ITRAQ-based proteomics reveals the potential mechanism of fluoride-induced myocardial contraction function damage

Xie, Jiaxin; Yan, Xiu-Tian; Xu, Guoqiang; Tian, Xiaolin; Dong, Nisha; Feng, Jing; Liu, Penghui; Li, Meng; Zhao, Yannan; Wei, Cailing; Lyu, Yi; Ma, Guijin; Song, Guohua; Wang, Tong; Yan, Xiaoyan

doi:10.1016/j.ecoenv.2020.110605

Cited by 19 publications

(4 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[51][52][53] In recent years, increased correlation has been confirmed between chronic fluoride exposure and human diseases (e.g., bone weakness, osteoarthritis, and myocardial damage). 2,54,55 Therefore, it is essential to determine the key intracellular signaling in fluorideinduced toxicity. For example, fluoride suppresses the development of spleen via MAPK/ERK signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Fluoride exposure confers NRF2 activation in hepatocyte through both canonical and non‐canonical signaling pathways

Li,

Wang,

Liu

et al. 2023

Environmental Toxicology

View full text Add to dashboard Cite

Due to the high abundance in the Earth's crust and industrial application, fluoride is widely present in our living environment. However, excessive fluoride exposure causes toxicity in different organs. As the most important detoxification and excretion organ, liver is more easily involved in fluoride toxicity than other organs, and oxidative stress is considered as the key mechanism related with fluoride hepatotoxicity. In this study, we mainly investigated the role of nuclear factor erythroid‐derived 2‐like 2 (NRF2, a core transcription factor in oxidative stress) in fluoride exposure‐induced hepatotoxicity as well as the related mechanism. Herein, liver cells (BNL CL.2) were treated with fluoride in different concentrations. The hepatotoxicity and NRF2 signaling pathway were analyzed respectively. Our results indicated that excessive fluoride (over 1 mM) resulted in obvious toxicity in hepatocyte and activated NRF2 and NRF2 target genes. The increased ROS generation after fluoride exposure suppressed KEAP1‐induced NRF2 ubiquitylation and degradation. Meanwhile, fluoride exposure also led to blockage of autophagic flux and upregulation of p62, which contributed to activation of NRF2 via competitive binding with KEAP1. Both pharmaceutical activation and genetic activation of NRF2 accelerated fluoride exposure‐induced hepatotoxicity. Thus, the upregulation of NRF2 in hepatocyte after fluoride exposure can be regarded as a cellular self‐defense, and NRF2‐KEAP1 system could be a novel molecular target against fluoride exposure‐induced hepatotoxicity.

show abstract

Section: Discussionmentioning

confidence: 99%

Fluoride exposure confers NRF2 activation in hepatocyte through both canonical and non‐canonical signaling pathways

Li,

Wang,

Liu

et al. 2023

Environmental Toxicology

View full text Add to dashboard Cite

show abstract

“…Excess fluoride in drinking water is known to cause fluoride poisoning. In addition, fluoride was added to the drinking water of the rats in order not to create any other stress in addition to the oral gavage stress in the rats (Xie et al 2020 ).The animal experiment phase of the study continued for 8 weeks.…”

Section: Methodsmentioning

confidence: 99%

“…Symptomatic fluorosis causes more damage to hard tissues such as teeth and skeletal structures. However, fluoride also damages other organs (heart, brain, liver, kidney) (Orta 2012 ; Wang et al 2018 ; Xie et al 2020 ). Fluoride toxicity creates widespread damage on various tissues through oxidative stress and apoptosis (Liu et al 2019 ).…”

Section: Introductionmentioning

confidence: 99%

The inducing of caspase and Bcl-2 pathway with royal jelly decreases the muscle tissue damage exposed with fluoride in rats

