Protective effect of resveratrol on fluoride induced alteration in protein and nucleic acid metabolism, DNA damage and biogenic amines in rat brain

Pal, Sudipta; Sarkar, Chaitali

doi:10.1016/j.etap.2014.07.009

Cited by 38 publications

(25 citation statements)

References 48 publications

(31 reference statements)

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“…This formation could induce cytosine deamination into uracil, which further lead to DNA damage [25,40]. Meanwhile, Fluoride is an exogenously oxidative inducer, which can trigger the production of free radicals [38]. Similarly, a mass of radicals like HSO 3 -will appear in the process of cellular oxidization of SO 2 .…”

Section: Discussionmentioning

confidence: 99%

“…(2) The main ways of DNA damage are deamination, depurination, depyrimidine and so on. Fluoride may directly bind to DNA chain, owing its powerful affinity for uracil and amide bond through -NH···F -interactions based on its active biochemical oxidant [38,39]. After SO 2 enters the body, via breathing, food or water, it could be converted to HSO 3 -, SO 3 2-and H -quickly in the interstitial fluid.…”

Section: Discussionmentioning

confidence: 99%

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Combination of Fluoride and SO2 Induce DNA Damage and Morphological Alterations in Male Rat Kidney

Gao

Liang

Zhang

et al. 2018

Cell Physiol Biochem

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Background/Aims: We investigated the combined toxic effect of sodium fluoride (NaF) and sulfur dioxide (SO₂) on kidney morphological changes and DNA damage in male Wistar rats. Methods: In this study we selected totally 96 male Wistar rats (12-week-old) then randomly group-housed them into four cages, treated with deionized water, NaF, SO₂ and co-treatment of NaF and SO₂ respectively. Morphological changes of kidney were detected by hematoxylin and eosin (H&E) staining at 2, 4, 6 and 8 weeks. Correspondingly, tailing ratio and comet length were measured by BAB Bs Comet Assay System, including DNA damage special unit were calculated to evaluate the grades of kidney DNA damage at the same time. Results: Treated groups showed a body weight decrease when compared to control group. However, no significant difference in the relative weight of kidney was found in all four groups. It is noteworthy that at 2, 4, 6 and 8 weeks after exposure, the morphological alteration of renal tubules were observed in all treated groups, especially in group-IV. Also, at 4 and 6 weeks, notable DNA damage was found in all treated groups, as assessed by significantly increasing trend of comet length tailing ratio. Conclusion: The study manifests that presence of NaF and SO₂ will not only induce renal tissue lesions but also impact DNA integrity. In addition, this combined exposure exhibits a synergistic effect, characterizing a dose-dependence and time correlation. These findings may provide novel insights regarding perturbations of DNA damage and its functions as a potential new mechanism, by which cautious interpretation of NaF and SO₂ co-exposure evolved in both animals and human beings is necessary.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Combination of Fluoride and SO2 Induce DNA Damage and Morphological Alterations in Male Rat Kidney

Gao

Liang

Zhang

et al. 2018

Cell Physiol Biochem

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“…Some researches showed that vitamins C and E [42], resveratrol [43], arjunolic acid (AA) [44] and epigallocatechin gallate (EGCG) [45] could protect endometrium, brain and hepatocytes against the fluoride-induced damage in rats. Moreover, it could be seen that these antidotes exhibited the role of resisting fluorosis mainly through the mechanism of inhibiting oxidative stress and DNA damage.…”

Section: Nac Pretreatment Reduced Fluoride-induced Oxidative Stress Amentioning

confidence: 99%

Ameliorative effects of N-acetylcysteine on fluoride-induced oxidative stress and DNA damage in male rats’ testis

Feng

Huang

Yang

et al. 2015

Mutation Research/Genetic Toxicology and Environmental Mutagene

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“…Fluoride can induce oxidative damage and apoptosis in neurons, which might be regulated by antiapoptotic genes and death receptor-mediated pathway [11][12][13]. Fluoride affects the brain by inhibiting some enzymes associated with energy production and transfer, membrane transport, and synaptic transmission [14]. Chronic or subchronic fluoride exposure may lead to reduction of acetylcholinesterase activity and nicotinic acetylcholine receptor level, as well as alteration in the neurotransmitter level [15,16].…”

Section: Introductionmentioning

confidence: 99%

Fluoride-Induced Neuron Apoptosis and Expressions of Inflammatory Factors by Activating Microglia in Rat Brain

Yan

Liu

et al. 2015

Mol Neurobiol

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Excessive exposure to fluoride results in structural and functional damages to the central nervous system (CNS), and neurotoxicity of fluoride may be associated with neurodegenerative changes. Chronic microglial activation appears to cause neuronal damage through producing proinflammatory cytokines and is involved in many neurodegenerative disorders. It is not known about effects on microglia of fluoride. In the present study, healthy adult Wistar rats were exposed to 60 and 120 ppm fluoride in drinking water for 10 weeks, and control rats received deionized water. After 10 weeks, rats were sacrificed under anesthesia then apoptosis in neuron and inflammatory factors secreted by microglia were determined. We found that apoptosis of neurons in fluoride-treated rat brain increased and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive immunofluorescence increased with increasing fluoride concentrations. Bax protein expression increased and Bcl-2 protein expression decreased in fluoride-treated rat brain compared with that of the control rat brain. The microglia in the hippocampus and cortex of fluoride-treated rats were activated by immunostaining with OX-42, a marker of activated microglia, and OX-42-positive microglia cells were more abundant in the hippocampus than in the cortex. The levels of IL-1β and IL-6 protein expression in OX-42-labeled microglial cells were significantly increased in the cortex and hippocampus of rats exposed to fluoride, and TNF-α immunoreactivity in microglial cells of the hippocampus was significantly higher in the 120 ppm fluoride-treated group than that in the control group. Our results indicate that fluoride induced neuron apoptosis and expressions of inflammatory factors by activating microglia in rat brain.

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Protective effect of resveratrol on fluoride induced alteration in protein and nucleic acid metabolism, DNA damage and biogenic amines in rat brain

Cited by 38 publications

References 48 publications

Combination of Fluoride and SO2 Induce DNA Damage and Morphological Alterations in Male Rat Kidney

Combination of Fluoride and SO2 Induce DNA Damage and Morphological Alterations in Male Rat Kidney

Ameliorative effects of N-acetylcysteine on fluoride-induced oxidative stress and DNA damage in male rats’ testis

Fluoride-Induced Neuron Apoptosis and Expressions of Inflammatory Factors by Activating Microglia in Rat Brain

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