Effect of arsenic and/or fluoride gestational exposure on renal autophagy in offspring mice

Guo, Qiang; Sun, Zilong; Niu, Ruiyan; Manthari, Ram Kumar; Yuan, Mengke; Yang, Kaidong; Cheng, Min; Gong, Zeen; Wang, Jundong

doi:10.1016/j.chemosphere.2019.124861

Cited by 20 publications

(7 citation statements)

References 31 publications

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“…In our study, the expression of Beclin-1 was increased in uoride group, which was in agree with other report by Guo et al who reported that 100 mg/L NaF increased the autophagy-related proteins in mice [12]. In particular, we observed that nano-Se could regulate the expression of Cyt-C and Beclin-1/Bcl-2 signaling pathway to target apoptosis and autophagy and mediate the liver damage affected by uorosis.…”

Section: Discussionsupporting

confidence: 93%

Ameliorative Effects of Nano-Selenium Against Fluoride Stress Induced Hepatocytes Autophagy and Apoptosis in Mice

Wang

Liu

Han

et al. 2020

Preprint

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Background: Fluorine is widespread in the environment, and the injurious impacts of fluoride underscore its significance for public health. The long-term presence of fluorine in environment could be a risk in hepatotoxicity for both human beings and animals. Important role of selenium in mitigation of heavy metal toxicity via regulating autophagy and apoptosis is well-known. Further, nano-Se is a common artificial nano material, with higher biological activity and lower toxicity. The aim of the current study was to examine whether nano-Se supplementation can reduce the effects of fluoride-induced hepatocytes autophagy and apoptosis. Results: Here, we report that fluoride exposure induces apoptosis and autophagy with nucleus broken, dissolved and disappeared of hepatocyte, contributing to its hepatotoxicity. More importantly, Cyt-C and Beclin-1/Bcl-2 pathways are involved in the regulation of autophagy and apoptosis via targeting Caspase-9, Caspase-3, P53, Bax, LC3, ATG-5, P62 and mTOR expressions. Conclusion: Nano-Se is capable to alleviate fluoride-induced hepatocyte damage, that selenium can be prefer to prevent chronic fluorosis-induced autophagy and apoptosis by regulating Cyt-C and Beclin-1/Bcl-2 signaling pathway. In precisely, NaF-induced the liver injury by activating autophagy and apoptosis, which indicate that fluorine exposure, pose an ecological risk to human beings and animals. Nano-Se has protective effects against fluoride-induced hepatocytes.

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Section: Discussionsupporting

confidence: 93%

Ameliorative Effects of Nano-Selenium Against Fluoride Stress Induced Hepatocytes Autophagy and Apoptosis in Mice

Wang

Liu

Han

et al. 2020

Preprint

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“…The kidney is a key target organ for the toxicity and accumulation of arsenic; therefore, arsenic is a nephrotoxic toxicant. Meanwhile, many studies have demonstrated that arsenic exposure could lead to renal injury by inducing oxidative stress, inflammation, apoptosis, and autophagy. − However, the influence of arsenic in the kidney and its underlying nephrotoxicity mechanisms remain largely undetermined. In this study, we investigate the underlying mechanisms of SIRT1-/PINK1-mediated mitophagy in NaAsO 2 -induced AKI in mice and in HK-2 cells.…”

Section: Discussionmentioning

confidence: 99%

Arsenic Exposure-Induced Acute Kidney Injury by Regulating SIRT1/PINK1/Mitophagy Axis in Mice and in HK-2 Cells

