Alterations of nAChRs and ERK1/2 in the brains of rats with chronic fluorosis and their connections with the decreased capacity of learning and memory

Liu, Yanjie; Gao, Qin; Wu, Chuncheng; Guan, Zhi‐Zhong

doi:10.1016/j.toxlet.2009.11.002

Cited by 42 publications

(34 citation statements)

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“…Fluoride primarily has a negative effect on bones and teeth called skeletal fluorosis and dental fluorosis. But epidemiologic studies show that it also affects the nervous system (Freni 1994;Liu et al 2010;Wang et al 2007), reproductive system (Freni 1994), cardiovascular system (Song et al 1990), and so on. Fluoride can concentrate in the cardiovascular system resulting in arterial calcifications (Tuncel 1984), arteriosclerosis (Naresh Kumar et al 2010), and myocardial damage (Cicek et al 2005).…”

Section: Introductionmentioning

confidence: 99%

Inflammatory responses induced by fluoride and arsenic at toxic concentration in rabbit aorta

Niu

Sun

et al. 2012

Arch Toxicol

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Epidemiological and experimental studies have demonstrated the atherogenic effects of environmental toxicant arsenic and fluoride. Inflammatory mechanism plays an important role in the pathogenesis of atherosclerosis. The aim of the present study is to determine the effect of chronic exposure to arsenic and fluoride alone or combined on inflammatory response in rabbit aorta. We analyzed the expression of genes involved in leukocyte adhesion [P-selectin (P-sel) and vascular cell adhesion molecule-1(VCAM-1)], recruitment and transendothelial migration of leukocyte [interleukin-8 (IL-8) and monocyte chemotactic protein-1 (MCP-1)] and those involved in pro-inflammatory cytokines [interleukin-6 (IL-6)]. We found that fluoride and arsenic alone or combined increased the expression of VCAM-1, P-sel, MCP-1, IL-8, and IL-6 at the RNA and protein levels. The gene expressions of inflammatory-related molecules were attenuated when co-exposure to the two toxicants compared with just one of them. We also examined the lipid profile of rabbits exposed to fluoride and (or) arsenic. The results showed that fluoride slightly increased the serum lipids but arsenic decreased serum triglyceride. We showed that inflammatory responses but not lipid metabolic disorder may play a crucial role in the mechanism of the cardiovascular toxicity of arsenic and fluoride.

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Section: Introductionmentioning

confidence: 99%

Inflammatory responses induced by fluoride and arsenic at toxic concentration in rabbit aorta

Niu

Sun

et al. 2012

Arch Toxicol

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“…Both the impaired learning and memory of rats with chronic fluorosis (Gao et al, 2009;X. Liu et al, 2010a;Y.J. Liu et al, 2010b), and the reduced intelligence quotient of children living in areas with endemic fluorosis (Rocha-Amador et al, 2007;Saxena et al, 2012;Tang et al, 2008) are particularly noteworthy.…”

Section: Discussionmentioning

confidence: 99%

“…Liu et al, 2010a;Y.J. Liu et al, 2010b;Gao et al, 2008;Guan et al, 1989Guan et al, , 1998Guan et al, , 2000.…”

Section: Discussionmentioning

confidence: 99%

“…Liu et al, 2010a;Y.J. Liu et al, 2010b); the resulting homogenates were centrifuged at 14,000 ×g for 40 min at 4°C; and the protein concentrations of the supernatants thus obtained were determined.…”

Section: Quantitation Of Rage and Nox 2 Proteins By Western Blottingmentioning

confidence: 99%

“…In addition, the reduced capacity for learning and memory due to fluorosis has attracted increasing attention in recent years (X. Liu et al, 2010a;Y.J. Liu et al, 2010b;Rocha-Amador et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Activation of the AGE/RAGE system in the brains of rats and in SH-SY5Y cells exposed to high level of fluoride might connect to oxidative stress

Zhang

Lou

Guan

2015

Neurotoxicology and Teratology

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Emodin protected against synaptic impairment and oxidative stress induced by fluoride in SH‐SY5Y cells by modulating ERK1/2/Nrf2/HO‐1 pathway

Lai

Chen

Ding

et al. 2020

Environmental Toxicology

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Excessive fluoride exposure contributes to neurotoxic effects. Emodin exhibits antioxidative functions in the central nervous system (CNS); however, its neuroprotective mechanism against fluoride remains to be elucidated. Our aim was to explore the neuroprotective efficacy and the possible mechanisms of emodin. In our study, synaptic proteins and oxidative stress damage were examined after human neuroblastoma SH‐SY5Y cells were treated with high doses of NaF for 24 hours. Moreover, pretreatment with emodin was used to shed light on the neuroprotective effects in NaF‐induced toxicity in SH‐SY5Y cells. We found that NaF significantly lowered the protein expressions of SNAP 25, synaptophysin and PSD 95 in SH‐SY5Y cells. In addition, NaF exposure increased the protein expression of p‐ERK1/2 and decreased the protein expressions of Nrf2 and HO‐1, as well as facilitated increasing ROS, 4‐hydroxynonenal (4‐HNE), and 8‐Hydroxy‐2′‐deoxyguanosine (8‐OHdG). Pretreatment with emodin significantly recovered these alterations caused by NaF. These data implied that the neuroprotective effects of emodin and pointed to the promising utilization for protecting against neurotoxicity induced by fluoride.

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Alterations of nAChRs and ERK1/2 in the brains of rats with chronic fluorosis and their connections with the decreased capacity of learning and memory

Cited by 42 publications

References 42 publications

Inflammatory responses induced by fluoride and arsenic at toxic concentration in rabbit aorta

Inflammatory responses induced by fluoride and arsenic at toxic concentration in rabbit aorta

Activation of the AGE/RAGE system in the brains of rats and in SH-SY5Y cells exposed to high level of fluoride might connect to oxidative stress

Emodin protected against synaptic impairment and oxidative stress induced by fluoride in SH‐SY5Y cells by modulating ERK1/2/Nrf2/HO‐1 pathway

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