Green Tea Diet Can Effectively Antagonize the Toxicity Induced by Environmental-Related Concentrations of BPA: An Implication from and Studies.

The neurotoxicity of bisphenol A (BPA) exposure has been confirmed and , and inflammatory response is considered the main pathway. Green tea is a healthy life habit as it is rich in various anti-inflammatory components. To confirm that green tea diet is an effective measure to antagonize BPA-induced neurotoxicity, mice were treated with 0.

Bisphenol a accelerates the glucolipotoxicity-induced dysfunction of rat insulinoma cell lines: An implication for a potential risk of environmental bisphenol a exposure for individuals susceptible to type 2 diabetes.

Epidemiological studies have suggested a correlation between bisphenol A (BPA) and type 2 diabetes (T2DM). The effects of BPA on β-cell dysfunction may reveal the risks from an in vitro perspective. We used the rat insulinoma (INS-1) cell lines (a type of β-cells) to set up normal or damaged models (DM), which were exposed to various concentrations of BPA (0.

Environmental dose of 16 priority-controlled PAHs induce endothelial dysfunction: An in vivo and in vitro study.

Polycyclic aromatic hydrocarbons (PAHs) exposure is related to the occurrence of cardiovascular diseases (CVDs). Endothelial dysfunction is considered an initial event of CVDs. To confirm the relationship of PAHs exposure with endothelial dysfunction, 8-week-old male SD rats and primary human umbilical vein endothelial cells (HUVECs) were co-treated with environmental doses of 16 priority-controlled PAHs for 90 d and 48 h, respectively.

Trace metal exposure and risk assessment of local dominant fish species in the Beijiang River Basin of China: A 60 years' follow-up study.

The Beijiang River, one of the Pearl River tributaries located in Guangdong, China, plays a critical role in providing water and fishery resources for the Pearl River Delta and receiving a large amount of domestic and industrial wastewater. However, due to the lack of historical monitoring data, we are unable to fully understand the relationship between the industrial and agricultural development and the environment. In this study, fish specimens collected from the Beijiang River Basin over a span of nearly 60 years (1963-2021) are used as research objects and the concentrations of ten trace metals (TMs) in two locally dominant fish species were determined by an inductively coupled plasma mass spectrometer.

Low-dose bisphenols exposure sex-specifically induces neurodevelopmental toxicity in juvenile rats and the antagonism of EGCG.

Bisphenols (BPs) can negatively affect neurobehaviors in rats, whereas the mechanism remains unclear. Here, the mechanism of BPs-induced neurodevelopmental toxicity and its effective detoxification measures were investigated in vitro and in vivo. In in vitro experiments, primary hippocampal neurons from neonatal rats of different genders were treated with bisphenol A (BPA), bisphenol S (BPS) and bisphenol B (BPB) at 1 nM-100 μM, epigallocatechin gallate (EGCG) and G15, an antagonist of G protein-coupled estrogen receptor (GPER) for 7 d.

In vitro and in silico assessment of GPER-dependent neurocytotoxicity of emerging bisphenols.

To rapidly assess the toxicity of bisphenols (BPs) via the activation of G protein-coupled estrogen receptor (GPER), eight BPs action on GPER were evaluated by molecular docking and molecular dynamics (MD) simulation and then confirmed with IMR-32 cells. The target BPs significantly promoted the production of reactive oxygen species (ROS), reduced cell viability, activated the expression of apoptosis-related proteins and increased the apoptosis rate of IMR-32 cells. Intracellular Ca level increased significantly after the treatments with bisphenol A (BPA), bisphenol E (BPE), bisphenol C (BPC) and bisphenol AP (BPAP), suggesting the activation of GPER.

Involvement of NLRP3/Caspase-1/GSDMD-Dependent pyroptosis in BPA-Induced apoptosis of human neuroblastoma cells.

Bisphenol A (BPA) induces neurotoxicity via enhancing cell apoptosis and inflammation potently (effective at nanomolar concentrations), but its mechanisms remain unidentified. In this study, human neuroblastoma cell lines, IMR-32 and SK-N-SH cells, isolated from a male and a female subject, respectively, were exposed to BPA at various concentrations, with epigallocatechin gallate (EGCG, an antioxidant from green tea), Z-YVAD-FMK (a caspase-1 inhibitor), and ICI182.780 [an estrogen receptor (ER) inhibitor] as modulators.

Environmental dose of 16 priority-controlled PAHs mixture induce damages of vascular endothelial cells involved in oxidative stress and inflammation.

Epidemiological studies have shown that cardiovascular diseases caused by PM pollution account for the second death rate in China. Polycyclic aromatic hydrocarbons (PAHs) are one important group of persistent organic pollutants absorbed on PM. Though individual PAH is related to vascular disease, the relationship between environmental PAHs exposure and vascular damages is still unclear.

