Hypericin, a medicinal compound from St. John's Wort, inhibits genotoxicity induced by mutagenic agents in V79 cells.

a.sfakia shared this article with you from Inoreader Hypericin, a medicinal compound from St. John's Wort, inhibits genotoxicity induced by mutagenic agents in V79 cells. Via pubmed: "drug chem toxicol"[... Hypericin, a medicinal compound from St. John's Wort, inhibits genotoxicity induced by mutagenic agents in V79 cells. Drug Chem Toxicol. 2020 Oct 13;:1-6 Authors: de Souza LM, de Sousa FD, Cruz RCR, Tavares DC, Francielli de Oliveira P Abstract This study evaluated the cytotoxic, genotoxic, and the modulatory effects on DNA damage of hypericin in Chinese hamster lung fibroblasts (V79 cells). The hypericin is a natural polycyclic quinone, mainly extracted from St. John's Wort (Hypericum perforatum L.). Along with hyperforin, the hypericins are responsible for the antidepressant activity of St. John's Wort. Cytotoxicity was assessed by the XTT colorimetric assay and the nuclear division index (NDI). The genotoxic activity was studied by the micronucleus test at concentrations of 30, 60, 120, and 240 μg/mL. Mutagenic agents, methyl methanesulfonate (MMS, 44 μg/mL), doxorubicin (DXR, 0.5 μg/mL), and etoposide (VP16, 1 μg/mL) were used in combination with different concentrations of hypericin in order to evaluate the modulatory effect on DNA damage. Results showed that the hypericin was cytotoxic at concentrations above 156.2 μg/mL and genotoxic above 120 μg/mL. The hypericin significantly reduced DNA d amage frequency induced by DXR, at concentrations of 30 and 60 μg/mL, and MMS at a concentration of 30 μg/mL, but was unable to reduce damage when combined with VP-16. These results demonstrate the non-photoactivated hypericin toxicological safety limits, its protective effect on DNA damage and provide a basis for future studies that may characterize better its chemopreventive mechanism. PMID: 33050761 [PubMed - as supplied by publisher] View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.