Co-exposure to arsenic and fluoride on oxidative stress, glutathione linked enzymes, biogenic amines and DNA damage in mouse brain

Flora, Sjs; Mittal, Megha; Mishra, Deepshikha

doi:10.1016/j.jns.2009.07.001

Cited by 110 publications

(61 citation statements)

References 40 publications

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“…In the present study, neurotransmitters such as AchE (acetylecholinesterase), norepinephrin (NP), dopamine (DA), and 5-hydroxytriptamin (5-HT) were significantly decreased in fluoride-intoxicated rats. Our findings is well corroborated with the previous reports of Flora, Mittal, and Mishra (2009) in Fl-intoxicated rats. This may be due to the over production of free radicals mediated lipid peroxidation in brain which will affect the synthesis of neurotransmitters.…”

Section: Discussionsupporting

confidence: 93%

“…This may be due to the over production of free radicals mediated lipid peroxidation in brain which will affect the synthesis of neurotransmitters. Moreover, the decreased levels of NE and DP due to the decreased activity of enzymes involved in their synthesis like tyrosine hydroxylase, DOPA decarboxylase and dopamine β-hydroxylase or to the enhanced release of catechol-O-methyl transferase caused by increased ROS-mediated lipidperoxidation and nitric oxide activity by Fl (Flora et al, 2009). Similarly, a significant decreased activity of AChE in Fl-exposed animals was reported by Long et al (2002) in rats.…”

Section: Discussionmentioning

confidence: 81%

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A mechanism underlying the neurotoxicity induced by sodium fluoride and its reversal by epigallocatechin gallate in the rat hippocampus: involvement of NrF2/Keap-1 signaling pathway

Thangapandiyan

Abdulla

Yakulasamy

et al. 2018

JoBAZ

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Background: Fluoride (Fl) exposure engenders neurodegeneration and induces oxidative stress in the brain. Therefore, the mechanism of Fl-induced neurotoxic effects needs to be determined. The aim of this study was to investigate the neuroprotective effects of EGCG (40 mg/kg) on Fl (25 mg/kg/bw)-induced oxidative stress mediated neurotoxicity with special emphasis on the hippocampus (4 weeks).Results: Fl-intoxicated rat shows an increased Fl concentration along with the decreased neurotransmitter (AChE, NP, DA and 5-HT) activity in the brain. The oxidative stress markers (ROS, TBARS, NO, and PC) was significantly increased with decreased enzymatic (SOD, CAT, GPx, GR, GST, and G6PD) and nonenzymatic antioxidants (GSH, TSH, and Vit.C) in the rat hippocampus. Moreover, results showed that increases in intrinsic and extrinsic apoptotic pathway leading to DNA damage and cell death were also proved by the immunohistochemical, histological, and ultra-structural studies in the Fl-treated rat hippocampus. In this context, pre-administration of EGCG significantly improved the oxidative stress, biochemical changes, cellular apoptotic and histological alternations by Fl in the hippocampus of rats. Conclusions: These results confirmed the EGCG supplementation might attenuate the Fl-induced neurotoxicity via Nrf2/Keap1 signaling pathway in the rat hippocampus.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 81%

A mechanism underlying the neurotoxicity induced by sodium fluoride and its reversal by epigallocatechin gallate in the rat hippocampus: involvement of NrF2/Keap-1 signaling pathway

Thangapandiyan

Abdulla

Yakulasamy

et al. 2018

JoBAZ

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“…We also found GS activity of brain increased with pup's age. In contrast to the recently reported that a notable decrease in AChE level was observed in Astreated rat brain [48], the activity of AChE increased linearly with As dose in pup's hippocampus in our studies, and mean activity of AChE was significantly higher in 100 mg/L As-exposed pup's hippocampus than in the control group on PND 28 and 42.…”

Section: Effect Of Arsenic On Activities Of Gs and Ache In Pups' Braincontrasting

confidence: 99%

Prenatal and early life arsenic exposure induced oxidative damage and altered activities and mRNA expressions of neurotransmitter metabolic enzymes in offspring rat brain

Shi

Guo

et al. 2010

J Biochem & Molecular Tox

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To better understand the effect of arsenic on central nervous system by prenatal and early life exposure, the oxidative stress and neurotransmitter metabolic enzymes were determined in offspring rats' brain cortex and hippocampus. Forty-eight pregnant rats were randomly divided into four groups, each group was given free access to drinking water that contained 0, 10, 50, and 100 mg/L NaAsO(2) from gestation day 6 (GD 6) until postnatal day 42 (PND 42). Once pups were weaned, they started to drink the same arsenic (As)-containing water as the dams. The level of malondialdehyde in 100 mg/L As-exposed pup's brain on PND 0 and cortex on PND 28 and 42 were significantly higher than in the control group (p < 0.05). Reduced glutathione (GSH) levels showed a clear decreasing trend in pup's cortex and hippocampus on PND 42. Activity of acetylcholinesterase was significantly higher in 100 mg/L As-exposed pup's hippocampus than in control group on PND 28 and 42. mRNA expression of glutamate decarboxylase (GAD(65) and GAD(67)) in 100 mg/L As-exposed pup's cortex or hippocampus on PND 28 and 42 were significantly higher than in control (p < 0.05). These alterations in the neurotransmitters and reduced antioxidant defence may lead to neurobehavioral and learning and memory changes in offspring rats.

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“…(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%

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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Co-exposure to arsenic and fluoride on oxidative stress, glutathione linked enzymes, biogenic amines and DNA damage in mouse brain

Cited by 110 publications

References 40 publications

A mechanism underlying the neurotoxicity induced by sodium fluoride and its reversal by epigallocatechin gallate in the rat hippocampus: involvement of NrF2/Keap-1 signaling pathway

A mechanism underlying the neurotoxicity induced by sodium fluoride and its reversal by epigallocatechin gallate in the rat hippocampus: involvement of NrF2/Keap-1 signaling pathway

Prenatal and early life arsenic exposure induced oxidative damage and altered activities and mRNA expressions of neurotransmitter metabolic enzymes in offspring rat brain

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

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