Disease relevance of (2S,3R,4S,5R,6R)-2-(C-allyl-N-sulfoxy-carbonimidoyl)thio-3,4,5-trihydroxy-6-methylol-tetrahydropyran

• Degradation of sinigrin by Lactobacillus agilis strain R16 [1].
• Sinigrin could also be used as a growth substrate by Sphingobacterium sp. strain OTG1, although at concentrations exceeding 0.15 mM degradation was not complete [2].
• A human digestive strain of Bacteroides thetaiotaomicron was tested for its ability to metabolise sinigrin, a glucosinolate commonly found in Brassica vegetables [3].
• Three strains of Bifidobacterium sp., B. pseudocatenulatum, B. adolescentis, and B. longum were studied for their ability to digest glucosinolates, sinigrin (SNG) and glucotropaeolin (GTL), in vitro [4].
• We used raw juice extracted from Brussels sprouts rich in the glucosinolate sinigrin to explore the effect of naturally occurring glucosinolate breakdown products on cell cycle progression and apoptosis in human colorectal carcinoma cells (HT29) [5].

High impact information on (2S,3R,4S,5R,6R)-2-(C-allyl-N-sulfoxy-carbonimidoyl)thio-3,4,5-trihydroxy-6-methylol-tetrahydropyran

• Metabolism of sinigrin (2-propenyl glucosinolate) by the human colonic microflora in a dynamic in vitro large-intestinal model [6].
• The V(max) and K(m) values for the hydrolysis of allyl glucosinolate (sinigrin) were 2.06 micromol/min per mg of protein and 23 microM in the absence of ascorbate and 280 micromol/min per mg of protein and 250 microM in the presence of 500 microM ascorbate, respectively [7].
• There was no statistically significant induction of apoptosis in animals fed sinigrin alone [8].
• Inhibition of dimethylhydrazine-induced aberrant crypt foci and induction of apoptosis in rat colon following oral administration of the glucosinolate sinigrin [8].
• In the present study we explored the effect of sinigrin on the intestinal mucosa of rats previously treated with dimethylhydrazine (DMH) [8].

Biological context of (2S,3R,4S,5R,6R)-2-(C-allyl-N-sulfoxy-carbonimidoyl)thio-3,4,5-trihydroxy-6-methylol-tetrahydropyran

• The contrary effects on NNK-induced hepatic DNA methylation by sinigrin and I3C, two major components of cruciferous vegetables, demonstrate the complexities of dietary modulation of carcinogenesis [9].
• Sinigrin inhibited lipid peroxidation by 71% at 250 microg/ml [10].
• One- and two-dimensional (1)H NMR spectroscopy were used to study the biotransformation of two dietary glucosinolates, sinigrin (SIN), and glucotropaeolin (GTL) by the human digestive microflora in vitro [11].
• The embryos of high and low glucosinolate genotypes were equally capable of absorbing sinigrin from the medium [12].
• Gnotobiotic rats harbouring the bacterial strain were orally dosed with 50 micromol sinigrin [3].

Anatomical context of (2S,3R,4S,5R,6R)-2-(C-allyl-N-sulfoxy-carbonimidoyl)thio-3,4,5-trihydroxy-6-methylol-tetrahydropyran

• This may be due to increased apoptotic deletion of damaged stem cells in the crypts of animals fed sinigrin [8].
• These results suggested that dietary sinigrin might reduce the incidence of NNK-induced hepatic tumors with no effect on NNK tumorigenesis of the lung and nasal cavity, whereas I3C might increase hepatic tumor incidence and reduce NNK tumorigenesis of the lung and nasal cavity [9].
• Over a time course of 100 h, protein bodies within aleurone-like cells degraded, fused to form the cell vacuole and lost all myrosinase labelling but retained residual sinigrin labelling [13].
• Aqueous extracts of cooked and autolysed Brussels sprouts and sinigrin decreased DNA strand breaks in human lymphocytes exposed to 100 microM H2O2 for 5 min on ice, although the level of EndoIII and FPG sensitive sites was not reduced [14].
• In larval feces, only trace amounts of glucosinolates (sinalbin and sinigrin) could be detected [15].

Associations of (2S,3R,4S,5R,6R)-2-(C-allyl-N-sulfoxy-carbonimidoyl)thio-3,4,5-trihydroxy-6-methylol-tetrahydropyran with other chemical compounds

• Effects of dietary sinigrin or indole-3-carbinol on O6-methylguanine-DNA-transmethylase activity and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced DNA methylation and tumorigenicity in F344 rats [9].
• Allyl isothiocyanate (AITC) is formed from sinigrin, a glucosinolate that is present in many Brassica vegetables [16].
• Cleavage assays with the 3CLpro demonstrated that IC50 values were in micromolar ranges for I. indigotica root extract, indigo, sinigrin, aloe emodin and hesperetin [17].
• In this study, the ability of allyl nitrile, a hydrolysis product of the glucosinolate sinigrin, to increase tissue levels of the phase 2 detoxication enzymes glutathione S-transferase and quinone reductase and GSH in a variety of mouse tissues was examined [18].

Gene context of (2S,3R,4S,5R,6R)-2-(C-allyl-N-sulfoxy-carbonimidoyl)thio-3,4,5-trihydroxy-6-methylol-tetrahydropyran

• The stereochemistry of hydrolysis of sinigrin by Sinapis alba myrosinase was followed by 1H NMR and the enzyme was found to operate with a mechanism retaining the anomeric configuration at the cleavage point exactly like the related O-glycosidases found in family 1 [19].
• Crude preparations of soluble proteins from leaf and flower extracts of wild-type Arabidopsis showed myrosinase activity when sinigrin was used as substrate [20].

Analytical, diagnostic and therapeutic context of (2S,3R,4S,5R,6R)-2-(C-allyl-N-sulfoxy-carbonimidoyl)thio-3,4,5-trihydroxy-6-methylol-tetrahydropyran

• The bioassay results showed that dietary sinigrin had no effect on NNK tumorigenesis in these target tissues [9].
• Reversed-phase ion-pair liquid chromatography has been investigated for directly analyzing sinigrin in mustard seed without desulfatation [21].
• After extraction by phosphate buffer (pH 7.0) from the grind-pastes of inactivated-myrosinase mustard seeds, sinigrin was first isolated through deproteinization and centrifugation, followed by filtration and injection into the chromatographic system [21].
• The glucosinolate content in membrane eluates is determined by HPLC using sinigrin standards [22].
• We have studied the effect of preincubating human lymphocytes with aqueous extracts of raw, cooked and autolysed Brussels sprouts and the glucosinolate, sinigrin, on hydrogen peroxide-induced DNA damage, strand breaks and base oxidation, in vitro by means of the Comet assay [14].

References