期刊
ANTIOXIDANTS
卷 11, 期 6, 页码 -出版社
MDPI
DOI: 10.3390/antiox11061125
关键词
cancer; saffron; safranal; natural products; DNA damage; hepatocellular carcinoma; hypoxanthine
资金
- Tamkeen under the NYU Abu Dhabi Research Institute [73 71210 CGSB9]
- NYUAD Faculty Research Funds [AD060]
- ZCHS Fund [31R174]
- Terry Fox Foundation Fund [21S103]
This study investigates the impact of safranal on HCC cells and finds that it can induce oxidative damage and protein destabilization, possibly through increasing reactive oxygen species and hypoxanthine levels.
The spice saffron (Crocus sativus) has anticancer activity in several human tissues, but the molecular mechanisms underlying its potential therapeutic effects are poorly understood. We investigated the impact of safranal, a small molecule secondary metabolite from saffron, on the HCC cell line HepG2 using untargeted metabolomics (HPLC-MS) and transcriptomics (RNAseq). Increases in glutathione disulfide and other biomarkers for oxidative damage contrasted with lower levels of the antioxidants biliverdin IX (139-fold decrease, p = 5.3 x 10(5)), the ubiquinol precursor 3-4-dihydroxy-5-all-trans-decaprenylbenzoate (3-fold decrease, p = 1.9 x 10(-5)), and resolvin E1 (-3282-fold decrease, p = 4(5)), which indicates sensitization to reactive oxygen species. We observed a significant increase in intracellular hypoxanthine (538-fold increase, p = 7.7 x 10(-6)) that may be primarily responsible for oxidative damage in HCC after safranal treatment. The accumulation of free fatty acids and other biomarkers, such as S-methyl-5 '-thioadenosine, are consistent with safranal-induced mitochondrial de-uncoupling and explains the sharp increase in hypoxanthine we observed. Overall, the dual omics datasets describe routes to widespread protein destabilization and DNA damage from safranal-induced oxidative stress in HCC cells.
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