Effects of chronic fluoride intake on the antioxidant systems of the liver and kidney in rats

Iano, Flávia Godoy; Ferreira, Maria Cecília de Freitas; Quaggio, Giovana Brino; Fernandes, Marcelo Adorna; Oliveira, Rodrigo Cardoso de; Ximenes, Valdecir Farias; Buzalaf, Marília Afonso Rabelo

doi:10.1016/j.jfluchem.2014.09.029

Cited by 37 publications

(27 citation statements)

References 33 publications

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“…Vitamin C has been shown to scavenge aqueous superoxide and hydroxyl radical and acts a chain‐breaking antioxidant in lipid peroxidation . In agreement with previous report , our study reveals that fluoride intoxication impairs the hepatic antioxidant machinery due to its pro‐oxidant including Nox4 and also inhibitory mechanism. Therefore, there was an imbalance between ROS production and antioxidant defense mechanism leading to oxidative damage in the fluoride treated liver tissue.…”

Section: Discussionsupporting

confidence: 92%

“…Antioxidant enzymes are the primary defense system that protects the hepatocytes from the free radicals mediated oxidative insults and maintains cellular redox homeostasis. SOD and CAT are the first line defense enzymes against superoxide and hydroxyl radical produced during fluoride toxicity . GSH is sulfhydryl tripeptide that protects the cell membrane from the peroxides and free radicals attacks caused by fluoride intoxication .…”

Section: Discussionmentioning

confidence: 99%

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Caffeic acid, a phyto polyphenol mitigates fluoride induced hepatotoxicity in rats: A possible mechanism

et al. 2015

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Fluoride induced hepatotoxicity has been extensively studied in both humans and animals. However, the mechanism underlying in the hepatotoxicity of experimental fluorosis remains obscure. The severity of fluoride toxicity was reduced by oral administration of certain plant derived antioxidants. Caffeic acid (CA) a polyphenolic compound has diverse range of pharmacological activity in the biological system. Therefore, the present study was aimed to investigate the protective mechanism of CA, against fluoride induced hepatotoxicity in rats. The rats were treated with 300 ppm of NaF via drinking water ad libitum alone and in combination with CA at a dose of 50 mg/kg daily for 30 days by oral intubation. CA treatment significantly prevented fluoride induced hepatic damage as evident from the histopathological studies and declined levels of serum fluoride and liver marker enzymes. A significant decrease in the levels of enzymatic (SOD2, CAT, GPx, and GSTpi class) and nonenzymatic (GSH and Vitamin C) antioxidants along with increased ROS, lipid peroxidation, protein carbonyl content, and nitrate levels by fluoride were also prevented in these groups. In addition, CA inhibits fluoride induced apoptosis by altering the Bax and caspase-3p20 expressions. Further, fluoride induced upregulation of Nox4, p38α MAPK, Hsp60, and downregulation of Hsp27 are the indicators for the detection of oxidative damage, apoptosis, and mitochondrial stress was also modulated by CA. These findings reveal that CA supplementation has a protective effect against fluoride induced hepatotoxicity in rats.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Caffeic acid, a phyto polyphenol mitigates fluoride induced hepatotoxicity in rats: A possible mechanism

et al. 2015

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“…After this step, the samples were transferred to microtubes and centrifuged at 3,500 rpm for 10 min. Supernatants were collected and the absorbances (abs) were measured in microplates on a spectrophotometer (Molecular Devices, Spectra Max M2, Sunnyvale, United States) at 535 nm (Iano et al, ).…”

Section: Methodsmentioning

confidence: 99%

Influence of iron on modulation of the antioxidant system in rat brains exposed to lead

et al. 2016

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The objective of this study was to evaluate markers of oxidative stress in the brains of rats exposed to lead acetate (Pb(C H O ) ), either associated or not associated with ferrous sulfate (FeSO ). A total of 36 weaning rats (Rattus norvegicus) were divided into 6 groups of six animals and exposed to lead acetate for six weeks. In the control group (control), the animals received deionized water. The Pb260 and Pb260 + Fe received 260 µM lead acetate, and the Pb1050 and Pb1050 + Fe received 1050 µM lead acetate. The Pb260 + Fe and Pb1050 + Fe were supplemented with 20 mg of ferrous sulfate/Kg body weight every 2 days. Group Fe received deionized water and ferrous sulfate. The rat brains were collected to analyze the enzymatic activity of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and the concentration of reduced glutathione (GSH), lipid peroxidation (TBARS), and total antioxidant substance (TAS) (DPPH technique). The activity of SOD and GPx in the experimental groups decreased compared to the control, together with the concentration of GSH (p < 0.05). For CAT analysis, SOD tended to increase in concentration in the experimental groups without a concomitant exposure to FeSO , whereas GPx showed a slight tendency to increase in activity compared to the control. For TAS-DPPH , there was a decrease in the experimental groups (p < 0.05). According to the results, SOD, GPx, and GSH were affected by lead acetate and exposure to ferrous sulfate changed this dynamic. However, further studies are needed to verify whether ferrous sulfate acts as a protectant against the toxic effects of lead. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 813-822, 2017.

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“…Once fluoride is incorporated into the bone, especially in the crystal structures or the bone matrix, it can be slowly removed with a half-life of 120 weeks for adults and 70 weeks for children [ 16 ]. Previous studies with rats chronically exposed to fluoride demonstrate the impairment in essential organs on metabolism and excretion processes, as liver and kidney, by oxidative stress, which is a critical cell damage [ 13 , 17 ].…”

Section: Introductionmentioning

confidence: 99%

Chronic Exposure to Sodium Fluoride Triggers Oxidative Biochemistry Misbalance in Mice: Effects on Peripheral Blood Circulation

Miranda

Gomes

Bittencourt

et al. 2018

Oxidative Medicine and Cellular Longevity

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The excessive fluoride (F) exposure is associated with damage to cellular processes of different tissue types, due to changes in enzymatic metabolism and breakdown of redox balance. However, few studies evaluate doses of F compatible with human consumption. Thus, this study evaluated the effects of chronic exposure to sodium fluoride (NaF) on peripheral blood of mice from the evaluation of biochemical parameters. The animals were divided into three groups (n = 10) and received three concentrations of NaF in the drinking water for 60 days: 0 mg/L F, 10 mg/L F, and 50 mg/L F. The blood was then collected for trolox equivalent antioxidant capacity (TEAC), thiobarbituric acid reactive substances (TBARS), concentrations of nitric oxide (NO), superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH). The results showed that doses of 10 mg/L F and 50 mg/L F were able to increase TBARS concentration and decrease NO levels and CAT activity in the blood, but there was no statistical difference for SOD levels. The 50 mg/L F group showed an increase in TEAC levels and a decrease in the GSH content when compared to the control group. In this way, oxidative changes in blood from chronic exposure to F, especially at the highest dose, indicate that F may be a toxic agent and, therefore, the long-term exposure to excessive doses should be avoided.

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Effects of chronic fluoride intake on the antioxidant systems of the liver and kidney in rats

Cited by 37 publications

References 33 publications

Caffeic acid, a phyto polyphenol mitigates fluoride induced hepatotoxicity in rats: A possible mechanism

Caffeic acid, a phyto polyphenol mitigates fluoride induced hepatotoxicity in rats: A possible mechanism

Influence of iron on modulation of the antioxidant system in rat brains exposed to lead

Chronic Exposure to Sodium Fluoride Triggers Oxidative Biochemistry Misbalance in Mice: Effects on Peripheral Blood Circulation

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