Fluoride as a pro-inflammatory factor and inhibitor of ATP bioavailability in differentiated human THP1 monocytic cells.
Chronic exposure of humans to fluorine compounds in the air, water and food may be atherogenic via the activation of oxidative stress and increased ROS production. The most important factor that promotes the formation of ROS seems to be the oxidoreduction of electron carriers in the critical points of the respiratory chain, which depends, among other things, on the cellular demand for ATP. This paper examines the effect of fluorides in concentrations determined in human serum on the intracellular synthesis of ROS, the activity of the respiratory chain enzymes and the synthesis of ATP via oxidative and substrate-level phosphorylation. The incubation of macrophages in fluoride solutions significantly decreased the amount of synthesized cellular ATP and increased formation of ROS and apoptosis in a dose-dependent pattern. The addition of respiratory chain inhibitors resulted in a significant decrease in the synthesized ROS. Sodium fluoride probably promotes oxidative stress in macrophages, which is manifested by a strong increase in ROS synthesis and a decrease in ATP. We suppose that fluoride may destabilize the action of respiratory chain. Our results indicate that the respiratory chain is the main site of ROS synthesis. One cannot exclude the stimulating role of fluorine compounds on the formation of ROS that is independent of the respiratory chain.
Gutowska
I
I
Department of Biochemistry and Human Nutrition, Pomeranian Medical University, Zołnierska 48 Str., Szczecin, Poland. gutowska@sci.pam.szczecin.pl <gutowska@sci.pam.szczecin.pl>
Baranowska-Bosiacka
I
I
Baśkiewicz
M
M
Milo
B
B
Siennicka
A
A
Marchlewicz
M
M
Wiszniewska
B
B
Machaliński
B
B
Stachowska
E
E
D000255:Adenosine Triphosphate / Q000378:metabolism*; D017209:Apoptosis / Q000187:drug effects; D001682:Biological Availability; D002454:Cell Differentiation; D002460:Cell Line; D004305:Dose-Response Relationship, Drug; D004579:Electron Transport / Q000187:drug effects; D004734:Energy Metabolism / Q000187:drug effects*; D004785:Environmental Pollutants / Q000633:toxicity*; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D008264:Macrophages / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D010085:Oxidative Phosphorylation / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects; D017382:Reactive Oxygen Species / Q000378:metabolism; D012969:Sodium Fluoride / Q000633:toxicity*
D004785:Environmental Pollutants; D018836:Inflammation Mediators; D017382:Reactive Oxygen Species; D000255:Adenosine Triphosphate; D012969:Sodium Fluoride