Aslan

Can

Gök

et al. 2021

Environ Sci Pollut Res

View full text Add to dashboard Cite

Graphical abstract In this study, 42 Wistar albino male rats ( n = 42, 8 weeks old) were used. Rats were divided into 6 groups and 7 rats included each group. Groups: (i) Control group: Standard diet; (ii) RJ (royal jelly) group: Standard diet + royal jelly; (iii) F50 group: Standard diet + 50 mg/kg fluoride; (iv): F100 group: Standard diet + 100 mg/kg fluoride; (v) F50+RJ group: Standard diet + 50 mg/kg fluoride + royal jelly; (vi): F100+RJ group: Standard diet + 100 mg/kg fluoride + royal jelly. After 8 weeks, the rats were decapitated, and their muscle tissues were removed. Expression levels of Caspase-3, Caspase-6, Bax, tumor necrosis factor-α (TNF-α), interleukin 1 alpha (IL1-α) and Bcl-2 proteins in muscle tissue were determined by western blotting method. Histopathological analyses were also performed on the muscle tissue. Malondialdehyde (MDA), glutathione (GSH) and catalase (CAT) analyses were determined by a spectrophotometer. According to the obtained results, Bcl-2, TNF-α and IL1-α protein expression was increased in damage groups compared to the control and royal jelly groups, while Caspase-3, Caspase-6 and Bax protein expression levels decreased in damage groups. MDA level increased in damage groups compared to the control and royal jelly groups, while CAT and GSH levels increased with royal jelly application in royal jelly-given group in comparison to the flouride-exposed group. According to histopathological analysis results, edema and inflammatory cell formations were found in the injury groups, a tendency to decrease in these injuries was observed in the treatment groups. Based on these results, we can say that royal jelly has protective effects on muscle tissue against fluoride damage.

show abstract

“…Symptomatic uorosis causes more damage to hard tissues such as teeth and skeletal structures. However, uoride also damages other organs (heart, brain, liver, kidney) (Orta 2012;Wang et al 2018;Xie et al 2020). Fluoride toxicity creates widespread damage on various tissues through oxidative stress and apoptosis (Liu et al 2019).…”

Section: Introductionmentioning

confidence: 99%

The inducing of caspase and bcl-2 pathway with royal jelly decreases the muscle tissue damage exposed with fluoride in rats

Aslan

Can

Gök

et al. 2021

Preprint

View full text Add to dashboard Cite

In this study, 42 Wistar albino female rats (n = 42, 8 weeks old) were used. Rats were divided into 6 groups and 7 rats included each group. Groups: (i) Control Group: Standard diet; (ii) RJ (royal jelly) Group: Standard diet + royal jelly; (iii) F50 Group: Standard diet + 50 mg/kg fluoride; (iv): F100 Group: Standard diet + 100 mg/kg fluoride; (v) F50 + RJ Group: Standard diet + 50 mg/kg fluoride + royal jelly; (iv): F100 + RJ Group: Standard diet + 100 mg/kg fluoride + royal jelly. After the 8-week study period, the rats were decapitated and their muscle tissues were removed. Expression levels of Caspase-3, Caspase-6, Bax, Tnf-α, IL1-α and Bcl-2 proteins in muscle tissue were determined by Western Blotting method. Histopathological analyzes were also performed on the muscle tissue. MDA, GSH, and CAT analyzes were determined by spectrophotometric analysis. According to our findings, Bcl-2, Tnf-α and IL1-α protein expression were increased in damage groups compared to control and royal jelly groups, Caspase-3, Caspase-6 and Bax protein expression levels decreased in damage groups. There was an increase in MDA level in damage groups compared to the control and royal jelly groups, CAT and GSH levels decreased in damage groups. According to histopathological analysis results, edema and inflammatory cell formations were found in the injury groups, a tendency to decrease in these injuries was observed in the treatment groups. Based on these results, we can say that royal jelly has protective effects against fluoride damage.

show abstract

ITRAQ-based proteomics reveals the potential mechanism of fluoride-induced myocardial contraction function damage

Cited by 19 publications

References 34 publications

Fluoride exposure confers NRF2 activation in hepatocyte through both canonical and non‐canonical signaling pathways

Fluoride exposure confers NRF2 activation in hepatocyte through both canonical and non‐canonical signaling pathways

The inducing of caspase and Bcl-2 pathway with royal jelly decreases the muscle tissue damage exposed with fluoride in rats

The inducing of caspase and bcl-2 pathway with royal jelly decreases the muscle tissue damage exposed with fluoride in rats

Contact Info

Product

Resources

About