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Chemical Compound Review

Sulforafan     1-isothiocyanato-4- methylsulfinyl-butane

Synonyms: Sulforaphan, Sulforathane, sulforaphane, Sulphoraphane, CHEMBL48802, ...
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Disease relevance of Sulforathane


High impact information on Sulforathane

  • Chemical inducers such as sulforaphane are known to react with Keap1 cysteine residues, thereby promoting Nrf2 nuclear accumulation and hence ARE activation [8].
  • Induction of phase 2 genes by sulforaphane protects retinal pigment epithelial cells against photooxidative damage [9].
  • Significant protection of RPE cells was obtained by prior treatment with phase 2 gene inducers, such as the isothiocyanate sulforaphane or a bis-2-hydroxybenzylideneacetone Michael reaction acceptor [9].
  • We cloned, overexpressed, and purified murine Keap1 and demonstrated on native gels the formation of complexes of Keap1 with the Neh2 domain of Nrf2 and their concentration-dependent disruption by inducers such as sulforaphane and bis(2-hydroxybenzylidene)acetone [10].
  • Thus, the dual actions of sulforaphane in inhibiting Helicobacter infections and blocking gastric tumor formation offer hope that these mechanisms might function synergistically to provide diet-based protection against gastric cancer in humans [2].

Chemical compound and disease context of Sulforathane


Biological context of Sulforathane

  • Since phase 2 enzyme induction is often associated with reduced susceptibility of animals and their cells to the toxic and neoplastic effects of carcinogens and other electrophiles, it was important to establish whether sulforaphane could block chemical carcinogenesis [1].
  • Neither quinone-induced oxidative stress nor sulforaphane disrupts association between Keap1 and Nrf2 [16].
  • Thus, the presumed natural antioxidants sulforaphane and curcumin may exert their anti-inflammatory and anticarcinogenic effects not only by induction of phase 2 enzymes but also by the up-regulation of the selenoprotein GI-GPx [17].
  • A marked decline in the protein level of X-linked inhibitor of apoptosis on treatment with sulforaphane was also observed [18].
  • This sulforaphane-induced cell cycle arrest was correlated with an increased expression of cyclins A and B1 [5].

Anatomical context of Sulforathane


Associations of Sulforathane with other chemical compounds


Gene context of Sulforathane

  • Overexpression of individual p38 mitogen-activated protein (MAP) kinase (MAPK) isoforms also suppressed constitutive as well as sulforaphane- or Nrf2-induced ARE-dependent gene expression [12].
  • Collectively, our results indicate that transcriptional activation of Nrf2/ARE is critical in sulforaphane-mediated induction of HO-1, which can be modulated in part by the blockade of p38 MAPK signaling pathway [12].
  • Furthermore, a dominant-negative mutant of Ras had little effect on ERK2 activation by tBHQ and SUL, implicating a Ras-independent mechanism [13].
  • Pretreatment with MEK1-ERK inhibitor U0126 and JNK inhibitor SP600125 substantially attenuated the decrease in cell viability induced by SFN, PEITC and AITC [24].
  • The induction of UGT1A1 and GSTA1 mRNA by sulforaphane was time and concentration dependent [25].

