Results of a 30-day safety assessment in young mice orally exposed to polystyrene nanoparticles.

Polystyrene nanoparticles (PSNPs) are a newly emerging pollutant in the natural environment. However, due to the lack of sufficient toxicological studies in mammals, the potential effects of PSNPs on human health remain largely undefined. Therefore, in this study, young mice aged four weeks old were subjected to oral administration of 0, 0.

Exposure to carbon black nanoparticles during pregnancy aggravates lipopolysaccharide-induced lung injury in offspring: an intergenerational effect.

Carbon black nanoparticles (CBNPs) are one of the most frequently used nanoparticles. Exposure to CBNPs during pregnancy (PrE to CBNPs) can directly induce inflammation, lung injury, and genotoxicity in dams and results in abnormalities in offspring. However, whether exposure to CBNPs during pregnancy enhances the susceptibility of offspring to environmental stimuli remains unknown.

Autophagy deficiency exacerbates acute lung injury induced by copper oxide nanoparticles.

Copper oxide nanoparticles (CuONPs) are one of the widely used metal nanoparticles in the industrial and commercial fields. Autophagy is an intracellular degradation system that delivers cytoplasmic constituents to the lysosome and has been linked to nanoparticles-induced toxicity. In particular, the roles of autophagy in response to CuONPs have been explored in vitro, although the conclusions are controversial.

Pulmonary Exposure to Copper Oxide Nanoparticles Leads to Neurotoxicity via Oxidative Damage and Mitochondrial Dysfunction.

Copper oxide nanoparticles (CuONPs) are widely used in pharmaceutical, food, and textile industries. They have been shown to cause lung, liver, and kidney damage. However, whether an intratracheal instillation of CuONPs would affect the brain and its underlying mechanisms remain poorly studied.

Arsenite induces ferroptosis in the neuronal cells via activation of ferritinophagy.

Ferroptosis is a novel form of cell death that involves in the pathophysiological process of diverse brain diseases. However, how arsenite induces ferroptosis in the neuronal cells remains unsolved. In this study, by using in vitro and in vivo models, we demonstrated that arsenite was able to trigger ferroptosis in the neuronal cells.

Lysosomal dysfunction is associated with persistent lung injury in dams caused by pregnancy exposure to carbon black nanoparticles.

Aims: Carbon black nanoparticles (CBNPs) are widely used in industrial field. Sensitive stages such as pregnancy are assumed to be more susceptible to stimulus, however whether pregnancy exposure to CBNPs (PrE-to-CBNPs) would cause long-term toxic effects in dams and the underlying mechanisms remain poorly addressed. The present study is aimed to determine the long-term toxic effects of PrE-to-CBNPs in dams.

Synaptic dopamine release is positively regulated by SNAP-25 that involves in benzo[a]pyrene-induced neurotoxicity.

Benzo[a]pyrene (B[a]P) is a ubiquitous neurotoxic pollutant that widely distributes in the natural environment. However, the exact mechanism of B[a]P-induced neurotoxicity has not been well established. As one key synaptic protein, SNAP-25 plays an important role in the regulation of neurotransmitter release, including synaptic dopamine release.

Exposure to carbon black nanoparticles during pregnancy persistently damages the cerebrovascular function in female mice.

Maternal exposure to carbon black nanoparticles (CBNPs) during pregnancy have been well documented to induce harmful outcomes of offspring on brain function. However, it remains largely unknown whether females exposed to CBNPs during sensitive period of pregnancy can cause the neurotoxic effects on their own body after parturition. In this study, our results showed that pregnancy CBNPs exposure induced the persistent pathological changes in the cerebral cortex tissues and impaired cerebrovascular function of mice manifested by significant alterations of endothelin-1, endothelial nitric oxide synthase, vascular endothelial growth factor-A and ATP-binding cassette transporter G1.

Gas chromatography-mass spectrometry based metabolomics profile of hippocampus and cerebellum in mice after chronic arsenic exposure.

Intake of arsenic (As) via drinking water has been a serious threat to global public health. Though there are numerous reports of As neurotoxicity, its pathogenesis mechanisms remain vague especially its chronic effects on metabolic network. Hippocampus is a renowned area in relation to learning and memory, whilst recently, cerebellum is argued to be involved with process of cognition.

