unclear .
Both sulforaphane and broccoli sprouts high in glucoraphanin decreased blood pressure in hypertensive rats .
Sulforaphane also reduced heart damage after infarct in rats .
SFN further possesses antithrombotic activities. SFN inhibited human platelet aggregation and reduced blood clot formation .
SFN reduced the mortality of acute lung thromboembolism in mice .
Finally, sulforaphane is beneficial in stroke. In rodents, SFN decreased brain infarct (damaged tissue from a stroke) volume, and maintained the blood-brain barrier (BBB) integrity and neurological function after stroke [74, 75].
A vegetable-rich diet is one of the first recommendations for weight management. Vegetables are low in calories and high in nutrients, and they are considered essential to a healthy lifestyle. However, the role of sulforaphane specifically is unclear.
In mice with Western diet-induced obesity, 3 weeks of sulforaphane supplementation reduced weight gain, leptin and insulin levels, and improved insulin resistance, glucose tolerance, and cholesterol .
Similarly, in another study, sulforaphane inhibited high-fat-diet-induced obesity and fat accumulation in mice. It also reduced total cholesterol, leptin, and liver triglyceride levels .
14) Immune Function
There is some evidence that sulforaphane benefits immunity, but human studies are lacking.
In cell and animal studies, sulforaphane has had anti-inflammatory effects, but it’s unclear to what extent these might apply to human health. However, people who eat a diet rich in vegetables like broccoli and brussels sprouts tend to have less inflammation than those who don’t eat as many vegetables; sulforaphane may play a role.
Indeed, in another study, treatment with SFN decreased inflammation in mice with colitis .
Sulforaphane decreases autoimmune inflammation .
SFN can be beneficial against T-cell driven autoimmune disorders, such as multiple sclerosis-like diseases in animals, but studies in humans are still lagging.
NRF2-deficient mice have exacerbated pathology in this model .
Sulforaphane activated the Nrf2/ARE pathway, which helps combat the disease .
A sulforaphane-rich diet improved osteoarthritis in mice. Sulforaphane inhibited key metalloproteinases implicated in osteoarthritis, independently of Nrf2, and blocked inflammation through NF-κB to protect against cartilage destruction .
Some of the SFN effects may be mediated by Nrf2 because enhanced oxidative stress and cartilage damage were observed in Nrf2-deficient mice with arthritis .
SFN reduced the severity of arthritis in mice by decreasing pro-inflammatory cytokines .
Several inflammatory autoimmune diseases, such as rheumatoid arthritis and osteoarthritis, trigger the transformation of monocytes into proinflammatory macrophages (M1 type). In a cell study, sulforaphane blocked the inflammatory responses specific to M1 macrophages (Th1) and shifted macrophage production to M2 macrophages, which tend to decrease inflammation and encourage tissue repair .
16) Depression and Anxiety
Researchers are currently investigating whether sulforaphane could combat mental illness, but human studies have not yet been conducted.
Repeated SFN administration reversed depression- and anxiety-like behaviors in chronically stressed mice, likely by inhibiting the hypothalamic-pituitary-adrenal (HPA) axis and inflammatory responses to stress [88, 89].
In another study, Nrf2 deficiency in mice resulted in depressive-like behavior, while the induction of Nrf2 by sulforaphane had antidepressant-like effects .
Also, dietary intake of glucoraphanin during the juvenile and adolescent periods in mice prevented the onset of depression-like behaviors at adulthood .
17) Brain Function
Sulforaphane appears to affect brain activity in animals, but its role in the human brain and cognition is unknown. Future clinical trials will offer more information and determine whether sulforaphane could benefit people with neurodegenerative disease.
Sulforaphane promoted microglia differentiation from pro-inflammatory M1 to anti-inflammatory M2 state. This reduced brain inflammation and restored spatial learning and coordination in rats .