Analytical, diagnostic and therapeutic context of Sulforathane


  1. Anticarcinogenic activities of sulforaphane and structurally related synthetic norbornyl isothiocyanates. Zhang, Y., Kensler, T.W., Cho, C.G., Posner, G.H., Talalay, P. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  2. Sulforaphane inhibits extracellular, intracellular, and antibiotic-resistant strains of Helicobacter pylori and prevents benzo[a]pyrene-induced stomach tumors. Fahey, J.W., Haristoy, X., Dolan, P.M., Kensler, T.W., Scholtus, I., Stephenson, K.K., Talalay, P., Lozniewski, A. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  3. Powerful and prolonged protection of human retinal pigment epithelial cells, keratinocytes, and mouse leukemia cells against oxidative damage: the indirect antioxidant effects of sulforaphane. Gao, X., Dinkova-Kostova, A.T., Talalay, P. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
  4. Sulforaphane causes autophagy to inhibit release of cytochrome C and apoptosis in human prostate cancer cells. Herman-Antosiewicz, A., Johnson, D.E., Singh, S.V. Cancer Res. (2006) [Pubmed]
  5. Sulforaphane, a naturally occurring isothiocyanate, induces cell cycle arrest and apoptosis in HT29 human colon cancer cells. Gamet-Payrastre, L., Li, P., Lumeau, S., Cassar, G., Dupont, M.A., Chevolleau, S., Gasc, N., Tulliez, J., Tercé, F. Cancer Res. (2000) [Pubmed]
  6. Sulforaphane enhances the therapeutic potential of TRAIL in prostate cancer orthotopic model through regulation of apoptosis, metastasis, and angiogenesis. Shankar, S., Ganapathy, S., Srivastava, R.K. Clin. Cancer Res. (2008) [Pubmed]
  7. Sulforaphane, a dietary component of broccoli/broccoli sprouts, inhibits breast cancer stem cells. Li, Y., Zhang, T., Korkaya, H., Liu, S., Lee, H.F., Newman, B., Yu, Y., Clouthier, S.G., Schwartz, S.J., Wicha, M.S., Sun, D. Clin. Cancer Res. (2010) [Pubmed]
  8. Modifying specific cysteines of the electrophile-sensing human Keap1 protein is insufficient to disrupt binding to the Nrf2 domain Neh2. Eggler, A.L., Liu, G., Pezzuto, J.M., van Breemen, R.B., Mesecar, A.D. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  9. Induction of phase 2 genes by sulforaphane protects retinal pigment epithelial cells against photooxidative damage. Gao, X., Talalay, P. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  10. Direct evidence that sulfhydryl groups of Keap1 are the sensors regulating induction of phase 2 enzymes that protect against carcinogens and oxidants. Dinkova-Kostova, A.T., Holtzclaw, W.D., Cole, R.N., Itoh, K., Wakabayashi, N., Katoh, Y., Yamamoto, M., Talalay, P. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  11. Phenethyl isothiocyanate and sulforaphane and their N-acetylcysteine conjugates inhibit malignant progression of lung adenomas induced by tobacco carcinogens in A/J mice. Conaway, C.C., Wang, C.X., Pittman, B., Yang, Y.M., Schwartz, J.E., Tian, D., McIntee, E.J., Hecht, S.S., Chung, F.L. Cancer Res. (2005) [Pubmed]
  12. Mechanism of Action of Sulforaphane: Inhibition of p38 Mitogen-Activated Protein Kinase Isoforms Contributing to the Induction of Antioxidant Response Element-Mediated Heme Oxygenase-1 in Human Hepatoma HepG2 Cells. Keum, Y.S., Yu, S., Chang, P.P., Yuan, X., Kim, J.H., Xu, C., Han, J., Agarwal, A., Kong, A.N. Cancer Res. (2006) [Pubmed]
  13. Role of a mitogen-activated protein kinase pathway in the induction of phase II detoxifying enzymes by chemicals. Yu, R., Lei, W., Mandlekar, S., Weber, M.J., Der, C.J., Wu, J., Kong, A.T. J. Biol. Chem. (1999) [Pubmed]