Volatile organic compounds from second-hand smoke may increase susceptibility of children through oxidative stress damage.

Although humans are generally exposed to second-hand smoke (SHS), volatile organic compounds (VOCs) exposure derived from SHS and its health hazard to non-smokers are rarely investigated. Thus, we examined the effects of SHS on VOCs exposure and oxidative stress damage via a passive smoking simulation experiment in 6 children and 7 adults. To further validate the studied urinary VOC metabolites as biomarkers for passive smoking, 259 children were recruited.

Human exposure and health risk assessment of an increasingly used antibacterial alternative in personal care products: Chloroxylenol.

The ban of some antibacterial ingredients, such as triclosan (TCS) and triclocarban (TCC), in personal care products (PCPs) in some countries (but not in China) has resulted in the increasing use of antibacterial alternatives, such as chloroxylenol (PCMX). However, the underlying human health risks and environmental impacts of PCMX exposure are largely unknown. Thus, the distribution characteristics of PCMX in PCPs and susceptible populations and the major routes and health risks of human exposure to PCMX were investigated.

Exposure to volatile organic compounds may be associated with oxidative DNA damage-mediated childhood asthma.

Volatile organic compounds (VOCs) are important and ubiquitous air pollutants, which may lead to a significant increase in the prevalence of respiratory diseases. To investigate the relationships between VOCs exposure and childhood asthma, 252 asthmatic children and 69 healthy children were recruited. Urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG, a biomarker of oxidative DNA damage), trans-3'-hydroxycotinine (OH-Cot, a biomarker of passive smoking) and 27 VOC metabolites were simultaneously determined by an ultra-high-performance liquid chromatography-tandem mass spectrometer.

Sex-specific oxidative damage effects induced by BPA and its analogs on primary hippocampal neurons attenuated by EGCG.

BPA analogs, including bisphenol S (BPS) and bisphenol B (BPB), have been used to replace BPA since it was banned to be added. To investigate whether BPA and its analogs cause oxidative damage effects on primary hippocampal neurons of rats, reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), mitochondrial membrane potential (MMP), apoptosis and cell viability assays were conducted after hippocampal neurons exposure to different concentrations of BPA, BPS, and BPB (1, 10, 100 nM and 1, 10, 100 μM). Moreover, the effects of EGCG (5 and 6 μM for male and female, respectively) added on neurons exposed to BPA were assessed.

Bisphenol A(BPA), BPS and BPB-induced oxidative stress and apoptosis mediated by mitochondria in human neuroblastoma cell lines.

The analogues of biphenol A (BPA), including bisphenol S (BPS) and bisphenol B (BPB), are commonly used to replace the application of BPA in containers and wrappers of daily life. However, their safeties are questioned due to their similar chemical structure and possible physiological effects as BPA. To investigate the neurotoxic effects of BPA, BPS, and BPB as well as their underlying mechanism, IMR-32 cell line from male and SK-N-SH cell line from female were exposed respectively to BPA, BPS and BPB with concentrations of 1 nM, 10 nM, 100 nM, 1 μM, 10 μM, and 100 μM for 24 h.

Co-exposure to polycyclic aromatic hydrocarbons, benzene and toluene may impair lung function by increasing oxidative damage and airway inflammation in asthmatic children.

As previous studies found that the direct associations between urinary polycyclic aromatic hydrocarbon (PAH), benzene and toluene (BT) metabolites and the decreased lung function were not conclusive, we further investigated relationship of oxidative damage and airway inflammation induced by PAHs and BTs exposure with lung function. A total of 262 children diagnosed with asthma and 72 heathy children were recruited. Results showed that asthmatic children had higher levels of PAHs and BTs exposure, as well as Malonaldehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) compared with healthy children.

Association between 10 urinary heavy metal exposure and attention deficit hyperactivity disorder for children.

Attention deficit hyperactivity disorder (ADHD) is associated with heavy metal exposure during adolescent development. However, the direct clinical evidence is limited. To investigate the possible association between environmental heavy metal exposure and ADHD, a case-control study was conducted with children aged 6-14 years in Guangzhou, China.

Maternal exposure to environmental bisphenol A impairs the neurons in hippocampus across generations.

Humans from fetal to adult stages are chronically and passively exposed to bisphenol A (BPA, an endocrine disruptor) due to its ubiquitous existence in daily life. To investigate the long-term neurotoxicity of maternal exposure to BPA for offspring, mice were used as the animal model. In this study, pregnant mice (F0) were orally dosed with BPA (i.

