Showing papers in "Toxicology and Applied Pharmacology in 2020"

TL;DR: Investigation of the anti-inflammatory effect and action mechanism of Aureusidin in LPS-induced mouse macrophage RAW264.7 cells suggested that lipopolysaccharide (LPS)-induced nitric oxide (NO), tumor necrosis factor-α (TNF-α) and prostaglandin E2 (PGE2) production were obviously inhibited by Aureusids, and may be an attractive therapeutic candidate for the inflammation-related diseases.

TL;DR: It is shown that RA improved locomotor recovery after SCI and significantly mitigated neurological deficit, increased neuronal preservation, and reduced apoptosis, which may be due to its antioxidant and anti-inflammatory properties, which are mediated by modulation of the Nrf2/HO-1 and TLR4/NF-κB pathways.

TL;DR: It is concluded that the HTPP assay can be used as an efficient, cost-effective and reproducible screening method for characterizing the biological activity and potency of environmental chemicals for potential use in in vitro-based safety assessments.

TL;DR: The results suggest that specific surface area, crystal phase and shape of TiO2 NMs are important predictors for the observed pulmonary effects of TiOs, including profound effects related to the tube shape.

TL;DR: Pooled analyses of serum lipoprotein cholesterol suggest that PFOA increased serum cholesterol, particularly in male mice, and generated new insight on the effects of PfoA on cholesterol regulation in the liver and the role of hPPARα.

TL;DR: Although occupational exposure to antimony and its compounds can produce pulmonary toxicity, human carcinogenic impacts have not been observed, and inhalation studies with respirable antimony trioxide particles administered to rats and mice have induced carcinogenic responses in the lungs and related tissue sites.

TL;DR: Altogether, miR-187-5p/apaf-1 axis participated in oxidative stress-mediated apoptosis caused by NH3 via mitochondrial pathway in the livers of chickens for fattening, and may provide new ideas to study the mechanism of liver apoptotic damage induced byNH3 exposure.

TL;DR: It is shown that inhibition of p38 MAPK-DRP1 signaling pathway may be a viable therapeutic strategy of PD on maintenance of mitochondrial homeostasis and restores the mitochondrial dysfunction and cell death in α-synuclein A53T model.

TL;DR: There is no consensus on a consistent miRNA profile for arsenic-induced cancers because most studies analyze only particular miRNAs, and identifying miRNA expression changes common among humans, rodents and cell lines might guide future miRNA investigations.

TL;DR: It is demonstrated that ferroptotic stimuli caused injury in neuron-like PC12 cells by modulating the expression of proteins involved in iron metabolism and lipid peroxidation at multiple levels, such as altering iron import/export, activating ferritinophagy, and decreasing glutathione (GSH) level.

TL;DR: The results indicate that 10 days of exposure to DEHP and DiNP changed the distribution of ovarian follicle populations and sex steroid hormones at multiple time points, including the last time point, 9 months post-dosing.

TL;DR: VLD showed a strong trend toward increasing the antioxidant defense machinery of fibrotic tissue, and it was confirmed that GLP-1Rs were not implicated in the observed hepatoprotection.

TL;DR: The data indicated that autophagy could be activated to protect testes from DEHP-induced reproductive damage by inhibiting PI3K-Akt-mTOR signaling pathway in the 250 mg/kg/day DEHP group.

TL;DR: The hypothesis that phthalate metabolites influence the expression of genes involved in sex steroid synthesis, cell cycle regulation, cell death, oxidative stress, and key receptors is tested as well as production of sex steroid hormones by mouse antral follicles, suggesting mixtures of phthalates can directly impact follicle health.

TL;DR: It is suggested that PFOS treatment did interfere with lipid loss associated with switch to a SD and similarly augmented hepatic lipid accumulation in mice established on an HFD.

