On the cytotoxicity and genotoxicity of allyl and phenethyl isothiocyanates and their parent glucosinolates sinigrin and gluconasturtiin

Dietary isothiocyanates, GSTM1, GSTT1, NAT2 polymorphisms and bladder cancer risk

“…Second, it has been observed in other studies that prolonged exposure to high levels of electrophilic ITCs in the urine has a carcinogenic effect on bladder epithelium. [24][25][26][27] As GSTM1 or GSTT1 null genotypes have slow ITC metabolism, which leads to extended exposure of ITC metabolites to bladder epithelium, the GSTM1 or GSTT1 null genotypes may not provide an extra protective effect. Furthermore, we observed no significant associations between GSTM1/ GSTT1 polymorphisms and bladder cancer risk in this study, suggesting the effects of genetic modification might be minimal in this study.…”

Identification and quantification of glucosinolates in Korean leaf mustard germplasm (Brassica juncea var. integrifolia) by liquid chromatography–electrospray ionization/tandem mass spectrometry

“…Sinigrin and gluconasturtiin were higher than other vegetables in the Brassicaceae family ( Table 2). The degradation product of sinigrin, namely allylisothiocyanate (AITC), has a unique pungent and spicy taste that is characteristics of the leaf mustard [8] and is known to effectively inhibit carcinogenesis by inducing cell cycle arrest and apoptosis in prostate, ovarian and liver cancers (Musk et al [26]; [22,32]). In addition, the degradation product [30]; [10,16,29,32]) and is certified as being among the 40 most important anticancer drugs by the National Cancer Institute (NCI) in the USA [23].…”

A Toxic Mutator and Selection Alternative to the Non-Mendelian RNA Cache Hypothesis for hothead Reversion

“…The HTH gene encodes a product whose closest characterized relative is an MBC oxidoreductase that hydrolyzes the aromatic mandelonitrile in stone fruits (Zheng and Poulton, 1995) ( Figure 1A). Arabidopsis has complex metabolic pathways for the production of glucosinolates (Wittstock and Halkier, 2002;Brown et al, 2003), some of which are aromatic and resemble mandelonitrile (Figure 1), and aromatic glucosinolates and their derivatives are mutagenic (Musk et al, 1995;Kassie et al, 1999;Kassie and Knasmuller, 2000;Canistro et al, 2004). The sticky surface properties of the HTH phenotype, which suggest alterations of cuticle, cell wall, and perhaps membranes, might also be an effect of the toxic mutator.…”

“…Aromatic glucosinolates are abundant in Arabidopsis seeds and flowers (Wittstock and Halkier, 2002;Brown et al, 2003), and a block in their metabolism could lead to toxicity and mutagenicity (Musk et al, 1995;Kassie et al, 1999;Kassie and Knasmuller, 2000;Canistro et al, 2004) and to genomic instability (Henikoff, 2005). The delayed and progressive onset of reversion could arise from suppressor mutations that ameliorate the toxic effect.…”