Chen S.-Y.Lu F.-J.Gau R.-J.Yang M.-L.TIEN-SHANG HUANG2020-06-032020-06-0320020959-4973https://www.scopus.com/inward/record.uri?eid=2-s2.0-0036667949&doi=10.1097%2f00001813-200208000-00011&partnerID=40&md5=cc4836856e340b2b91065387903067b8https://scholars.lib.ntu.edu.tw/handle/123456789/496839Treatment of carcinoma cell lines with 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2), a natural ligand of the peroxisome proliferator-activated receptor-γ, has been reported to induce apoptosis and/or inhibit proliferation. In this study, we investigated the cytotoxic effect and the action mechanisms of 15d-PGJ2 in a thyroid papillary cancer cell line, CG3. The results indicate that 15d-PGJ2 caused cytotoxicity and increased the amount of intracellular reactive oxygen species (ROS) in these cells. Mitochondrial oxidative phosphorylation inhibitors (carbonyl cyanide m-chlorophenylhydrazone, oligomycin, cyclosporin A and rotenone), NADPH oxidase inhibitor (diphenyleneiodonium), xanthine oxidase inhibitor (allopurinol) and NO synthase inhibitor (N-monomethyl-L-arginine acetate) did not reduce the generation of ROS. However, catalase, N-acetyl-cysteine and the iron chelator desferrioxamine decreased the intracellular ROS of 15d-PGJ2-treated CG3 cells. Furthermore, 15d-PGJ2 enhanced the accumulation of iron in the CG3 cells. These data suggest that 15d-PGJ2 induces the generation of ROS by enhancing the accumulation of intracellular iron and that the increased oxidative stress may cause apoptosis of CG3 cells. ? 2002 Lippincott Williams & Wilkins.[SDGs]SDG315 deoxy delta12,14 prostaglandin J2; acetylcysteine; allopurinol; catalase; cyclosporin A; deferoxamine; diphenyliodonium salt; iron; n(g) methylarginine acetate; nitric oxide synthase inhibitor; oligomycin; peroxisome proliferator activated receptor gamma; reactive oxygen metabolite; reduced nicotinamide adenine dinucleotide phosphate oxidase; rotenone; unclassified drug; xanthine oxidase inhibitor; 15 deoxy delta(12,14) prostaglandin J2; 15-deoxy-delta(12,14)-prostaglandin J2; biological response modifier; caspase; diagnostic agent; drug derivative; dyes, reagents, indicators, markers and buffers; iron chelating agent; prostaglandin D2; reactive oxygen metabolite; antineoplastic activity; apoptosis; article; cancer cell culture; controlled study; cytotoxicity; enzyme inhibition; human; human cell; iron chelation; iron storage; mitochondrial respiration; oxidative stress; priority journal; thyroid papillary carcinoma; apoptosis; cell count; cell culture; cell survival; drug effect; enzyme activation; lipid peroxidation; metabolism; papillary carcinoma; pathology; stimulation; thyroid tumor; Apoptosis; Biological Response Modifiers; Carcinoma, Papillary; Caspases; Cell Count; Cell Survival; Enzyme Activation; Humans; Indicators and Reagents; Iron; Iron Chelating Agents; Lipid Peroxidation; Oxidative Stress; Prostaglandin D2; Reactive Oxygen Species; Stimulation, Chemical; Thyroid Neoplasms; Tumor Cells, Culturedjournal article10.1097/00001813-200208000-00011121873332-s2.0-0036667949