Integrated Epigenetics, Transcriptomics, and Metabolomics to Analyze the Mechanisms of Benzo[a]pyrene Neurotoxicity in the Hippocampus.

Benzo[a]pyrene (B[a]P) is a common environmental pollutant that is neurotoxic to mammals, which can cause changes to hippocampal function and result in cognitive disorders. The mechanisms of B[a]P-induced impairments are complex .To date there have been no studies on the association of epigenetic, transcriptomic, and metabolomic changes with neurotoxicity after B[a]P exposure.

m6A Demethylase FTO Regulates Dopaminergic Neurotransmission Deficits Caused by Arsenite.

Arsenite exposure is known to increase the risk of neurological disorders via alteration of dopamine content, but the detailed molecular mechanisms remain largely unknown. In this study, using both dopaminergic neurons of the PC-12 cell line and C57BL/6J mice as in vitro and in vivo models, our results demonstrated that 6 months of arsenite exposure via drinking water caused significant learning and memory impairment, anxiety-like behavior and alterations in conditioned avoidance and escape responses in male adult mice. We also were the first to reveal that the reduction in dopamine content induced by arsenite mainly resulted from deficits in dopaminergic neurotransmission in the synaptic cleft.

[Changes of cerebral cortical metabolomics in rats following benzo[a]pyrene exposure].

Objective: To analyze the changes in endogenous small molecule metabolites after benzo[a]pyrene (B[a]P) exposure in rat cerebral cortex and explore the mechanism of B[a]P neurotoxicity.

Methods: Five-day-old SD rats were subjected to gavage administration of 2 mg/kg B[a]P for 7 consecutive weeks. After the exposure, the rats were assessed for spatial learning ability using Morris water maze test, ultrastructural changes of the cortical neurons under electron microscope, and metabolite profiles of the cortex using GC/MS.

Postnatal Subacute Benzo(a)Pyrene Exposure Caused Neurobehavioral Impairment and Metabolomic Changes of Cerebellum in the Early Adulthood Period of Sprague-Dawley Rats.

Benzo(a)pyrene (BaP) is a widespread environmental contaminant that has been associated with neurotoxicity in mammals. It has strong toxic effects on the developing central nervous system. Cerebellum is associated with locomotor activity and anxiety behavior, but there is very little research about the toxic effects of BaP in cerebellum.

Disruption of glutamate neurotransmitter transmission is modulated by SNAP-25 in benzo[a]pyrene-induced neurotoxic effects.

Benzo[a]pyrene (B[a]P), a ubiquitous chemical contaminant in the environment, is a well-established neurotoxicant to human. However, the molecular mechanisms for B[a]P neurotoxicity are still unclear. In the present study, after treating Sprague-Dawley rats with 0.

Effects of benzo(a)pyrene exposure on the ATPase activity and calcium concentration in the hippocampus of neonatal rats.

Objectives: To investigate whether postnatal benzo(a)pyrene (B(a)P) exposure caused the impairments on the process of neurodevelopment and the alteration in the calcium medium in the neonatal rats.

Material And Methods: Eighty neonatal Sprague Dawley (SD) rats were randomly divided into 5 groups (untreated control group, vehicle group, 0.02 mg/kg, 0.

Effects of coke oven emissions and benzo[a]pyrene on blood pressure and electrocardiogram in coke oven workers.

Objective: To evaluate the effects of occupational exposures to coke oven emissions (COEs) and benzo[a]pyrene (B[a]P) on the prevalence of hypertension and abnormal electrocardiogram (ECG) in coke oven workers.

Methods: We included 880 coke oven workers and 710 oxygen employees in the exposed and control groups, respectively. Blood pressure (BP), ECG, blood lipid levels, and glucose levels of all subjects were measured.

[Effect of Benzo [α]pryene and Butylated Hydroxylanisole on Learning and Memory in Rats].

Objective: To investigate the neurotoxic effect of benzo[α]pryene (B[α]P) and protective effect of butylated hydroxyl anisole (BHA) on learning and memory in hippocampus of rats.

Methods: Ninety male, SD rats were randomly divided into blank control group, solvent control group, B[α]P exposed group [(2 mg/(kg x d)], BRA group [50 mg/(kg x d)] and B[α]P + BHA combined group. Rats were given the appropriate dose oral treatment according to body mass and group (the same volume of saline and peanut oil were given to blank and solvent control group, respectively) for 90 d.

