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Nutrients 2018, 10(6), 718; https://doi.org/10.3390/nu10060718

Induction of Apoptosis and Cytotoxicity by Isothiocyanate Sulforaphene in Human Hepatocarcinoma HepG2 Cells

1
UPM-MAKNA Cancer Research Laboratory, Institute of Bioscience, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia
2
Consiglio per la Ricerca in Agricoltura e L’analisi Dell’economia Agraria, Centro di Ricerca Agricoltura e Ambiente (CREA-AA), Via di Corticella 133, 40128 Bologna, Italy
3
Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey GU2 7XH, UK
4
Laboratory of Molecular Biomedicine, Institute of Bioscience, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia
5
Laboratory of Food Safety and Food Integrity, Institute of Tropical Agriculture and Food Security, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia
6
Department of Food Science, Faculty of Food Science and Technology, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia
*
Author to whom correspondence should be addressed.
Received: 18 May 2018 / Revised: 31 May 2018 / Accepted: 1 June 2018 / Published: 4 June 2018
(This article belongs to the Special Issue Plant Food, Nutrition and Human Health)
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Abstract

Glucoraphenin, a glucosinolate present in large quantities in radish is hydrolysed by myrosinase to form the isothiocyanate sulforaphene, which is believed to be responsible for its chemopreventive activity; however, the underlying mechanisms of action have not been investigated, particularly in human cell lines. The aim of the study is to assess the cytotoxicity of sulforaphene in HepG2 cells and evaluate its potential to enhance apoptosis. The cytotoxicity of sulforaphene in HepG2 cells was carried out ensuing an initial screening with two other cell lines, MFC-7 and HT-29, where sulforaphene displayed highest toxicity in HepG2 cells following incubation at 24, 48 and 72 h. In contrast, the intact glucosinolate showed no cytotoxicity. Morphological studies indicated that sulforaphene stimulated apoptosis as exemplified by cell shrinkage, blebbing, chromatin condensation, and nuclear fragmentation. The Annexin V assay revealed significant increases in apoptosis and the same treatment increased the activity of caspases -3/7 and -9, whereas a decline in caspase-8 was observed. Impairment of cell proliferation was indicated by cell cycle arrest at the Sub G0/G1 phase as compared to the other phases. It may be concluded that sulforaphene, but not its parent glucosinolate, glucoraphenin, causes cytotoxicity and stimulates apoptosis in HepG2 cells. View Full-Text
Keywords: glucoraphenin; sulforaphene; HepG2 cells; apoptosis; cell cycle arrest glucoraphenin; sulforaphene; HepG2 cells; apoptosis; cell cycle arrest
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).
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Kntayya, S.B.; Ibrahim, M.D.; Mohd Ain, N.; Iori, R.; Ioannides, C.; Abdull Razis, A.F. Induction of Apoptosis and Cytotoxicity by Isothiocyanate Sulforaphene in Human Hepatocarcinoma HepG2 Cells. Nutrients 2018, 10, 718.

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