Liu,

et al. 2023

J. Agric. Food Chem.

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Groundwater resources are often contaminated by arsenic, which poses a serious threat to human and animal's health. Some studies have demonstrated that acute arsenic exposure could induce kidney injury because the kidney is a key target organ for toxicity, but the exact mechanism remains unclear. Hence, we investigated the effect of SIRT1-/PINK1-mediated mitophagy on NaAsO 2 -induced kidney injury in vivo and in vitro. In our study, NaAsO 2 exposure obviously induced renal tubule injury and mitochondrial dysfunction. Meanwhile, NaAsO 2 exposure could inhibit the mRNA/protein level of SIRT1 and activate the mitophagy-related mRNA/protein levels in the kidney of mice. In HK-2 cells, we also confirmed that NaAsO 2 -induced nephrotoxicity depended on the activation of mitophagy. Moreover, the activation of SIRT1 by resveratrol alleviated NaAsO 2induced acute kidney injury via the activation of mitophagy in vivo and in vitro. Interestingly, the inhibition of mitophagy by cyclosporin A (CsA) further exacerbated NaAsO 2 -induced nephrotoxicity and inflammation in HK-2 cells. Taken together, our study found that SIRT1-regulated PINK1-/Parkin-dependent mitophagy was implicated in NaAsO 2 -induced acute kidney injury. In addition, we confirmed that PINK1-/Parkin-dependent mitophagy played a protective role against NaAsO 2 -induced acute kidney injury. Therefore, activation of SIRT1 and mitophagy may represent a novel therapeutic target for the prevention and treatment of NaAsO 2 -induced acute renal injury.

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“…In rat kidney epithelial cells (NRK-52E) treated with high concentrations of NaF, in the first 12 h of exposure only, autophagy was induced, and after 24 h, the markers associated with apoptosis or necrosis were increased too [ 188 ]. In a study conducted on the offspring of rats whose mothers were administered fluorine and/or arsenic, a significant increase was observed in renal tissue in the expression of a number of genes closely related to autophagy, i.e., LC3, LC3I, LC3II, Beclin-1, ULK1, Atg13, and Atg14, with a concomitant decrease in mTOR and Bcl-2 levels [ 189 ]. A similar study undertaken by another team confirmed increases in the number of autophagosomes and in the expression of autophagy markers in kidney tissue of the offspring of dams (mother rat) exposed to fluorine compounds [ 190 ].…”

Section: Autophagy—its Role In the Pathogenesis Of Cancermentioning

confidence: 99%

Fluoride in the Central Nervous System and Its Potential Influence on the Development and Invasiveness of Brain Tumours—A Research Hypothesis

Żwierełło

Maruszewska

Skórka-Majewicz

et al. 2023

IJMS

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The purpose of this review is to attempt to outline the potential role of fluoride in the pathogenesis of brain tumours, including glioblastoma (GBM). In this paper, we show for the first time that fluoride can potentially affect the generally accepted signalling pathways implicated in the formation and clinical course of GBM. Fluorine compounds easily cross the blood–brain barrier. Enhanced oxidative stress, disruption of multiple cellular pathways, and microglial activation are just a few examples of recent reports on the role of fluoride in the central nervous system (CNS). We sought to present the key mechanisms underlying the development and invasiveness of GBM, as well as evidence on the current state of knowledge about the pleiotropic, direct, or indirect involvement of fluoride in the regulation of these mechanisms in various tissues, including neural and tumour tissue. The effects of fluoride on the human body are still a matter of controversy. However, given the growing incidence of brain tumours, especially in children, and numerous reports on the effects of fluoride on the CNS, it is worth taking a closer look at these mechanisms in the context of brain tumours, including gliomas.

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Effect of arsenic and/or fluoride gestational exposure on renal autophagy in offspring mice

Cited by 20 publications

References 31 publications

Ameliorative Effects of Nano-Selenium Against Fluoride Stress Induced Hepatocytes Autophagy and Apoptosis in Mice

Ameliorative Effects of Nano-Selenium Against Fluoride Stress Induced Hepatocytes Autophagy and Apoptosis in Mice

Arsenic Exposure-Induced Acute Kidney Injury by Regulating SIRT1/PINK1/Mitophagy Axis in Mice and in HK-2 Cells

Fluoride in the Central Nervous System and Its Potential Influence on the Development and Invasiveness of Brain Tumours—A Research Hypothesis

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