TL;DR: Arsenic exposure altered motor activity through the development and increased anxiety-like behaviors which were transmitted to the F2 generation, and a reduction in brain-derived neurotrophic factor expression and an increase in methylation on histone H3K4me3 in the nervous system were found.

TL;DR: Results support a strong correlation between ADC hydrophobicity, rate of non-specific uptake, peak tissue concentration of released payload, and resulting toxicology parameters and should be translatable to the clinic.

TL;DR: Mechanistic investigations revealed that all of the three substances induce apoptotic cell death via its intrinsic pathway by causing deformation of the nuclear membrane, disruption of the mitochondrial membrane potential (MMP), and elevated reactive oxygen species (ROS) production in both cell lines.

TL;DR: Pristimerin protected mice from dextran sulfate sodium (DSS)-induced colitis, restoring epithelial damage and reducing tissue inflammation and inflammatory cell infiltration, and inhibited Wnt/β-catenin signaling via activation of GSK3β, thereby suppressing Wnt target gene expression in colon cancer HCT116 and HT-29 cells.

TL;DR: It is suggested that GNA induces ferroptosis in TGF-β1-stimulated melanoma cells via the p53/SLC7A11/GPX4 signaling pathway and upregulated the expression of p53, solute carrier family 7 member 11 and glutathione peroxidase 4 in the model cells, contributing to the mechanisms underlying GNA-induced ferroPTosis.

TL;DR: Chronic exposure to ACR caused gait abnormality and cognitive dysfunction, which was associated with neuronal lesions, decrease in synapse associated proteins including synapsin I (SYN1), synaptophysin (SYP) and postsynaptic density protein 95 (PSD95), neurogenesis suppression as shown by reduced brain derived neurotrophic factor (BDNF) and doublecortin (DCX) in the hippocampus and frontal cortex.

TL;DR: The results strongly suggest that BR treatment protected against cerulein-induced CP and associated fibrosis progression by inhibiting TGF-β1/Smad signaling and M2 macrophages polarization in an AMPK dependent manner.

TL;DR: It is demonstrated that NM induces structural and inflammatory changes in the lung that correlate with aberrations in pulmonary function and this mouse model will be useful for mechanistic studies of mustard lung injury and for assessing potential countermeasures.

TL;DR: The relationship between safety margin thresholds and torsadogenic risk predictivity suggests the threshold should be tailored to each specific context of use, and safety margin evaluation may need to be integrated with other information to form a more comprehensive risk assessment.

TL;DR: In a Tm-mediated liver injury model, luteolin decreased serum alanine aminotransferase and aspartate aminosferase activities, prevented degenerative changes and apoptosis of hepatocytes, and inhibited CHOP and glucose-regulated protein 78 expression in hepatic tissues, suggesting that lUTEolin may be an effective phytochemical to manage ER stress-related liver injury.

TL;DR: Across the three platforms, menthol adversely effected human bronchial epithelium in a manner that could lead to respiratory disease.

TL;DR: This review will summarize the literature on the non-lethal, adverse health effects associated with prenatal and early life exposure to cadmium and the implications of these exposures in the development of diseases later in life and highlight possible mechanisms responsible for these outcomes.

TL;DR: This review provided a comprehensive and in-depth elaboration of the cytotoxic mechanisms of ATO and its methylated metabolites based on in vivo or in vitro studies, trying to clarify the importance of achieving balance between the toxicity and anti-leukemic activity of ATo in APL treatment.

TL;DR: 4-methylpyrazole (4MP, Fomepizole) protects against APAP-induced liver injury by inhibiting reactive metabolite formation through Cyp2E1, and analysis of data from APAP overdose patients indicated that kidney dysfunction strongly correlated with severe liver injury, indicating its potential use in protection against AP AP-induced nephrotoxicity.

TL;DR: This study demonstrates that Erk/MAPK signaling is a major pathway involved in Cd-induced malignant transformation of normal prostate cells, and understanding these dominant oncogenic pathways may help develop optimal therapeutic strategies for PCa.