[button : interested : interested : CM135]
Published in National Center for Biotechnology Information on 10/14/2019, distributed under a Creative Commons Attribution License.
Action | Clinical implications |
---|---|
(1) Increases glutathione synthesis [117]. | This has implications for oxidative stress and detoxification because glutathione is a substrate for both pathways. Glutathione is also an antioxidant in its own right. |
(2) It inhibits some phase 1 detoxification enzymes that activate chemical carcinogens [118]. | This reduces the level of toxic intermediates with carcinogenic potential. It also allows phase 2 to “keep up” with phase 1 processing. |
(3) It increases the activity of phase 2 detoxifying enzymes. Sulforaphane is considered the most potent of the phase 2 inducing agents [79]. | As a monofunctional inducer, sulforaphane is considered to be an important component of the anticarcinogenic effect of broccoli. |
(4) It provides significant antioxidant activity, mainly due to its ability to induce glutathione synthesis. | Glutathione is a critical factor in protecting organisms from toxicity and disease [119]. The ability of sulforaphane to regulate glutathione synthesis is very significant. |
(5) It acts as a histone deacetylase inhibitor and provides DNA protection [120-122]. | The development of histone deacetylase inhibitors is a key avenue for anticancer drug research. |
(6) Induces apoptosis, inhibits MMP-2 (metastasis), and inhibits angiogenesis and cell cycle arrest [28, 105, 123, 124] (interacts at multiple levels). | Therapeutic interventions that exhibit several related activities targeting the same underlying defect are considered highly desirable. |
(7) Limits the pro-inflammatory effects of diesel chemicals by upregulating phase 2 enzymes [125]. | Environmental pollutants are known to contribute to various lung diseases. Removal of toxins reduces the propensity for disease. |
(8) Induces thioredoxin (Trx) as part of the ARE. | Thioredoxin is involved in cardioprotection by triggering several survival proteins [126]. Sulforaphane may have beneficial effects in cardiovascular diseases. |
(9) Bactericidal against Helicobacter pylori and also blocks gastric tumor formation in animals [127]. | Helicobacter is known to contribute to the development of gastric cancer. Elimination of the organism without the use of typical antimicrobial triple therapy could protect the microflora of the colon. |
(10) Protects dopaminergic cells from cytotoxicity and subsequent neuronal death (cell culture) [128]. | Dopaminergic neurons are associated with Parkinson’s disease. Drugs to treat Parkinsonism are not without risk and the disease is usually not detected until more than 50% of neurons are lost. A chemoprotective tool could prevent premature loss. |
(11) It increases p-53 (associated with tumor suppression) and the expression of bax proteins, thereby enhancing cellular protection against cancer [129]. | Sulforaphane is an attractive chemotherapeutic agent for tumors with p53 mutations [62]. |
(12) Limits of aflatoxin action on liver cells [26]. | Interventions that can provide significant protection from environmental and food pollutants could prevent the consequences of these factors. Appropriate doses of sulforaphane-producing agents have yet to be determined. |
(13) It increases natural killer cell activity and other markers of enhanced immune function [117]. | The immune system is a critical component of the body’s defenses against both inflammatory and infectious diseases. Most diseases benefit from a boost in immune function. |
(14) Suppresses NF-κB, a key regulator of inflammation [117]. NF-κB expression is downregulated by sulforaphane and as such downregulates inducible pro-inflammatory enzymes such as cyclooxygenase (COX-2) and NO synthase (iNOS). | As an inhibitor of NF-κB as well as an activator of Nrf2, SF modulates many cancer-related events, returnincluding susceptibility to carcinogens, cell death, cell cycle, angiogenesis, invasion and metastasis [117]. |
(15) Sulforaphane is not a direct antioxidant. Instead, it exhibits a weak pro-oxidant effect [130]. | Because sulforaphane is not directly antioxidant, but exerts its antioxidant effect primarily by inducing glutathionenu and other antioxidant compounds, it is considered to exhibit an indirect antioxidant effect. |
(16) Potent inducer of HO-1 (haem oxygenase-1). | Hemooxygenase-1 plays an important role in modulating the effects of oxidants in the lung [131]. |
The articles in Oxidative Medicine and Cellular Longevity are reproduced here courtesy of Hindawi Limited.
