ArticleToxicology letters2010
Goniothalamin-induced oxidative stress, DNA damage and apoptosis via caspase-2 independent and Bcl-2 independent pathways in Jurkat T-cells.
Article in Toxicology letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 56 citations in OpenAlex.
- Goniothalamin as a Styryl-Lactone Toxicophore in Cancer Models: Electrophile-Driven DNA Damage, Reactive Oxygen Species-Endoplasmic Reticulum Stress Signaling and Detoxification-Relevant Safety Considerations.Journal of biochemical and molecular toxicology · 2026Review
- Combination of Goniothalamin and Sol-Gel-Derived Bioactive Glass 45S5 Enhances Growth Inhibitory ActivityBioMed research international · 2022Article
- Antimutagenic, Cytoprotective and Antioxidant Properties ofMolecules (Basel, Switzerland) · 2021Article
- Therapeutic potential of xanthones fromThe Indian journal of medical research · 2020Article
- The Role of Caspase-2 in Regulating Cell Fate.Cells · 2020Review
- Goniothalamin Induces Necroptosis and Anoikis in Human Invasive Breast Cancer MDA-MB-231 Cells.International journal of molecular sciences · 2019Article
- Histological, Biochemical, and Hematological Effects of Goniothalamin on Selective Internal Organs of MaleJournal of toxicology · 2019Article
- Apoptosis Induction via ATM Phosphorylation, Cell Cycle Arrest, and ER Stress by Goniothalamin and Chemodrugs Combined Effects on Breast Cancer-Derived MDA-MB-231 Cells.BioMed research international · 2018Article
- Article
- Herbal Formulation C168 Attenuates Proliferation and Induces Apoptosis in HCT 116 Human Colorectal Carcinoma Cells: Role of Oxidative Stress and DNA Damage.Evidence-based complementary and alternative medicine : eCAM · 2016Article
- Threshold Dose of Three Types of Quantum Dots (QDs) Induces Oxidative Stress Triggers DNA Damage and Apoptosis in Mouse Fibroblast L929 Cells.International journal of environmental research and public health · 2015Article
- Upregulation of cyclin-dependent kinase inhibitors CDKN1B and CDKN1C in hepatocellular carcinoma-derived cells via goniothalamin-mediated protein stabilization and epigenetic modifications.Toxicology reports · 2015Article
- Emerging anticancer potentials of goniothalamin and its molecular mechanisms.BioMed research international · 2014Review
- Toxic effect of silica nanoparticles on endothelial cells through DNA damage response via Chk1-dependent G2/M checkpoint.PloS one · 2013Article
- A bacterial biosensor for oxidative stress using the constitutively expressed redox-sensitive protein roGFP2.Sensors (Basel, Switzerland) · 2010Article
- Rosiglitazone enhances the apoptotic effect of 5-fluorouracil in colorectal cancer cells with high-glucose-induced glutathione.Science progressArticle
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
Goniothalamin (GTN) isolated from Goniothalamus sp. has been demonstrated to induce apoptosis in a variety of cancer cell lines including Jurkat T leukemia cells. However, the mechanism of GTN-induced apoptosis upstream of mitochondria is still poorly defined. In this study, GTN caused a decrease in GSH with an elevation of reactive oxygen species as early as 30 min and DNA damage as assessed by Comet assay. Analysis using topoisomerase II processing of supercoiled pBR 322 DNA showed that GTN caused DNA damage via a topoisomerase II-independent pathway suggesting that cellular oxidative stress may contribute to genotoxicity. A 12-fold increase of caspase-2 activity was observed in GTN-treated Jurkat cells after 4h treatment and this was confirmed using Western blotting. Although the caspase-2 inhibitor Z-VDVAD-FMK inhibited the proteolytic activity of caspase-2, apoptosis ensued confirming that caspase-2 activity was not crucial for GTN-induced apoptosis. However, GTN-induced apoptosis was completely abrogated by N-acetylcysteine further confirming the role of oxidative stress. Since cytochrome c release was observed as early as 1h without any appreciable change in Bcl-2 protein expression, we further investigated whether overexpression of Bcl-2 confers resistance in GTN-induced cytotoxicity. Using a panel of Jurkat Bcl-2 transfectants, GTN cytotoxicity was not abrogated in these cells. In conclusion, GTN induces DNA damage and oxidative stress resulting in apoptosis which is independent of both caspase-2 and Bcl-2.
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