Inflammation-like glial response in rat brain induced by prenatal PFOS exposure

Zeng, Huai-cai; Zhang, Ling; Li, Yuanyuan; Wang, Yan‐Jian; Xia, Wei; Lin, Yi; Jie, Wei; Xu, Shunqing

doi:10.1016/j.neuro.2010.10.001

Cited by 58 publications

(36 citation statements)

References 48 publications

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“…The contributions of microglia and subsequent inflammation to the neurotoxicity after PFOS exposure have been hardly investigated by researchers. Some investigators have reported PFOS-induced inflammation in rodents (H. C. Zeng et al, 2011;G. H. Dong et al, 2012), whereas other investigators have found the immunosuppressive effects of PFOS in rodents (D. E. Keil et al, 2008;L.…”

Section: Discussionmentioning

confidence: 99%

Reactive oxygen species mediate nitric oxide production through ERK/JNK MAPK signaling in HAPI microglia after PFOS exposure

Wang

Nie

Zhang

et al. 2015

Toxicology and Applied Pharmacology

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Section: Discussionmentioning

confidence: 99%

Reactive oxygen species mediate nitric oxide production through ERK/JNK MAPK signaling in HAPI microglia after PFOS exposure

Wang

Nie

Zhang

et al. 2015

Toxicology and Applied Pharmacology

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“…It also induces brain oxidative stress by dysregulating cyclin-dependant kinase 5 and peroxiredoxin, and causes an inflammatory glial response 57. It impairs calcium signalling,58 and interferes with gene transcription related to neuroactive ligand-receptor interaction, the cell cycle, cell communication, long-term potentiation and depression, and peroxisome proliferator-activated receptor (PPAR) signalling 59.…”

Section: Discussionmentioning

confidence: 99%

Pop, heavy metal and the blues: secondary analysis of persistent organic pollutants (POP), heavy metals and depressive symptoms in the NHANES National Epidemiological Survey

et al. 2014

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ObjectivesPersistent environmental pollutants, including heavy metals and persistent organic pollutants (POPs), have a ubiquitous presence. Many of these pollutants affect neurobiological processes, either accidentally or by design. The aim of this study was to explore the associations between assayed measures of POPs and heavy metals and depressive symptoms. We hypothesised that higher levels of pollutants and metals would be associated with depressive symptoms.SettingNational Health and Nutrition Examination Survey (NHANES).ParticipantsA total of 15 140 eligible people were included across the three examined waves of NHANES.Primary and secondary outcome measuresDepressive symptoms were assessed using the nine-item version of the Patient Health Questionnaire (PHQ-9), using a cut-off point of 9/10 as likely depression cases. Organic pollutants and heavy metals, including cadmium, lead and mercury, as well as polyfluorinated compounds (PFCs), pesticides, phenols and phthalates, were measured in blood or urine.ResultsHigher cadmium was positively associated with depression (adjusted Prevalence Ratios (PR)=1.48, 95% CI 1.16 to 1.90). Higher levels of mercury were negatively associated with depression (adjusted PR=0.62, 95% CI 0.50 to 0.78), and mercury was associated with increased fish consumption (n=5500, r=0.366, p<0.001). In addition, several PFCs (perfluorooctanoic acid, perfluorohexane sulfonic acid, perfluorodecanoic acid and perfluorononanoic acid) were negatively associated with the prevalence of depression.ConclusionsCadmium was associated with an increased likelihood of depression. Contrary to hypotheses, many of persistent environmental pollutants were not associated or negatively associated with depression. While the inverse association between mercury and depressive symptoms may be explained by a protective role for fish consumption, the negative associations with other pollutants remains unclear. This exploratory study suggests the need for further investigation of the role of various agents and classes of agents in the pathophysiology of depression.

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“…In rats, prenatal exposure to ATR decreased striatal dopamine and decreased locomotor activity (Bardullas et al, 2011, Lin et al, 2013a, Rodríguez et al, 2012). Prenatal exposures to perfluorooctanoic acids (PFOAs), as fire retardants, increased home-cage activity in male mice, and enhanced astrogliosis and pro-inflammatory cytokines in the hippocampus and cortex of rats (Onishchenko et al, 2011, Zeng et al, 2011). Mice exposed to low dose TCDD in the perinatal period exhibited hypo-activation of the prefrontal cortex, increased brain monoamines and increased social behavior abnormalities (Ahmed, 2011, Endo et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Sex-specific enhanced behavioral toxicity induced by maternal exposure to a mixture of low dose endocrine-disrupting chemicals

et al. 2014

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Humans are increasingly and consistently exposed to a variety of endocrine disrupting chemicals (EDCs), chemicals that have been linked to neurobehavioral disorders such as ADHD and autism. Many of such EDCs have been shown to adversely influence brain mesocorticolimbic systems raising the potential for cumulative toxicity. As such, understanding the effects of developmental exposure to mixtures of EDCs is critical to public health protection. Consequently, this study compared the effects of a mixture of four EDCs to their effects alone to examine potential for enhanced toxicity, using behavioral domains and paradigms known to be mediated by mesocorticolimbic circuits (Fixed Interval (FI) schedule controlled behavior, novel object recognition memory and locomotor activity) in offspring of pregnant mice that had been exposed to vehicle or relatively low doses of four EDCs, Atrazine (ATR – 10mg/kg), Perfluorooctanoic acid (PFOA – 0.1 mg/kg), Bisphenol-A (BPA - 50μg/kg), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD – 0.25μg/kg) alone or combined in a mixture (MIX), from gestational day 7 until weaning. EDC-treated males maintained significantly higher horizontal activity levels across 3 testing sessions, indicative of delayed habituation, whereas no effects were found in females. Statistically significant effects of MIX were seen in males, but not females, in the form of increased FI response rates, in contrast to reductions in response rate with ATR, BPA and TCDD, and reduced short term memory in the novel object recognition paradigm. MIX also reversed the typically lower neophobia levels of males compared to females. With respect to individual EDCs, TCDD produced notable increases in FI response rates in females, and PFOA significantly increased ambulatory locomotor activity in males. Collectively, these findings show the potential for enhanced behavioral effects of EDC mixtures in males and underscore the need for animal studies to more fully investigate mixtures, including chemicals that converge on common physiological substrates to examine potential mechanisms of toxicity with full dose effect curves to assist in interpretations of relevant mechanisms.

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Inflammation-like glial response in rat brain induced by prenatal PFOS exposure

Cited by 58 publications

References 48 publications

Reactive oxygen species mediate nitric oxide production through ERK/JNK MAPK signaling in HAPI microglia after PFOS exposure

Reactive oxygen species mediate nitric oxide production through ERK/JNK MAPK signaling in HAPI microglia after PFOS exposure

Pop, heavy metal and the blues: secondary analysis of persistent organic pollutants (POP), heavy metals and depressive symptoms in the NHANES National Epidemiological Survey

Sex-specific enhanced behavioral toxicity induced by maternal exposure to a mixture of low dose endocrine-disrupting chemicals

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