Myrosinase
Episodes
In this clip, Dr. Jed Fahey discusses whether or not microwaving broccoli preserves the heat-sensitive myrosinase enzyme enough to convert glucoraphanin into sulforaphane.
Dr. Jed Fahey describes the effects of freezing and freeze-drying of broccoli sprouts on sulforaphane production.
Dr. Jed Fahey discusses the importance of having active myrosinase in dietary supplements for optimizing the conversion of glucoraphanin to sulforaphane.
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In this clip, Dr. Jed Fahey discusses whether or not microwaving broccoli preserves the heat-sensitive myrosinase enzyme enough to convert glucoraphanin into sulforaphane.
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Dr. Jed Fahey describes the effects of freezing and freeze-drying of broccoli sprouts on sulforaphane production.
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Dr. Jed Fahey discusses the importance of having active myrosinase in dietary supplements for optimizing the conversion of glucoraphanin to sulforaphane.
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Dr. Jed Fahey describes some of the factors that influence the conversion of myrosinase-driven conversion of glucoraphanin to sulforaphane.
Topic Pages
News & Publications
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Sulforaphane improves behavioral symptoms of autism. molecularautism.biomedcentral.com
Autism – often referred to as autism spectrum disorder, or ASD – is a neurodevelopmental disorder characterized by impaired social interaction and communication, as well as restrictive, repetitive patterns of behavior. The disorder typically manifests in early childhood and is slightly more common among boys than girls. Roughly one in 54 people living in the United States has ASD. Findings from a recent clinical trial suggest that sulforaphane improves behavioral symptoms associated with autism.
Sulforaphane is a bioactive compound derived from precursors (glucoraphanin and myrosinase) in broccoli and broccoli sprouts. It exhibits antioxidant and anti-inflammatory properties and may be beneficial against a wide range of chronic and acute diseases, including cardiovascular disease, neurological disease, cancer, and others. Previous research has demonstrated that sulforaphane reduces behavioral symptoms of autism in young men. Sulforaphane exerts its therapeutic effects through a variety of mechanisms, the most notable of which is the activation of Nrf2, a cellular protein that regulates the expression of antioxidant and stress response proteins that provide protection against oxidative stress due to injury and inflammation. Sulforaphane is the most potent naturally occurring inducer of Nrf2.
The randomized, placebo-controlled trial, which involved 45 children (ages 3 to 12 years) with autism, occurred in three distinct phases. During the first phase, half of the children received a commercially available dietary supplement containing glucoraphanin and myrosinase (yielding approximately 15 micromoles of sulforaphane) every day for 15 weeks, while the other half received a placebo. During the second phase, which also lasted 15 weeks, all the children received the supplement. During the third phase, which lasted six weeks, none of the children received the supplement. Before and after the intervention, caregivers and investigators evaluated the participants' symptoms using standardized behavioral assessments. Investigators collected blood and urine samples from the participants to assess metabolic and biochemical changes.
They found that behavioral symptoms among the children who received the sulforaphane supplement improved during the first phase (compared to those on the placebo), but the differences between the two groups were not statistically significant. However, both groups' behavioral symptoms improved during the second phase, as did markers of oxidative stress, mitochondrial respiration, inflammation, and heat shock proteins. The supplement elicited no adverse effects and was well tolerated.
These findings suggest that sulforaphane improves behavioral symptoms associated with autism. However, the study investigators caution that further study is needed to fully elucidate the clinical effects and mechanisms of action associated with the compound’s effects on autism.
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Gut microbial conversion of glucosinolates to isothiocyanates is highly variable in humans. cancerpreventionresearch.aacrjournals.org
Glucoraphanin, a precursor to sulforaphane, is a type of glucosinolate found primarily in broccoli and kale. Its conversion to sulforaphane requires myrosinase, an enzyme co-located within the leaves, stems, and other components of the plants in which it is found. Cooking temperatures inactivate myrosinase, effectively preventing isothiocyanate conversion and allowing unhydrolyzed glucosinolates to pass into the gut. In humans, myrosinase-producing gut bacteria can convert these glucosinolates to their cognate isothiocyanates. Findings from a 2012 study indicate that microbial conversion of glucosinolates to isothiocyanates is highly variable.
