Fluoride Increases Superoxide Production and Impairs the Respiratory Chain in ROS 17/2.8 Osteoblastic Cells

Abstract

It is known that fluoride produces oxidative stress. Inflammation in bone tissue and an impairment of the respiratory chain of liver have been described in treatments with fluoride. Whether the impairment of the respiratory chain and oxidative stress are related is not known. The aim of this work was to study the effects of fluoride on the production of superoxide radical, the function of the respiratory chain and the increase in oxidative stress in ROS 17/2.8 osteoblastic cells. We measured the effect of fluoride (100 µM) on superoxide production, oxygen consumption, lipid peroxidation and antioxidant enzymes activities of cultured cells following the treatment with fluoride. Fluoride decreased oxygen consumption and increased superoxide production immediately after its addition. Furthermore, chronic treatment with fluoride increased oxidative stress status in osteoblastic cells. These results indicate that fluoride could damage bone tissue by inhibiting the respiratory chain, increasing the production of superoxide radicals and thus of the others reactive oxygen species.

The trypanocidal benznidazole promotes adaptive response to oxidative injury: Involvement of the nuclear factor-erythroid 2-related factor-2 (Nrf2) and multidrug resistance associated protein 2 (MRP2)

“…CAT activity was quantified in cell lysates as described by Fina et al (2014). The method is based on the consumption of hydrogen peroxide in a reaction medium of PBS-EDTA (6.30 mM) pH 7.00 and hydrogen peroxide 0.02 M as substrate.…”

“…GPx was quantified in cell lysates as described by Fina et al (2014) following the GRx catalyzed consumption of NADPH coupled to the GPx catalyzed reaction of H 2 O 2 with GSH. Reactions were performed in a buffer consisting of KH 2 PO 4 /K 2 HPO 4 (50 mM), EDTA (1 mM) pH 7.40 supplemented with 1 mM NaN 3 , 200 μM NADPH, 1 mM GSH and 1 U/ml glutathione reductase.…”

Single oral acute fluoride exposure causes changes in cardiac expression of oxidant and antioxidant enzymes, apoptotic and necrotic markers in male rats

“…F -, being highly basic, easily crosses the cell membrane by simple diffusion and inhibit respiratory chain by increasing the superoxide radical (O 2 -), hydrogen peroxide, and hydroxyl radical, peroxynitrite formation and disturb the redox homeostasis in both in vivo [5] and in vitro [6] models. Increased generation of reactive oxygen species (ROS) plays a key role in the oxidation of lipids, proteins and DNA in the myocardium and leads to the alteration in the normal cardiac contractile function.…”

The intracellular mediation during chronic fluoride intoxication in rats

“…The detected phenomenon was very common and was confirmed for many cells 29 . The inclusion of Ca 2+ -dependent potassium conductivity can also be one of the mechanisms of the cell's adaptation process to long-term external stress 30,31 .…”