[div : row]
[div : col-sm-6]
[additional_content : 65]
[div]
[div : col-sm-6]
[additional_content : 96]
[div]
[div : clearfix]
[div]
[div]
28. Fimognari C., Hrelia P. Sulforaphane as a promising molecule to fight cancer. Mutation research/reviews in mutation research. 2007; 635(2-3):90-104. doi: 10.1016/j.mrrev.2006.10.004. [PubMed] [CrossRef] [Google Scholar]
62. Juge N., Mithen R. F., Traka M. Molecular basis of sulforaphane chemoprevention: a comprehensive review. Cellular and Molecular Life Sciences.2007; 64:1105 – 1127. DOI: 10.1007/S00018-007-6484-5. [PubMed] [CrossRef] [Google Scholar]
79. Zhang Y, Talalay P, Cho CG, Posner G. H. A major inducer of anticarcinogenic protective enzymes from broccoli: isolation and elucidation of structure. Proceedings of the National Academy of Sciences of the United States of America. 1992;89(6):2399-2403. doi: 10.1073/pnas.89.6.2399. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
105 Myzak M. C., Dashwood R. H. Histone deacetylases as targets for dietary cancer-preventive agents: lessons learned with butyrate, diallyl disulfide, and sulforaphane. Contemporary Drug Targets. 2006; 7(4):443-452. DOI: 10.2174/138945006776359467. [PubMed] [CrossRef] [Google Scholar]
106. Dashwood RH, Myzak MC, Ho E. Dietary HDAC inhibitors: time to rethink weak ligands in cancer chemoprevention? Carcinogenesis. 2006; 27(2):344-349. DOI: 10.1093/Carcin/BGI253. [Free PMC Article] [PubMed] [CrossRef] [Google Scholar]
117. Zhang Y, Tang L. Discovery and development of sulforaphane as a cancer chemopreventive phytochemical. Acta Pharmacologica Sinica. 2007;28(9):1343-1354. doi: 10.1111/j.1745-7254.2007.00679.x. [PubMed] [CrossRef] [Google Scholar]
118. Singh S. V., Srivastava S. K., Choi S., et al. Sulforaphane-induced cell death in human prostate cancer cells is initiated by reactive oxygen species. The Journal of Biological Chemistry. 2005;280(20):19911-19924. doi: 10.1074/jbc.m412443200. [PubMed] [CrossRef] [Google Scholar]
119 Pastore A, Federici G, Bertini E, Piemonte F. Analysis of glutathione: implication in redox and detoxification. Clinica Chimica Acta. 2003;333(1):19-39. doi: 10.1016/s0009-8981(03)00200-6. [PubMed] [CrossRef] [Google Scholar]
120 Myzak M. C., Karplus P. A., Chung F. L., Dashwood R. H. A Novel Mechanism of Chemoprotection by Sulforaphane. Cancer Research. 2004;64(16):5767-5774. doi: 10.1158/0008-5472.can-04-1326. [PubMed] [CrossRef] [Google Scholar]
121 Steinkellner H, Rabot S, Freywald C., et al. Effects of cruciferous vegetables and their constituents on drug metabolizing enzymes involved in the bioactivation of DNA-reactive dietary carcinogens. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis. 2001;480-481:285-297. doi: 10.1016/s0027-5107(01)00188-9. [PubMed] [CrossRef] [Google Scholar]
122 Myzak M. C., Hardin K., Wang R., Dashwood R. H., Ho E. Sulforaphane inhibits histone deacetylase activity in BPH-1, LnCaP and PC-3 prostate epithelial cells. Carcinogenesis. 2006;27(4):811-819. doi: 10.1093/carcin/bgi265. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
123 Fimognari C, Berti F, Cantelli-Forti G., Hrelia P. Effect of sulforaphane on micronucleus induction in cultured human lymphocytes by four different mutagens. Environmental and Molecular Mutagenesis. 2005;46(4):260-267. doi: 10.1002/em.20156. doi: 10.1002/em.20156. [PubMed] [CrossRef] [Google Scholar]
124 Tang L, Zhang Y, Jobson HE, et al. Potent activation of mitochondria-mediated apoptosis and arrest in S and M phases of cancer cells by a broccoli sprout extract. Molecular Cancer Therapeutics. 2006;5(4):935-944. doi: 10.1158/1535-7163.mct-05-0476. [PubMed] [CrossRef] [Google Scholar]
125 Ritz S. A., Wan J., Diaz-Sanchez D. Sulforaphane-stimulated phase II enzyme induction inhibits cytokine production by airway epithelial cells stimulated with diesel extract. American Journal of Physiology-Lung Cellular and Molecular Physiology. 2007;292(1):L33-L39. doi: 10.1152/ajplung.00170.2006. [PubMed] [CrossRef] [Google Scholar]
126. mukherjee S, Gangopadhyay H, Das D. K. Broccoli: a unique vegetable that protects mammalian hearts through the redox cycling of the thioredoxin superfamily. Journal of Agricultural and Food Chemistry. 2008;56(2):609-617. doi: 10.1021/jf0728146. [PubMed] [CrossRef] [Google Scholar]
127 Fahey JW, Haristoy X, Dolan P. M., et al. Sulforaphane inhibits extracellular, intracellular, and antibiotic-resistant Helicobacter pylori strains and prevents benzo[a]pyrene-induced gastric tumors.Proceedings of the National Academy of Sciences of the United States of America. 2002; 99(11):7610-7615. DOI: 10.1073/PNAS.112203099. [Free PMC Article] [PubMed] [CrossRef] [Google Scholar]
128. Han J. M., Lee Y. J., Lee S. Y., et al. Protective effect of sulforaphane against dopaminergic cell death. The Journal of Pharmacology and Experimental Therapeutics. 2007;321(1):249-256. doi: 10.1124/jpet.106.110866. [PubMed] [CrossRef] [Google Scholar]
129 Fimognari C, Nusse M, Berti F, Iori R, Cantelli-Forti G, Hrelia P. Cyclin D3 and p53 mediate sulforaphane-induced cell cycle delay and apoptosis in non-transformed human T lymphocytes. Cellular and Molecular Life Sci. 2002;59(11):2004-2012. doi: 10.1007/pl00012523. [PubMed] [CrossRef] [Google Scholar]
130. Lee Y.-J., Lee S.-H. Sulforaphane Induces Antioxidative and Antiproliferative Responses by Generating Reactive Oxygen Species in Human Bronchial Epithelial BEAS-2B Cells. Journal of Korean Medical Science. 2011;26(11):1474-1482. doi: 10.3346/jkms.2011.26.11.1474. [PMC free article] [PubMed] [CrossRef] [Google Scholar].
131. Hisada T, Salmon M, Nasuhara Y, Chung K. F. Involvement of haemoxygenase-1 in ozone-induced airway inflammation and hyperresponsiveness. European Journal of Pharmacology. 2000;399(2-3):229-234. doi: 10.1016/s0014-2999(00)00369-1. [PubMed] [CrossRef] [Google Scholar].
https://www.carnomed.sk/produkty/sulforafan-extra.htm
https:// www.carnomed.sk/produkty/sulforafan-extra-xl-pure-gold-edition.htm