  14. Targeting cell cycle machinery as a molecular mechanism of sulforaphane in prostate cancer prevention. Wang, L., Liu, D., Ahmed, T., Chung, F.L., Conaway, C., Chiao, J.W. Int. J. Oncol. (2004) [Pubmed]
  15. Protection against UV-light-induced skin carcinogenesis in SKH-1 high-risk mice by sulforaphane-containing broccoli sprout extracts. Dinkova-Kostova, A.T., Jenkins, S.N., Fahey, J.W., Ye, L., Wehage, S.L., Liby, K.T., Stephenson, K.K., Wade, K.L., Talalay, P. Cancer Lett. (2006) [Pubmed]
  16. Keap1 is a redox-regulated substrate adaptor protein for a Cul3-dependent ubiquitin ligase complex. Zhang, D.D., Lo, S.C., Cross, J.V., Templeton, D.J., Hannink, M. Mol. Cell. Biol. (2004) [Pubmed]
  17. The GI-GPx gene is a target for Nrf2. Banning, A., Deubel, S., Kluth, D., Zhou, Z., Brigelius-Flohé, R. Mol. Cell. Biol. (2005) [Pubmed]
  18. Bax and Bak are required for apoptosis induction by sulforaphane, a cruciferous vegetable-derived cancer chemopreventive agent. Choi, S., Singh, S.V. Cancer Res. (2005) [Pubmed]
  19. Dietary indoles and isothiocyanates that are generated from cruciferous vegetables can both stimulate apoptosis and confer protection against DNA damage in human colon cell lines. Bonnesen, C., Eggleston, I.M., Hayes, J.D. Cancer Res. (2001) [Pubmed]
  20. Inhibition of cytochromes P-450 and induction of glutathione S-transferases by sulforaphane in primary human and rat hepatocytes. Mahéo, K., Morel, F., Langouët, S., Kramer, H., Le Ferrec, E., Ketterer, B., Guillouzo, A. Cancer Res. (1997) [Pubmed]
  21. Effects of glutathione on antioxidant response element-mediated gene expression and apoptosis elicited by sulforaphane. Kim, B.R., Hu, R., Keum, Y.S., Hebbar, V., Shen, G., Nair, S.S., Kong, A.N. Cancer Res. (2003) [Pubmed]
  22. Nrf2 Possesses a Redox-sensitive Nuclear Exporting Signal in the Neh5 Transactivation Domain. Li, W., Yu, S.W., Kong, A.N. J. Biol. Chem. (2006) [Pubmed]
  23. Reversal of hypermethylation and reactivation of p16INK4a, RARbeta, and MGMT genes by genistein and other isoflavones from soy. Fang, M.Z., Chen, D., Sun, Y., Jin, Z., Christman, J.K., Yang, C.S. Clin. Cancer Res. (2005) [Pubmed]
  24. ERK and JNK signaling pathways are involved in the regulation of activator protein 1 and cell death elicited by three isothiocyanates in human prostate cancer PC-3 cells. Xu, C., Shen, G., Yuan, X., Kim, J.H., Gopalkrishnan, A., Keum, Y.S., Nair, S., Kong, A.N. Carcinogenesis (2006) [Pubmed]
  25. Sulforaphane and its glutathione conjugate but not sulforaphane nitrile induce UDP-glucuronosyl transferase (UGT1A1) and glutathione transferase (GSTA1) in cultured cells. Basten, G.P., Bao, Y., Williamson, G. Carcinogenesis (2002) [Pubmed]
  26. A major inducer of anticarcinogenic protective enzymes from broccoli: isolation and elucidation of structure. Zhang, Y., Talalay, P., Cho, C.G., Posner, G.H. Proc. Natl. Acad. Sci. U.S.A. (1992) [Pubmed]
  27. A novel mechanism of chemoprotection by sulforaphane: inhibition of histone deacetylase. Myzak, M.C., Karplus, P.A., Chung, F.L., Dashwood, R.H. Cancer Res. (2004) [Pubmed]
  28. Cancer chemopreventive potential of sulforamate, a novel analogue of sulforaphane that induces phase 2 drug-metabolizing enzymes. Gerhäuser, C., You, M., Liu, J., Moriarty, R.M., Hawthorne, M., Mehta, R.G., Moon, R.C., Pezzuto, J.M. Cancer Res. (1997) [Pubmed]
  29. Identification of Nrf2-regulated genes induced by the chemopreventive agent sulforaphane by oligonucleotide microarray. Thimmulappa, R.K., Mai, K.H., Srisuma, S., Kensler, T.W., Yamamoto, M., Biswal, S. Cancer Res. (2002) [Pubmed]
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