Previous research has demonstrated that sulforaphane administration promotes uniformly high urinary excretion of dithiocarbamate metabolites, accounting for as much as 90 percent of the administered sulforaphane over a 24-hour period. Dithiocarbamate levels in urine serve as a biomarker of glucosinolate intake.
The study involved two dissimilar groups of people: rural Han Chinese and racially mixed Baltimoreans. The participants abstained from cruciferous vegetable consumption for three days prior to the beginning of the study. They had not taken antibiotics for two weeks prior. Each of the participants kept a food diary, provided their medical history, and kept track of their bowel activity. The participants took a glucoraphanin-rich broccoli sprout extract that provided 200 micromoles of glucoraphanin in water. The authors of the study collected urine samples from 8 a.m. to 4 p.m. and from 4 p.m. until 8 a.m. on the following morning.
They found that microbial-induced conversion of glucoraphanin to sulforaphane is highly variable (ranging from 1 to 40 percent of dose) and subject to interindividual differences in gut bacteria populations. As such, conversion is distinguished by “high converters” – people with high elimination profiles, and “low converters”– those with low elimination profiles. The authors of the study identified no demographic factors that affected conversion efficiency, but they did note that conversion of glucoraphanin to dithiocarbamate was greater during the day.
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A substantial body of evidence from experimental, epidemiological, and clinical studies demonstrates the beneficial effects of sulforaphane consumption on human health. Many questions remain, however, regarding optimal formulation, bioavailability, and dosage of sulforaphane. A 2019 review discusses these and other aspects of the current state of evidence surrounding sulforaphane.
Sulforaphane is the end-product of a chemical reaction between two naturally occurring plant compounds – glucoraphanin and myrosinase. These compounds, often referred to as secondary metabolites, are not required for the plant’s growth or reproduction. Rather, they confer an advantage to the plant, particularly in terms of defense, participating in a dual-component chemical defense system – commonly referred to as the “mustard oil bomb” – that protects plants from environmental stressors. Glucoraphanin content in broccoli sprouts and mature broccoli vary across species and cultivar and is influenced by factors such as soil and growing conditions, harvest time, and post-harvest storage.
Most rodent studies of sulforaphane’s effects administer the end product via oral, intraperitoneal, or topical means. The median effective dose is 175 micromoles (~30 milligrams) per kilogram of the animal’s body weight when given orally; the median effective dose when given intraperitoneally is 113 micromoles (~20 milligrams) per kilogram. Most studies report beneficial outcomes, but this might be due to publication bias – the tendency for researchers to publish favorable results only. High doses (greater than 150 milligrams) elicited negative effects, including sleepiness, hypothermia, impaired motor coordination, and even death. When given with other drugs, sulforaphane potentiated some of the drugs' effects.
In humans, sulforaphane undergoes extensive biotransformation in the gut to yield mercapturic acid, which can be measured in urine and serves as a biomarker of intake. In general, sulforaphane is rapidly absorbed and eliminated, with most people excreting between 70 and 90 percent of the dose taken.
Clinical studies have assessed the merits of sulforaphane in a wide range of chronic and infectious diseases, including autism, aflatoxin toxicity, air pollution detoxication, cancer, cardiovascular disease, diabetes, neurodegenerative disease, Helicobacter pylori infection, and many others. Doses varied markedly and in terms of whether supplied as glucoraphanin (the precursor) or sulforaphane (the end product). The median dose of glucoraphanin was 190 micromoles (~76 milligrams) and of sulforaphane was 100 micromoles (~18 milligrams).
The authors of the review enumerate several issues that must be overcome in designing and conducting clinical studies with sulforaphane, but they stress the importance of plant-based diets as delivery modes for not only sulforaphane but other bioactive compounds that promote health. They also noted concerns that determining dose is inherently difficult in light of the differences in bioavailability of glucoraphanin and sulforaphane; translating animal data to humans poses many challenges.