Simultaneous determination of urinary 31 metabolites of VOCs, 8-hydroxy-2'-deoxyguanosine, and trans-3'-hydroxycotinine by UPLC-MS/MS: C- and N-labeled isotoped internal standards are more effective on reduction of matrix effect.

Human beings are inevitably exposed to volatile organic compounds (VOCs) of anthropogenic emissions as they are ubiquitous atmospheric pollutants. Smoking is an important exposure route of VOCs for the general population. Health effects induced by VOC exposure raise more concerns as they are identified with carcinogenicity, genotoxicity, neurotoxicity, and reproductive toxicity.

Association among blood BPDE-DNA adduct, serum interleukin-8 (IL-8) and DNA strand breaks for children with pulmonary diseases.

Exposure to benzo[a]pyrene (B[a]P) may be a risk factor for pulmonary diseases. To investigate the correlations among B[a]P exposure level, DNA strand breaks and pulmonary inflammation, we recruited 83 children diagnosed with pulmonary diseases and 63 healthy children from Guangzhou, China. Results showed that the levels of Benzo[a]pyrene diol epoxide (BPDE) DNA adduct in blood and IL-8 in serum in case group were significantly higher than those in control group ( < 0.

Low-dose bisphenol A exposure impairs learning and memory ability with alterations of neuromorphology and neurotransmitters in rats.

To investigate the developmental neurotoxicity of environmental bisphenol A (BPA) exposure for infants and children, postnatal rats were used as the animal model and were divided into four groups. Then, they were treated with different concentrations of BPA (i.e.

[Simultaneous determination of five neurotransmitters in neonatal rat hippocampus by adding vitamin C coupled with isotope dilution-ultra-high performance liquid chromatography-tandem mass spectrometry].

Analysis of neurotransmitters in brain tissue is useful for mechanistic studies of the central nervous system. Isotope dilution coupled with ultra-high performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) was developed for the simultaneous determination of glutamic acid, -amino butyric acid, acetylcholine, dopamine, and serotonin in the hippocampus tissue. A 2% (v/v) acetic acid in water-methanol (9:1, v/v) solution was used to prepare the standards and re-dissolute samples after nitrogen drying.

Neurotoxicity of BPA, BPS, and BPB for the hippocampal cell line (HT-22): An implication for the replacement of BPA in plastics.

Bisphenol A (BPA), a plastic additive, is ubiquitous in the environment and has endocrine disrupting effects. As many countries have prohibited the manufacture and sale of plastic products with BPA, BPA analogs have been used to replace BPA during production, including bisphenol S (BPS) and bisphenol B (BPB). To investigate the toxicities of BPA and its analogs on neurons, reactive oxygen species (ROS) assay, Annexin V-FITC (fluorescein) apoptosis detection assay, lactate dehydrogenase (LDH) cytotoxicity assay, and Cell Counting Kit-8 assay were conducted to comprehensively assess the influence of different concentrations of BPA, BPB, and BPS on ROS, apoptosis, damage, and proliferation for hippocampal HT-22 cells, respectively.

Relationship between bisphenol A exposure and attention-deficit/ hyperactivity disorder: A case-control study for primary school children in Guangzhou, China.

Bisphenol A (BPA) is an endocrine-disrupting chemical. Studies have shown that the exposure to BPA is associated with attention-deficit/hyperactivity disorder (ADHD) during adolescent development. However the direct clinical evidence is limited.

Regulation of Th17 Differentiation by IKKα-Dependent and -Independent Phosphorylation of RORγt.

Transcription factor retinoid acid-related orphan receptor (ROR)γt transcriptionally regulates the genes required for differentiation of Th17 cells that mediate both protective and pathogenic immunity. However, little is known about the function of posttranslational modifications in the regulation of RORγt activity. Mass spectrometric analysis of immunoprecipitated RORγt from Th17 cells identified multiple phosphorylation sites.

Neurotoxicity of low bisphenol A (BPA) exposure for young male mice: Implications for children exposed to environmental levels of BPA.

To investigate the neuron toxicities of low-dose exposure to bisphenol A (BPA) in children, mice were used as an animal model. We examined brain cell damage and the effects of learning and memory ability after BPA exposure in male mice (4 weeks of age) that were divided into four groups and chronically received different BPA treatments for 8 weeks. The comet assay and hippocampal neuron counting were used to detect the brain cell damage.

Exposure of children to BPA through dust and the association of urinary BPA and triclosan with oxidative stress in Guangzhou, China.

Both bisphenol A (BPA) and triclosan (TCS) are phenolic compounds widely used in a variety of household applications. These compounds could be released into the environment, enter the human body and cause a series of potential health hazards. Children are sensitive and susceptible to these contaminants.