Dynamic monitoring of depressive behavior induced by nonylphenol and its effect on synaptic plasticity in rats

Yu, Jian; Xu, Weihong; Luo, Yan; Ou, Wei; Li, Shengnan; Chen, Xu

doi:10.1016/j.scitotenv.2019.06.250

Cited by 28 publications

(4 citation statements)

References 19 publications

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“…[ 11 ] Yu et al showed that cells in the cerebral cortex of rats exposed to NP exhibited an irregular arrangement and cytoplasmic shrinkage. [ 7 ] Tabassum et al found degenerative neurons in the cerebral cortex of animals with potential cognitive impairment with NP exposure. [ 5 ] In our study, dark‐stained neurons were found in the cerebral cortex of rats exposed to NP.…”

Section: Discussionmentioning

confidence: 99%

“…[1,2] In addition, NP impairs neurogenesis, inhibits neuronal growth and differentiation, and causes changes in the morphology of dendrites and synapses. [2,7] NP exposure is known to increase Cas-3 activation, induce chromatin concentration, and DNA fragmentation. [6] The neurotoxicity of NP is due to oxidative stress through the mitochondrial apoptosis pathway and inflammatory signaling pathway, which affect the expression of apoptosis genes and inflammatory mediators.…”

Section: Introductionmentioning

confidence: 99%

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Therapeutic effect of thymoquinone on brain damage caused by nonylphenol exposure in rats

Ceylan

Akın

Karabulut

et al. 2023

J Biochem & Molecular Tox

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Nonylphenol (NP), causes various harmful effects such as cognitive impairment and neurotoxicity. Thymoquinone (TQ), has antioxidant, anti‐inflammatory, and neuroprotective properties. In this study, our aim is to investigate the effects of TQ on the brain damage caused by NP. Corn oil was applied to the control group. NP (100 mg/kg/day) was administered to the NP and NP + TQ groups for 21 days. TQ (5 mg/kg/day) was administered to the NP + TQ and TQ groups for 7 after 21 days. At the end of the experiment, the new object recognition test was applied to the rats and the rats were killed and their brain tissues were removed. Sections taken from brain tissues were stained with hematoxylin–eosin for histopathological evaluation. In addition, neuronal nuclei (NeuN), glial fibrillary acidic protein (GFAP), Cas‐3, and nerve growth factor (NGF) immunoreactivities were evaluated in brain tissue sections. In addition, malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) activities were determined. Comet assay was applied to determine DNA damage in cells. The results of our study showed that NP, caused behavioral disorders and damage to the cerebral cortex in rats. This damage in the form of neuron degeneration seen in the cortex was associated with apoptosis involving Cas‐3 activation, increased DNA damage, and free oxygen radicals. NP, SOD, and CAT caused a decrease in enzyme activities. In addition, the cellular protein NeuN was decreased, astrocytosis‐associated GFAP was increased, and growth factor NGF was decreased. When all our evaluations are taken together, treatment with TQ showed an ameliorative effect on the behavioral impairment and brain damage caused by NP exposure.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Therapeutic effect of thymoquinone on brain damage caused by nonylphenol exposure in rats

Ceylan

Akın

Karabulut

et al. 2023

J Biochem & Molecular Tox

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“…15−18 Numerous studies have illustrated the depressive effect of POPs, such as polychlorinated biphenyls, 19 bisphenol A, 20 and nonylphenol. 21 Nevertheless, there is a scarcity of research investigating the relationship between PFOS and depression, with existing findings presenting inconsistencies. 22,23 Conclusive evidence is required to ascertain whether PFOS can indeed cause depression.…”

Section: Introductionmentioning

confidence: 99%

“…Previous studies have shown that human exposure to PFOS and PFOS-related compounds is associated with various toxic effects, including immunotoxicity, hepatotoxicity, endocrine toxicity, cardiovascular toxicity, and neurotoxicity. − Numerous studies have illustrated the depressive effect of POPs, such as polychlorinated biphenyls, bisphenol A, and nonylphenol . Nevertheless, there is a scarcity of research investigating the relationship between PFOS and depression, with existing findings presenting inconsistencies. , Conclusive evidence is required to ascertain whether PFOS can indeed cause depression.…”

Section: Introductionmentioning

confidence: 99%

Hippocampal Proteomics Reveals the Role of Glutamatergic Synapse Activation in the Depression Induced by Perfluorooctane Sulfonate

Yang

Xiao

et al. 2023

J. Agric. Food Chem.

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Perfluorooctane sulfonate (PFOS), a new type of persistent organic pollutant in the environment of water, has drawn significant attention in recent years due to its widespread prevalence and high toxicity. Neurotoxicity is regarded as one of the major toxic effects of PFOS, while research studies on PFOS-induced depression and the underlying mechanisms remain scarce. In this study, behavioral tests revealed the depressive-like behaviors in PFOS-exposed male mice. Neuron damages including pyknosis and staining deepening were identified through hematoxylin and eosin staining. Then, we noticed the elevation of glutamate and proline levels as well as the decline of glutamine and tryptophan levels. Proteomics analysis identified 105 differentially expressed proteins that change in a dose-dependent manner and revealed that PFOS exposure activated the glutamatergic synapse signaling pathway, which were further confirmed by Western blot, and the data were consistent with the findings of the proteomics analysis. Additionally, the downstream signaling cyclic AMP-responsive element-binding protein (CREB)/brain-derived neurotrophic factor (BDNF) and synaptic plasticity-related postsynaptic density protein 95, synaptophysin, were downregulated. Our results highlight that PFOS exposure may inhibit the synaptic plasticity of the hippocampus via glutamatergic synapse and the CREB/BDNF signaling pathway to cause depressive-like behaviors in male mice.

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The mechanisms of learning and memory impairment caused by nonylphenol: a narrative review based on in vivo and in vitro studies

Rang

Liu

2022

Environ Sci Pollut Res

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Dynamic monitoring of depressive behavior induced by nonylphenol and its effect on synaptic plasticity in rats

Cited by 28 publications

References 19 publications

Therapeutic effect of thymoquinone on brain damage caused by nonylphenol exposure in rats

Therapeutic effect of thymoquinone on brain damage caused by nonylphenol exposure in rats

Hippocampal Proteomics Reveals the Role of Glutamatergic Synapse Activation in the Depression Induced by Perfluorooctane Sulfonate

The mechanisms of learning and memory impairment caused by nonylphenol: a narrative review based on in vivo and in vitro studies

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