In animals, sulforaphane has been found to benefit the brain in a number of ways. It:
- Improved cognitive performance and reduced working memory dysfunction in rats after traumatic brain injury 
- Weakened cognitive deficits in mouse models of psychiatric disease. Also, the intake of glucoraphanin during the juvenile and adolescent periods prevented the onset of cognitive deficits at adulthood 
- Alleviated brain swelling in rats, by attenuating the blood-brain barrier disruption, decreasing the levels of pro-inflammatory cytokines, and inhibiting NF-κB; it also increased AQP4 (a water channel protein) levels, thereby reducing brain swelling [98, 99]
- Prevented memory impairment and increased the survival of hippocampal neurons in diabetic rats 
SFN exerted protective effects against brain damage induced by acute CO poisoning in rats .
In a cell study, sulforaphane also protected human neurons against prion-mediated neurotoxicity .
Parkinson’s disease is characterized by selective loss of dopaminergic neurons in the substantia nigra of the brain. In animal models of Parkinson’s disease, sulforaphane improved deficits in motor coordination and inhibited dopaminergic neuronal loss [107, 108, 109, 110].
Abnormal production and aggregation of amyloid beta (Aβ) peptide are major factors implicated in the pathogenesis of Alzheimer’s disease (AD). Broccoli sprouts protected against Aβ-induced cell death, and sulforaphane inhibited Aβ-related inflammation [111, 112, 113].
Sulforaphane activated the protein degradation machinery that promotes huntingtin degradation and reduced huntingtin toxicity in mice .
Sulforaphane protected against seizures and elevated the seizure thresholds in mice .
Sulforaphane improved performance in a learning task in outpatients with schizophrenia .
Methamphetamine can induce psychosis in susceptible people. Sulforaphane weakened behavioral abnormalities in mice after administration of methamphetamine or phencyclidine, suggesting that it may help with schizophrenia .
Sulforaphane protected against antipsychotic-induced toxicity in dopaminergic neurons .
18) Substance Abuse
Researchers are currently investigating sulforaphane as a potential tool to combat addiction and substance abuse disorders. However, the only studies currently available were conducted on animals.
Sulforaphane weakened behavioral and neuropathological changes associated with methamphetamine exposure in mice. Pretreatment with sulforaphane weakened acute hyperlocomotion (increase in movement) in mice after a single administration of methamphetamine .
Also, the development of behavioral sensitization after repeated administrations of methamphetamine was significantly reduced by pretreatment with sulforaphane .
19) Pain Management
Sulforaphane may play a role in pain management, but human studies have not yet been conducted.
In mice, sulforaphane lessened pain, reduced pro-inflammatory cytokines, and increased anti-inflammatory cytokines. Sulforaphane blocked COX2 and iNOS in injured nerve cells, the 2 key enzymes implicated in inflammation and neuropathic pain .
In women, low levels of estrogen, such as during menopause or after an ovary removal surgery, can lead to reduced bone mass (osteoporosis). Researchers are currently investigating whether sulforaphane might help prevent bone loss.
Sulforaphane promoted bone formation and increased bone volume (∼20%) in both normal mice and mice without ovaries. Sulforaphane diminished bone resorption, thereby shifting the balance to a state favoring bone acquisition .
21) Muscle Damage
Muscles can be damaged by strenuous exercise or any number of disorders and diseases. According to animal studies, sulforaphane may help maintain and repair muscle tissue, but human studies have not yet been conducted.
In mouse models of Duchenne muscular dystrophy, sulforaphane significantly increased muscle mass, muscle force (∼30%), and running distance. Sulforaphane also reduced muscle hypertrophy, heart muscle hypertrophy, and inflammation .
22) Kidney Function
Sulforaphane may protect the kidneys from damaging chemicals, but this has only been studied in animals so far.
Chemotherapeutics, such as cisplatin, can be toxic to kidneys. In animals, sulforaphane prevented inflammation and kidney damage caused by cisplatin .
23) Hair Growth
Theoretically, sulforaphane’s interaction with DHT-degrading enzymes could prevent baldness and stimulate hair growth, but this has not yet been demonstrated in humans.
24) Alcohol Tolerance
Researchers are investigating whether sulforaphane could prevent alcohol toxicity in people who are sensitive.
Many East Asians are highly intolerant to even modest alcohol consumption. These people accumulate acetaldehyde, the primary metabolite of alcohol, because of a genetic polymorphism in aldehyde dehydrogenase (ALDH2) that metabolizes acetaldehyde to nontoxic acetate. Sulforaphane upregulated ALDH2 by dietary means, thereby reducing acetaldehyde toxicity .
