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Kasim Doronin
Kasim Doronin

Where To Buy Sulforaphane

The study found that sulforaphane effectively reduced fasting blood sugar levels by 6.5% and improved hemoglobin A1c, a marker of long-term blood sugar control. These effects were particularly strong in participants who were obese with poor diabetes control (17).

where to buy sulforaphane

To further boost your intake, add mustard seeds or mustard powder to your meals. These ingredients are rich in dietary myrosinase, which can help increase the availability of sulforaphane, particularly in cooked vegetables (30, 31).

Sulforaphane can be found in cruciferous vegetables like broccoli, kale, cabbage, and watercress. To maximize your sulforaphane intake, eat vegetables raw or cooked at low temperatures with a sprinkle of mustard seeds or mustard powder.

Glucoraphanin is chemically stable and biologically inert. However, following plant tissue injury, such as biting or chewing, glucoraphanin comes in contact with the enzyme myrosinase, a ß-thioglucosidase, which in the intact plant is physically separated from its substrate. Myrosinase catalyzes the hydrolysis of glucoraphanin to liberate glucose and form an unstable aglucone (Scheme 1d) that spontaneously rearranges to give rise to a range of products, the most reactive of which is the isothiocyanate sulforaphane. Importantly, mammalian cells do not produce myrosinases; however, the conversion of glucoraphanin to sulforaphane still occurs in mammals. It is carried out by the bacterial microflora of the gastrointestinal tract and can be greatly reduced by antibiotic treatment or mechanical bowel cleansing [26]. Of note, this microbially-mediated conversion of glucoraphanin has been exploited in a recent study to generate high concentrations of sulforaphane locally in the colon of mice [27].

On a weight basis, glucoraphanin (right axis) is most abundant in the seeds of the broccoli plant. Upon enzymatic conversion to sulforaphane, the capacity of extracts of these plants to induce or up-regulate phase 2 enzymes such as NQO1 in mammalian cells, follows precisely the same curve (left axis).

Animal studies have principally used three routes of administration for sulforaphane: Oral, intraperitoneal and topical. Figure 2 highlights the distributions of doses selected by investigators for oral or intraperitoneal dosing to mice. Oral administration is the route typically used by the NCI in chemopreventive agent development [39]. Yet, somewhat paradoxically as depicted in Figure 2, intraperitoneal administration has been the most commonly employed route for studies with sulforaphane. Presumably this choice reflects relative ease of administration to animals rather than attempted mimicry of a route most appropriate for administration of a dietary compound or matrix to humans.

Distribution of daily doses of sulforaphane administered to mice as reported in the literature based on route of administration and efficacy outcome. Top panel, oral (gavage or in diet); bottom panel, intraperitoneal administration. Where necessary, dose extrapolations assumed 25 g body weight and dietary intake of 4 g food/mouse/day [38].

Sulforaphane and its metabolites (dithiocarbamates) can be quantified collectively by cyclocondensation with 1,2-benzenedithiol, with sensitivity in the picomolar range [50]. This highly sensitive, simple and convenient method has been widely used to measure the levels of sulforaphane and its metabolites in blood, plasma, urine and tissues following sulforaphane administration to rodents and humans. The use of this method revealed that sulforaphane crosses the placental barrier based on detection of dithiocarbamates in embryos 2 h post-treatment of pregnant mice with a single (5 μmol) dose of sulforaphane [51]. In addition, methods have been developed to analyze the individual metabolites following their separation by liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS) [52,53]. Furthermore, the use of mass spectrometry coupled with stable isotope-labeled internal standards of sulforaphane [1-isothiocyanato-4-methyl-sulfinyl(1,1,2,2,3,3,4,4-2H8)butane] and its corresponding mercapturic acid pathway conjugates allows for quantitative, precise, sensitive, and specific analysis of sulforaphane and its metabolites [54].

