title: N-acetyl cysteine protects TMJ chondrocytes from oxidative stress.
abstract: Temporomandibular joint (TMJ) inflammation is closely associated with oxidative stress. This study tested the potential of N-acetyl cysteine (NAC), an anti-oxidant amino-acid derivative, in alleviating oxidative stress-related damage in TMJ chondrocytes. The inflammatory condition was simulated by the addition of hydrogen peroxide (H₂O₂) to TMJ-derived chondrocyte cultures. Exposure to H₂O₂ decreased the cell population by half within 2 days as a result of induced apoptosis and reduced proliferation. Gene expression of aggrecan and collagen II, as well as glycosaminoglycan production, were reduced by more than 70%. These compromised chondrocyte viability and function were fully restored by the addition of NAC to the cultures. NAC reduced the H₂O₂-elevated intracellular reactive oxygen species to the normal level and increased cellular glutathione reserves. These results indicate that NAC restores oxidative stress-induced cell death and severe functional impairment in TMJ chondrocytes, and warrant in vivo testing to explore its therapeutic potential as an anti-inflammatory agent.
authors.affiliation: Laboratory for Bone and Implant Sciences, The Jane and Jerry Weintraub Center for Reconstructive Biotechnology, Division of Advanced Prosthodontics, Biomaterials and Hospital Dentistry, UCLA School of Dentistry, 10833 Le Conte Avenue, CHS B3-088H, Los Angeles, CA 90095-1668, USA. takepr01@tmd.ac.jp
authors.forename: T
authors.initials: T
authors.lastname: Ueno
authors.forename: M
authors.initials: M
authors.lastname: Yamada
authors.forename: Y
authors.initials: Y
authors.lastname: Sugita
authors.forename: T
authors.initials: T
authors.lastname: Ogawa
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology* / Q000627:therapeutic use; D053674:Aggrecans / Q000096:biosynthesis; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D019902:Chondrocytes / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D024043:Collagen Type II / Q000096:biosynthesis; D016166:Free Radical Scavengers / Q000494:pharmacology* / Q000627:therapeutic use; D005978:Glutathione / Q000096:biosynthesis; D006025:Glycosaminoglycans / Q000096:biosynthesis; D006861:Hydrogen Peroxide / Q000494:pharmacology; D010003:Osteoarthritis / Q000188:drug therapy* / Q000378:metabolism / Q000601:surgery; D016877:Oxidants / Q000494:pharmacology; D018384:Oxidative Stress / Q000187:drug effects*; D019152:Paracentesis; D051381:Rats; D013705:Temporomandibular Joint Disorders / Q000188:drug therapy* / Q000378:metabolism / Q000601:surgery
chemical_list: D053674:Aggrecans; D000975:Antioxidants; D024043:Collagen Type II; D016166:Free Radical Scavengers; D006025:Glycosaminoglycans; D016877:Oxidants; D006861:Hydrogen Peroxide; D005978:Glutathione; D000111:Acetylcysteine