In mice, SFN dramatically increased tissue ALDH2 and doubled the rate of elimination of acetaldehyde after the administration of alcohol .
SFN activated human salivary aldehyde dehydrogenase (hsALDH) and increased its activity towards acetaldehyde .
Many more human trials will be required to determine whether these mechanisms play out in a living system.
25) In Pregnancy
In the quantities that we could reasonably ingest in our diets, sulforaphane is safe and possibly beneficial during pregnancy. However, despite animal research into its potential benefits to expectant mothers, we recommend against taking sulforaphane as a supplement without your doctor’s advice and supervision.
When glucoraphanin (the precursor to sulforaphane) was administered to pregnant female rats, their offspring had lower blood pressure and less tissue inflammation in adulthood, regardless of their subsequent diet .
26) Eye Health
Sulforaphane’s antioxidant activity may prevent damage to the retina, but the evidence is limited to cell and animal studies thus far.
Oxidative stress due to excessive light exposure can exacerbate a variety of human retinal diseases by accelerating photoreceptor cell death (photoreceptors are cells that receive light and translate it into nerve impulses) .
SFN protected human retinal cells from UVA light-induced damage .
Sulforaphane treatment significantly decreased ischemia (reduced oxygen and blood flow), a condition that induces loss of retinal function in mice .
SFN protected human lens cells against oxidative stress and could potentially delay the onset of cataracts .
Also, SFN may help prevent complications after cataract surgery .
Fuchs endothelial corneal dystrophy (FECD) is a condition in which a deficiency in Nrf2 is observed. SFN significantly improved oxidative stress-induced cell death in FECD human cells .
27) Wound Healing
Some researchers are investigating whether sulforaphane could improve healing and prevent excessive scarring. Sulforaphane inhibited cell growth and reduces collagen in keloids, a type of scar tissue .
28) Bladder Dysfunction
In rats with bladder outlet obstruction, SFN treatment increased bladder capacity and bladder compliance. The potential implication for human health is unclear so far .
Hutchinson-Gilford progeria syndrome (HGPS) is a rare childhood premature aging disorder linked to mutations in the LMNA gene. Protein clearance and autophagy are impaired in HGPS cells. SFN stimulated protein clearance by autophagy and reversed cellular phenotypic changes, both of which are the hallmarks of HGPS .
Sulforaphane has not been studied in the context of HGPS itself, only its markers. Future animal studies and clinical trials will be needed.
Sulforaphane Side Effects
Sulforaphane is considered safe when consumed in the amounts available in broccoli and other greens, and very few side effects have been observed in clinical trials of broccoli sprouts, their extracts, or purified sulforaphane. However, supplements are not standardized, and we do not have sufficient data to determine the safety of long-term sulforaphane use. Talk to your doctor to avoid adverse effects or unexpected interactions.
1) Genome Stability
Sulforaphane appears to increase the activation of many beneficial genes, including tumor suppressor genes. However, sulforaphane may also activate long terminal repeats (LTRs), DNA sequences found within our genome that impair genome stability and cause mutations .
Consumption of broccoli sprouts by human volunteers caused a 10-fold increase in LTR activation in white blood cells. These effects are transient, and it remains to be determined whether they are biologically meaningful .
Other studies on human volunteers recorded no abnormal events related to broccoli sprout consumption .
Genotoxic effects were observed in unpublished studies with pigs fed with 600 g of raw broccoli for 12 days. These pigs had an increase in DNA strand breaks by 21% in the colon .
Also, after feeding raw or steamed broccoli to mice and rats, an increase in DNA adducts (cancer-causing chemicals binding to DNA) was observed .
However, all these effects in animals were observed for mature broccoli plant consumption. An additional benefit of broccoli sprouts is that they contain negligible quantities of indole glucosinolates, which predominate in the mature vegetable, and may give rise to degradation products (e.g., indole-3-carbinol). This may enhance tumorigenesis .