Overall, in humans, sulforaphane is rapidly absorbed and eliminated with small inter-individual variations and typical urinary excretion of 70% to 90% of the dose. By contrast, the conversion of glucoraphanin is slow and with high inter-individual variations. The urinary excretion of sulforaphane metabolites following intervention with glucoraphanin-containing preparations typically range from 2% to 15% of the dose, being 1% to 45% at the extremes. The differences in inter-individual variations between sulforaphane and glucoraphanin make, at first glance, the use of sulforaphane much more attractive for the purposes of dose precision. However, in contrast to its stable glucosinolate precursor, sulforaphane is unstable, which has prompted the development of stabilized preparations, such as an α-cyclodextrin-encapsulated form of sulforaphane [66] and a stabilized version of pure plant-derived sulforaphane, known as Prostaphane (Nutrinov, Noyal sur Vilaine Cedex, France). Alternatively, glucoraphanin-rich preparations containing active myrosinase have also been used [67,68]. As formulations differ in their bioavailability (which provides a possible explanation for the differences in pharmacokinetic parameters reported in the various human studies), the excreted amount of sulforaphane metabolites in the urine, and not the amount in the administered preparation, provides a more reliable measure of the actual dose [69].

Similar to the studies of the pharmacokinetics of sulforaphane, nearly all human studies addressing the pharmacodynamics of sulforaphane have used glucoraphanin- or sulforaphane-rich broccoli-based preparations. Although there is currently no direct evidence for specific target engagement by sulforaphane in humans, there is clear evidence for its pharmacodynamic action. Thus, increased levels of the Nrf2-target enzymes A-class GSTs and NQO1 have been reported in plasma [70] and saliva [71] of human subjects consuming cruciferous vegetables. In agreement, administration of glucoraphanin/sulforaphane-rich preparations to healthy volunteers resulted in increased mRNA or protein levels of NQO1 and GSTs in PBMC, skin punch biopsies, as well as in nasal and buccal scrapings [72,73,74,75,76].

Yet, animal studies have not delivered all that might be expected of them. It is clear from the data presented in Figure 5 that the pre-clinical experimentalists have not thought carefully about the selection of dose (or route) and its relevance to clinical utility. Using oral dosing in mice and rat studies as examples, over two-thirds of the animal studies have used doses that exceed the highest (and bordering on intolerable) doses of sulforaphane used in humans, even after accounting for allometric scaling between rodents and humans. Few studies have included a dose-response; thus, the greater than 4-log spread of doses used in mice appears to be driven by needs for effect reporting in publications rather than optimization of translational science. Authors of this review have contributed to this dose skewing, among many investigators.

Comparisons of published oral doses of sulforaphane administered to mice or rats and sulforaphane (tablets or sulforaphane-rich broccoli preparations) or glucoraphanin-rich broccoli preparations administered to humans. The allometric scaling of the murine doses uses the correction factor of 0.081 and those for rat doses 0.162 [145]. Human doses were based on an estimate of 70 kg body weights in each study.

Biosynthesis of glucoraphanin, its hydrolysis to form the isothiocyanate sulforaphane, and metabolism of sulforaphane. The highly reactive isothiocyanate sulforaphane is produced in plants as an inert precursor, the glucosinolate glucoraphanin. Its biosynthetic pathway originates from the amino acid methionine and proceeds in three stages: (i) methionine side chain elongation by two methylene groups (a); (ii) formation of the core glucosinolate structure (b); (iii) secondary modification of the glucosinolate side chain (c); Upon disruption of the plant tissue integrity, glucoraphanin comes into contact with myrosinase, which catalyzes the hydrolysis of glucoraphanin to give sulforaphane (d); In mammalian cells, sulforaphane is metabolized through the mercapturic acid pathway, and can also undergo an interconversion to erucin (e).

We thank our many colleagues who have contributed to our studies on sulforaphane. Special thanks to Patricia Egner (Johns Hopkins University) for conducting the sulforaphane metabolite measures depicted in Figure 4.

The following are available online. Table S1: Summary of literature reporting oral dosing of mice with sulforaphane, Table S2: Summary of literature reporting intraperitoneal dosing of mice with sulforaphane, Table S3: Summary of literature reporting topical administration of sulforaphane to mice, Table S4: Summary of literature reporting oral dosing of rats with sulforaphane.

A complete guide for growing broccoli sprouts with tips for getting the MOST sulforaphane from your seeds! You'll also find out why broccoli sprouts are one of the most nutritious, healthiest foods we can imagine.

Out of all edible plants, the highest amount of sulforaphane is found in broccoli sprouts. Research suggests that sulforaphane is beneficial for human consumption in multiple ways.

Just make sure to reincorporate any of the "juices" that leach out while thawing. That liquid likely contains a considerable amount of sulforaphane! That's why I usually only use frozen broccoli sprouts in smoothies. 041b061a72


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