Clinical trials have shown that antioxidant supplementation increased the risk of lung and skin cancers, but the underlying molecular mechanism is unknown. Here, we show that epigallocatechin gallate (EGCG) as an exemplary antioxidant induced significant death and DNA damage in human lung and skin normal cells through a reductive mechanism. Our results show direct evidence of reductive DNA damage in the cells. We found that EGCG was much more toxic against normal cells than H₂O₂ and cisplatin as toxic and cancer-causing agents, while EGCG at low concentrations (≤100 μM) increased slightly the lung cancer cell viability. EGCG induced DNA double-strand breaks and apoptosis in normal cells and enhanced the mutation frequency. These results provide a compelling explanation for the clinical results and unravel a new reductive damaging mechanism in cellular processes. This study therefore provides a fresh understanding of aging and diseases, and may lead to effective prevention and therapies.
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http://dx.doi.org/10.1038/srep03169 | DOI Listing |
Hum Exp Toxicol
January 2025
Department of Gynecology and Obstetrics, Fuyong People's Hospital, Shenzhen, China.
Gestational diabetes mellitus (GDM) is a metabolic disorder that arises during pregnancy and heightens the risk of placental dysplasia. Ginsenoside Re (Re) may stabilize insulin and glucagon to regulate glucose levels, which may improve diabetes-associated diseases. This study aims to investigate the mechanism of Re in high glucose (HG)-induced apoptosis of trophoblasts through endoplasmic reticulum stress (ERS)-related protein CHOP/GADD153.
View Article and Find Full Text PDFACS Appl Mater Interfaces
January 2025
Key Laboratory of Cryogenics Science and Technology, Technical Institute of Physics and Chemistry, Chinese Academy of Sciences, Laboratory of Controllable Preparation and Application of Nanomaterials, Technical Institute of Physics and Chemistry, Chinese Academy of Sciences, Beijing 100190, China.
Sublethal tumor cells have an urgent need for energy, making it common for them to switch metabolic phenotypes between glycolysis and oxidative phosphorylation (OXPHOS) for compensatory energy supply; thus, the synchronous interference of dual metabolic pathways for limiting energy level is essential in inhibiting sublethal tumor growth. Herein, a multifunctional nanoplatform of Co-MOF-loaded anethole trithione (ADT) and myristyl alcohol (MA), modified with GOx and hyaluronic acid (HA) was developed, namely, CAMGH. It could synchronously interfere with dual metabolic pathways including glycolysis and OXPHOS to restrict the adenosine triphosphate (ATP) supply, achieving the inhibition to sublethal tumors after microwave (MW) thermal therapy.
View Article and Find Full Text PDFTheor Appl Genet
January 2025
School of Life Sciences, Guizhou Normal University, Guiyang, 550025, China.
A complete set of monosomic alien addition lines of Radish-Brassica oleracea exhibiting extensive variations was generated and well characterized for their chromosome behaviors and phenotypic characteristics. Monosomic alien addition lines (MAALs) are developed through interspecific hybridization, where an alien chromosome from a relative species is introduced into the genome of the recipient plant, serving as valuable genetic resources. In this study, an allotetraploid Raphanobrassica (RRCC, 2n = 36) was created from the interspecific hybridization between radish (Raphanus sativus, RR, 2n = 18) and Brassica oleracea (CC, 2n = 18).
View Article and Find Full Text PDFDrug Dev Ind Pharm
January 2025
Institute of Pharmaceutics, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China.
Objective: Boron Neutron Capture Therapy (BNCT) is a novel precision radiotherapy. The key to BNCT application lies in the effective targeting and retention of the boron-10 (B) carrier. Among the various compounds studied in clinical settings, 4-boronophenylalanine (BPA) become the most prevalent one currently.
View Article and Find Full Text PDFClin Transl Sci
January 2025
NIMML Institute, Blacksburg, Virginia, USA.
NIM-1324 is an oral investigational new drug for autoimmune disease that targets the Lanthionine Synthetase C-like 2 (LANCL2) pathway. Through activation of LANCL2, NIM-1324 modulates CD4+ T cells to bias signaling and cellular metabolism toward increased immunoregulatory function while providing similar support to phagocytes. In primary human immune cells, NIM-1324 reduces type I interferon and inflammatory cytokine (IL-6, IL-8) production.
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