2) Liver Toxicity
There is a single case report of liver toxicity after drinking large amounts of broccoli juice for 4 weeks (800 ml/day). Transaminases, aspartate aminotransferase, and c-glutamyltrans-peptidase were elevated but decreased to normal within 15 days .
This was also caused by consuming the mature plant; the contribution of sulforaphane is unknown. Until we know more, caution is advised.
The amount of sulforaphane (glucoraphanin) can vary widely in vegetables .
Broccoli is not the only cruciferous vegetable which has SFN, but it yields the highest amounts, with glucoraphanin content around 75% of total glucosinolates .
Do not confuse broccoli sprouts with Brussels sprouts.
Genetics And Sulforaphane Metabolism
GSTs are a large family of glutathione conjugating enzymes, which attach glutathione to the substance that needs to be detoxified out of the body. Three of them, GSTM1, GSTP1, and GSTT1 have been implicated in the metabolism of isothiocyanates, and sulforaphane in particular .
SNPs in the GSTM1 gene
Individuals with GSTM1-null mutations may benefit more from SFN due to the decreased degradation of SFN, which therefore increases exposure .
However, several other studies suggest otherwise. In these studies, GSTM1-positive individuals benefited more from either broccoli or cruciferous vegetable consumption compared to GSTM1-null individuals. GSTM1-null carriers excrete more SFN and SFN-metabolites, and excretion is faster .
SNPs in the GSTT1 gene
Null mutations in the GSTT1 gene result in the absence of a functional enzyme. The frequency of the GSTT1-null variation has been estimated to be between 10 and 21% for Caucasian populations and as high as 64% for Asian populations .
Broccoli sprouts are more effective in detoxification when GSTT1-positive carriers are exposed to airborne pollution compared to the null carriers .
SNPs in the GSTP1 gene
Sulforaphane Mechanism of Action
As an Indirect Antioxidant:
- SFN activates Nrf2 by binding Keap1 [8, 153]
- SFN reacts with Keap1, thereby releasing Nrf2 from Keap1 binding 
- SFN promotes ARE-driven gene expression [8, 153]
- SFN increases other phase II enzymes: NQO1, GSTA1, and HO-1 [27, 155, 156, 84]
- SFN inhibits phase I enzymes CYP1A1, CYP1A2, CYP1B1, CYP2B2, and CYP3A4 [57, 8]
- SFN blocks SXR 
- SFN inhibits NfkB [46, 8, 127]
- SFN decreases TNF-α, NLRP3, IL-1β, IL-18, IFN-gamma and IL6 [89, 98, 94, 86, 157, 123]
- SFN increases IL-10, IL-4, Arg1, and YM-1 [89, 123, 84, 158]
- SFN decreases NO, iNOS and COX-2 [98, 123, 159]
- SFN silences Th17/Th1 responses [31, 84]
- SFN decreases IL-17 [86, 31]
- SFN decreases TGF-β/Smad 
- SFN decreases IL-23 and IL-12 expression 
- SFN decreases MMP-9 [84, 159]
- SFN decreases LDH and PGE2 
- DNA hypermethylation can inhibit tumor suppressor genes and genes involved in cell cycle regulation and apoptosis (cell death). DNA methyltransferases (DNMTs) methylate DNA, and an overexpression of DNMTs is observed in a number of cancers, including leukemia, gastric, lung, and prostate cancer [8, 160]
- Sulforaphane inhibits DNMT1 and DNMT3A 
- SFN is one of the most potent (histone deacetylase) HDAC inhibitors found to date 
- SFN inhibits HDAC1, HDAC2, HDAC3, and HDAC4 [161, 8]
- SFN decreases miR-21 and TERT 
- SFN activates caspase-3, caspase-7, caspase-8, caspase-9 [160, 8]
- SFN decreases anti-apoptotic Bcl-2 and Bcl-XL [160, 8]
- SFN increases pro-apoptotic Bax 
- SFN induces p21 (CDKN1A) and p53 
- SFN inactivates PARP 
- SFN decreases HIF1A 
- SFN decreases β-catenin (CTNNB1) 
- SFN‐induced browning of white adipocytes (fat cells) 
- SFN decreases PPARγ and C/EBPα 
- SFN increases AMPK 
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