[Vitamin E prevents the toxic effect of benzo(a)pryene on reproductive system in male SD rats].

Objective: To investigate the protective effects and the potential mechanisms of vitamin E (VE) on benzo(a)pryene (B[a]P)-induced toxicity in the reproductive system of male rats. 


Methods: A total of 60 male Sprague Dawley (SD) rats, weighted 70-90 g, were randomly assigned to 6 groups: a control group, a vehicle group, a B[a]P group (5 mg/kg), a VE (10 mg/kg)+ B[a]P (5 mg/kg) group, a VE (50 mg/kg) + B[a]P (5 mg/kg) group and a VE (100 mg/kg)+B[a]P (5 mg/kg) group (n=10 per group). The rats were treated with B[a]P and/or VE once a day for 30 days via intragastric administration.

[Effects of benzo(a)pyrene exposure on the ATPase activity and content of Ca²⁺ in the hippocampus of neonatal SD rats].

Objective: To investigate the effect of benzo(α)pyrene on the ATPase activity and content of Ca²⁺ in the hippocampus of neonatal SD rats.

Methods: Sixty male and 60 female 4-days-old neonatal SD rats were randomly divided into 5 groups (n=24): a blank control group, a vehicle control group (peanut oil), 3 benzo(α)pyrene groups (0.02, 0.

Adverse effect of sub-chronic exposure to benzo(a)pyrene and protective effect of butylated hydroxyanisole on learning and memory ability in male Sprague-Dawley rat.

Previous studies demonstrate that benzo(a)pyrene (B(a)P) can affect hippocampal function and cause spatial cognition impairment. However, the mechanism is incomplete. Some evidence implies that B(a)P may cause an oxidative damage linking to the function of the hippocampus and antioxidant can prevent the oxidative damage in rats, but the ATPase and Ca(2+) in the hippocampus and the protective effect of butylated hydroxyanisole (BHA) have not been studied.

[Effects of benzo(a)pyrene exposure on oxidative stress and ATPase in the hippocampus of rats].

Objective: To investigate the effects of benzo[a]pyrene (B[a]P) exposure on the behaviors and hippocampal oxidative stress and ATPase in rats and the molecular mechanism of neurobehavioral toxicity of B[a]P.

Methods: A total of 120 male SD rats (21 days old) were randomly and equally assigned to five groups: blank control group, vegetable oil (solvent control) group, and 2.5, 5, and 10 mg/kg B[a]P exposure groups.

Neurotoxic effect of subacute benzo(a)pyrene exposure on gene and protein expression in Sprague-Dawley rats.

Benzo(a)pyrene (B[a]P) is an environmental carcinogen that induces tumors in many animal species, but the neurotoxic effects of B[a]P have not been well studied. In the present study, we investigated the effects of subacute exposure to B[a]P in Sprague-Dawley (SD) rats. Male rats received daily injections of either B[a]P (0, 1, 2.

The effect of occupational exposure to benzo[a]pyrene on neurobehavioral function in coke oven workers.

Background: Coke oven workers are regularly exposed to polycyclic aromatic hydrocarbons (PAHs). Benzo[a]pyrene (B[a]P), known as an indicator species for PAH contamination, is a neurobehavioral toxicant. The purpose of the study was to evaluate the relationship between B[a]P exposure, a B[a]P-related urinary metabolite and neurobehavioral function among coke oven workers.

The synergistic effect of benzo[a]pyrene and lead on learning and memory of mice.

In the present study, the single and combined neurotoxic effects of benzo[a]pyrene ([BaP] 0.0, 0.5, and 5.

Modulation of behavior and glutamate receptor mRNA expression in rats after sub-chronic administration of benzo(a)pyrene.

Objective: The present study aimed to test whether exposure to benzo(a)pyrene [B(a)P] affects spatial learning and short-term memory by modulating the expression of the Gria1 and Grin2a glutamate receptor subunit genes in the hippocampus.

Methods: Thirty-six 21-24-day-old, male rats were randomly assigned into high-, medium-, and low-dose toxin exposure groups (6.25, 2.