Maternal exposure to nonylphenol during pregnancy and lactation induces microglial cell activation and pro-inflammatory cytokine production in offspring hippocampus

Gu, Weijia; Wang, Yi; Qiu, Zhenmin; Dong, Jing; Wang, Yuan; Chen, Jie

doi:10.1016/j.scitotenv.2018.03.329

Cited by 25 publications

(14 citation statements)

References 53 publications

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“…25,26 The NP exposure rat model used herein was according to the NOAEL, 22,27 environmental concentration ranges in aquatic systems, 25,28 and previous studies that reported a toxic effect on the testis at doses starting from 5 mg/kg of NP. 20,22,[29][30][31][32]…”

Section: -Nonylphenol Bisphenol a Ftir Spectroscopy Leydig Cells Mult...mentioning

confidence: 99%

Multi‐ and transgenerational biochemical effects of low‐dose exposure to bisphenol A and 4‐nonylphenol on testicular interstitial (Leydig) cells

Xia

Guo

et al. 2022

Environmental Toxicology

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Bisphenol A (BPA) and 4-nonylphenol (NP) are well-known endocrine-disrupting chemicals (EDCs) that have been proven to affect Leydig cell (LC) functions and testosterone production, but whether BPA and NP have multi-and transgenerational biochemical effects on Leydig cells (LCs) is unknown. Fourier transform infrared (FTIR) spectroscopy is a powerful analytical technique that enables label-free and non-destructive analysis of the tissue specimen. Herein we employed FTIR coupled with chemometrics analysis to identify biomolecular changes in testicular interstitial (Leydig) cells of rats after chronic exposure to low doses of BPA and NP. Cluster segregations between exposed and control groups were observed based on the fingerprint region of 1800-900 cm À1 in all generations. The main biochemical alterations for segregation were amide I, amide II and nucleic acids. BPA and NP single and coexposure induced significant differences in the ratio of amide I to amide II compared to the corresponding control group in all generations. BPA exposure resulted in remarkable changes of cellular gene transcription and DNA oxidative damage across all generations. Direct exposure to BPA, NP, and BPA&NP of F0 and F1 generations could significantly decrease lipid accumulation in LCs in the F2 and F3 generations.The overall findings revealed that single or co-exposure to BPA and NP at environmental concentrations affects the biochemical structures and properties of LCs.

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Section: -Nonylphenol Bisphenol a Ftir Spectroscopy Leydig Cells Mult...mentioning

confidence: 99%

Multi‐ and transgenerational biochemical effects of low‐dose exposure to bisphenol A and 4‐nonylphenol on testicular interstitial (Leydig) cells

Xia

Guo

et al. 2022

Environmental Toxicology

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“…Activating the Akt / MAPK / AP-1 signaling by NP, can increase the secretion of inflammatory cytokines at the MG level and can initiate the CNS inflammation [ 39 ]. Neuroinflammation, caused by excessive MG activity is one of the most common causes of neurodegenerative diseases such as Alzheimer's, Parkinson's, and Huntington's disease [ 41 , 42 ].…”

Section: Effects Of Np On Different Neural Cellsmentioning

confidence: 99%

“…It seems that JNK has a central role in both pathways mentioned [ 63 ]. Based on the results of various studies, it can be concluded that NP activates the cell's inflammatory signaling, especially in the hippocampus and cortex, and increases the secretion of inflammatory cytokines, including IL-6, IL-1β, and TNF-α [ 41 ] (81). This means that NP can induce apoptosis not only by increasing the activity of inflammatory cytokines, including TNF-α, but also by stimulating JNK signaling.…”

Section: Apoptosis Signalingmentioning

confidence: 99%

The Investigation into Neurotoxicity Mechanisms of Nonylphenol: A Narrative Review

Lotfi

Hasanpour

Moghadamnia

et al. 2021

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Background: Nonylphenol (NP), as a chemical compound that widely used in industry, is the result of the nonylphenol ethoxylate decomposition and it is known as an estrogen-like compound. Numerous studies and researches have shown that it has many destructive functions of various organs such as the brain. This toxicant causes oxidative stress in the cortex and hippocampus cells, which are two essential regions to preserve memory and learning in the brain. Methods: This review examines recent findings to better understand the mechanisms of NP neurotoxicity. We used Scopus, Google Scholar and PubMed databases to find articles with focus on the destructive effects of NP on the oxidative stress pathway and its defense mechanisms. Results: NP has potential human health hazard associated with gestational, peri- and postnatal exposure. NP can disrupt brain homeostasis in different ways, such as activation of inflammatory factors in brain especially in hippocampus and cortex, disruption of the cell cycle, changes in neuron, dendrites and synapses morphology, disruption of extra and intracellular calcium ion balance and also memory and learning disorders

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“…inflammation (Schmatz et al 2010, Ingvorsen et al 2015, Ozias et al 2015, Alfaradhi et al 2016, Dewi et al 2017, Dudele et al 2017, Bansal et al 2018, Gu et al 2018, Zota et al 2018, Desplats et al 2019, Kelley et al 2019a, Song et al 2020) and an altered androgen milieu (Table 2) (Acromite et al 1999, Takeuchi et al 2004, Whyte et al 2007, Morisset et al 2013, Rutkowska & Rachon 2014, Vejrazkova et al 2014, Barrett & Swan 2015, Arnon et al 2016, Maliqueo et al 2017, Sathyanarayana et al 2017 in both humans and animals. These findings implicate androgens and inflammatory processes in the programming of insulin resistance.…”

Section: Journal Of Endocrinologymentioning

confidence: 99%

Developmental programming of insulin resistance: are androgens the culprits?

Puttabyatappa

Sargis

Padmanabhan

2020

Journal of Endocrinology

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Insulin resistance is a common feature of many metabolic disorders. The dramatic rise in the incidence of insulin resistance over the past decade has enhanced focus on its developmental origins. Since various developmental insults ranging from maternal disease, stress, over/undernutrition, and exposure to environmental chemicals can all program the development of insulin resistance, common mechanisms may be involved. This review discusses the possibility that increases in maternal androgens associated with these various insults are key mediators in programming insulin resistance. Additionally, the intermediaries through which androgens misprogram tissue insulin sensitivity, such as changes in inflammatory, oxidative, and lipotoxic states, epigenetic, gut microbiome and insulin, as well as data gaps to be filled are also discussed.

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Maternal exposure to nonylphenol during pregnancy and lactation induces microglial cell activation and pro-inflammatory cytokine production in offspring hippocampus

Cited by 25 publications

References 53 publications

Multi‐ and transgenerational biochemical effects of low‐dose exposure to bisphenol A and 4‐nonylphenol on testicular interstitial (Leydig) cells

Multi‐ and transgenerational biochemical effects of low‐dose exposure to bisphenol A and 4‐nonylphenol on testicular interstitial (Leydig) cells

The Investigation into Neurotoxicity Mechanisms of Nonylphenol: A Narrative Review

Developmental programming of insulin resistance: are androgens the culprits?

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