The Phenolic Composition and Antioxidant Properties of Figs (Ficus carica L.) Grown in the Black Sea Region.

This study compared the phenolic composition and antioxidant properties of three varieties of fig fruits (Ficus carica L) from the Eastern Black Sea region of Türkiye. Total polyphenol content (TPC), total flavonoid content (TFC), and phenolic compositions were analyzed in green, purple, and dark purple species. The mean TPC value was 42.10 ± 5.71 mg GAE/100 g FW, ranging from 35.98 to 47.30 mg GAE/100 g FW, and was highest in the dark purple species. The mean TFC value was 1.27 ± 0.93 mg QUE/100 FW g, ranging between 0.35 and 2.21 mg QUE/100 FW g, and was highest in the purple species. The samples' total antioxidant capacity was measured based on ferric reducing/antioxidant power (FRAP), the values ranging from 151.98 to 372.97 µmol FeSO4.7H2O/100 g FW, with an average value of 239.64 µmol FeSO4.7H2O/100 g FW, being highest in the dark purple species. The 2,2-Diphenyl-1-picrylhydrazyl (DPPH) radical scavenging activity of the fruits was expressed as SC50 (mg/mL), and the values ranged from 10.04 to 42.42 mg/mL, being highest in the purple species. The phenolic composition was analyzed using HPLC-PDA according to the method in which 25 phenolic standards were used. Chlorogenic acid and t-cinnamic acid were the most common phenolic compounds, with rutin, chrysin, apigenin, and luteolin being detected at different amounts. In conclusion, the purple species contained the highest flavonoid content, was rich in apigenin, luteolin, and chrysin, and possessed the highest DPPH radical scavenging activity.

Distinct Epigenetic Reprogramming, Mitochondrial Patterns, Cellular Morphology, and Cytotoxicity after Bee Venom Treatment.

BACKGROUND: Bee venom is a promising agent for cancer treatment due to its selective cytotoxic potential for cancer cells through apoptotic pathways. However, there is no evidence for changes in the epigenome and mitochondrial DNA copy numbers after bee venom application. The purpose of this study was to determine the impact of bee venom on cytosine modifications and mitochondrial DNA copy number variation. METHODS: A broad range of methods was applied to elucidate the impact of bee venom on neoplastic cells. These included MTT assay for detection of cytotoxicity, immunostaining of cytosine modifications and mitochondria, assessment of cellular morphology by flow cytometry, and quantification of mitochondrial DNA copy numbers using QPCR. RESULTS: Bee venom-induced cell death was selective for cancer cells, where it triggered a response characterized by alteration of cytosine modification. In contrast, normal cells were more resistant to DNA modifications. Furthermore, application of the venom resulted in variation of mitochondrial membrane permeability and mitochondrial DNA copy numbers, together with alterations in cell morphology, manifesting as reduced affected cell size. CONCLUSION: The study findings suggest that bee venom can be used as a selective DNA (de)methylating agent in cancer. Various agents (such as decitabine and 5-azacytidine) have been synthesized and developed for cancer treatment, and a range of syntheses and preparation and application methods have been described for these patented drugs. However, to the best of our knowledge, no previous research has investigated the use of bee venom or any component thereof for epigenetic therapy in cancer cells.