Intracellular effects of NSAIDs/ASA in oxidatively stressed human lens epithelial cells in culture.
The aim of the study was to examine the effects of nonsteroidal anti-inflammatory drugs (NSAIDs)/acetylsalicylic acid (ASA) on human lens epithelial cells (HLECs) during oxidative stress. HLECs were exposed to H2O2 in the absence or presence of indomethacin, diclofenac, celecoxib (NSAIDs) or ASA for 24 h. HLECs were assayed for changes in superoxide and peroxide production and for variations in glutathione. Mitochondrial depolarization was measured using the membrane potential-sensitive dye JC-1. The results of the study include reduction in superoxide and peroxide production as well as reduction in glutathione depletion in oxidatively stressed HLECs incubated with low concentrations of NSAIDs/ASA. However, no protection against H2O2-induced mitochondrial depolarization by NSAIDs/ASA could be seen. In conclusion, NSAIDs/ASA display reactive oxygen species-scavenging properties in H2O2-exposed HLECs in culture.
Petersen
A
A
Department of Medical Chemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy at Goteborg University, Goteborg, Sweden. anne.petersen@gu.se
Carlsson
T
T
Karlsson
J-O
JO
Zetterberg
M
M
D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D001241:Aspirin / Q000494:pharmacology*; D000068579:Celecoxib; D048429:Cell Size; D002478:Cells, Cultured; D004008:Diclofenac / Q000494:pharmacology; D004847:Epithelial Cells / Q000166:cytology / Q000187:drug effects; D016166:Free Radical Scavengers / Q000494:pharmacology; D005978:Glutathione / Q000037:antagonists & inhibitors / Q000378:metabolism; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D007425:Intracellular Membranes / Q000187:drug effects*; D007908:Lens, Crystalline / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism*; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects; D016877:Oxidants / Q000494:pharmacology; D018384:Oxidative Stress; D010545:Peroxides / Q000037:antagonists & inhibitors; D011720:Pyrazoles / Q000494:pharmacology; D017382:Reactive Oxygen Species / Q000378:metabolism; D013449:Sulfonamides / Q000494:pharmacology; D013481:Superoxides / Q000037:antagonists & inhibitors
D000894:Anti-Inflammatory Agents, Non-Steroidal; D016166:Free Radical Scavengers; D016877:Oxidants; D010545:Peroxides; D011720:Pyrazoles; D017382:Reactive Oxygen Species; D013449:Sulfonamides; D013481:Superoxides; D004008:Diclofenac; D006861:Hydrogen Peroxide; D005978:Glutathione; D000068579:Celecoxib; D001241:Aspirin; D007213:Indomethacin