title: Acrylamide-induced mitochondria collapse and apoptosis in human astrocytoma cells.
abstract: Acrylamide (ACR) can be produced during food processing and has neurotoxic effects in humans. This study aims to determine ACR induced apoptotic responses in human astrocytoma U-1240 MG cells to realize the incurred toxic mechanisms. Under 1 and 2mM ACR exposure, cell viability decreased as time increased. The increments in sub-G(1) phase were 87.5-fold, and pro-caspase 3 and PARP protein expressions decreased 35% and 54.5% respectively relative to the control after 2mM ACR treatment. Molecular evidence of Bax/bcl-2 ratio and cytochrome c expression increased 8.86-fold and 6.81-fold as well as pro-caspase 9 decreased 67.8% relative to the control respectively under 2mM ACR exposure. Trolox, an ROS scavenging agent, attenuated cell death and induced ROS production by 2mM ACR. The ultrastructure alterations of mitochondria showed marked vesicular matrix compartmentalization and cytoplasmic vacuole formation after 2mM ACR was treated for 48h, whereas those treated for 72h showed chromatin condensation, pyknosis, and swelling. These results indicate long-term exposure to ACR induced mitochondria collapse and finally led to apoptosis. Although 2mM ACR is higher than average daily intake dosage, workers in chemical industries may be exposed to sufficient doses to entail health risks.
authors.affiliation: School of Veterinary Medicine, National Taiwan University, No. 1, Section 4, Roosevelt Rd., Taipei 106, Taiwan, ROC.
authors.forename: Jong-Hang
authors.initials: JH
authors.lastname: Chen
authors.forename: Cheng-Hsien
authors.initials: CH
authors.lastname: Yang
authors.forename: Yan-Shiu
authors.initials: YS
authors.lastname: Wang
authors.forename: Jiann-Gwu
authors.initials: JG
authors.lastname: Lee
authors.forename: Chiung-Hsiang
authors.initials: CH
authors.lastname: Cheng
authors.forename: Chin-Cheng
authors.initials: CC
authors.lastname: Chou
mesh_terms: D020106:Acrylamide / Q000633:toxicity*; D017209:Apoptosis / Q000187:drug effects* / Q000502:physiology; D001254:Astrocytoma / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*; D053148:Caspase 3 / Q000378:metabolism; D045744:Cell Line, Tumor / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002839:Chromans / Q000494:pharmacology; D045304:Cytochromes c / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D016193:G1 Phase / Q000187:drug effects; D006801:Humans; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D018675:Toxicity Tests / Q000379:methods; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: C494826:BAX protein, human; D002839:Chromans; D017382:Reactive Oxygen Species; D051028:bcl-2-Associated X Protein; D020106:Acrylamide; D045304:Cytochromes c; D011065:Poly(ADP-ribose) Polymerases; D053148:Caspase 3; C010643:6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid