Embryonic Atrazine Exposure Elicits Alterations in Genes Associated with Neuroendocrine Function in Adult Male Zebrafish
The developmental origins of health and disease (DOHaD) hypothesis states that exposure to environmental stressors early in life can elicit genome and epigenome changes resulting in an increased susceptibility of a disease state during adulthood. Atrazine, a common agricultural herbicide used throughout the Midwestern United States, frequently contaminates potable water supplies and is a suspected endocrine disrupting chemical. In our previous studies, zebrafish was exposed to 0, 0.3, 3, or 30 parts per billion (μg/l) atrazine through embryogenesis, rinsed, and allowed to mature to adulthood. A decrease in spawning was ...
Source: Toxicological Sciences - August 30, 2016 Category: Toxicology Authors: Wirbisky, S. E., Sepulveda, M. S., Weber, G. J., Jannasch, A. S., Horzmann, K. A., Freeman, J. L. Tags: Neuroendocrine Effects of Atrazine in Zebrafish Source Type: research
From the Cover: Exposing Imidacloprid Interferes With Neurogenesis Through Impacting on Chick Neural Tube Cell Survival
In this study, using a chick embryo model, we investigated the effects of imidacloprid exposure on neurogenesis at the earliest stage and during late-stage embryo development. Exposing HH0 chick embryos to imidacloprid in EC culture caused neural tube defects (NTDs) and neuronal differentiation dysplasia as determined by NF/Tuj1 labeling. Furthermore, we found that F-actin accumulation on the apical side of the neural tube was suppressed by exposure to imidacloprid, and the expression of BMP4 and Shh on the dorsal and ventral sides of the neural tubes, respectively, were also reduced, which in turn affects the dorsolateral...
Source: Toxicological Sciences - August 30, 2016 Category: Toxicology Authors: Liu, M., Wang, G., Zhang, S.-Y., Zhong, S., Qi, G.-L., Wang, C.-J., Chuai, M., Lee, K. K. H., Lu, D.-X., Yang, X. Tags: Imidacloprid and Neural Tube Cell Integrity Source Type: research
From the Cover: Zinc Deficiency Worsens and Supplementation Prevents High-Fat Diet Induced Vascular Inflammation, Oxidative Stress, and Pathological Remodeling
Obesity has become a common public health problem in the world and raises the risk of various cardiovascular diseases. Zinc is essential for multiple organs in terms of normal structure and function. The present study investigated the effects of high fat diet (HFD) induced obesity on the aorta in mice, and evaluated whether it can be affected by zinc deficiency or supplementation. Four-week-old male C57BL/6J mice were fed HFD with varied amounts of zinc (deficiency, adequate and supplementation) for 3 and 6 months. Results showed that HFD feeding induced a time-dependent aortic remodeling, demonstrated by increased vessel ...
Source: Toxicological Sciences - August 30, 2016 Category: Toxicology Authors: Chen, J., Wang, S., Luo, M., Zhang, Z., Dai, X., Kong, M., Cai, L., Wang, Y., Shi, B., Tan, Y. Tags: Effects of Zinc Levels on Vascular Inflammation and Oxidative Stress Source Type: research
Association Between Variants in Arsenic (+3 Oxidation State) Methyltranserase (AS3MT) and Urinary Metabolites of Inorganic Arsenic: Role of Exposure Level
Variants in AS3MT, the gene encoding arsenic (+3 oxidation state) methyltranserase, have been shown to influence patterns of inorganic arsenic (iAs) metabolism. Several studies have suggested that capacity to metabolize iAs may vary depending on levels of iAs exposure. However, it is not known whether the influence of variants in AS3MT on iAs metabolism also vary by level of exposure. We investigated, in a population of Mexican adults exposed to drinking water As, whether associations between 7 candidate variants in AS3MT and urinary iAs metabolites were consistent with prior studies, and whether these associations varied ...
Source: Toxicological Sciences - August 30, 2016 Category: Toxicology Authors: Xu, X., Drobna, Z., Voruganti, V. S., Barron, K., Gonzalez-Horta, C., Sanchez-Ramirez, B., Ballinas-Casarrubias, L., Ceron, R. H., Morales, D. V., Terrazas, F. A. B., Ishida, M. C., Gutierrez-Torres, D. S., Saunders, R. J., Crandell, J., Fry, R. C., Loomi Tags: Arsenic Methyltransferase and Urinary Metabolites Source Type: research
From the Cover: Prenatal Nicotinic Exposure Attenuates Respiratory Chemoreflexes Associated With Downregulation of Tyrosine Hydroxylase and Neurokinin 1 Receptor in Rat Pup Carotid Body
Maternal cigarette smoke is the major risk of sudden infant death syndrome (SIDS). A depressed ventilatory response to hypoxia (HVR) and hypercapnia (HCVR) is thought to be responsible for the pathogenesis of SIDS and the carotid body is critically involved in these responses. We have recently reported that prenatal nicotinic exposure (PNE) over the full gestation induces depressed HVR in rat pups. Here, we asked whether PNE (1) depressed not only HVR but also HCVR that were dependent on the carotid body, (2) affected some important receptors and neurochemicals expressed in the carotid body, such as tyrosine hydroxylase (T...
Source: Toxicological Sciences - August 30, 2016 Category: Toxicology Authors: Zhao, L., Zhuang, J., Gao, X., Ye, C., Lee, L.-Y., Xu, F. Tags: Prenatal Nicotine Exposure and Chemoreflexes in Carotid Bodies Source Type: research
Editors Highlight: Characterization of Hepatotoxicity Mechanisms Triggered by Designer Cathinone Drugs ({beta}-Keto Amphetamines)
In conclusion, the present data shows that (1) cathinones induce in vitro hepatotoxic effects that vary in magnitude among the different analogues, (2) oxidative stress and mitochondrial dysfunction play a role in cathinones-induced hepatic injury, and (3) apoptosis appears to be an important pathway of cell death elicited by these novel drugs. (Source: Toxicological Sciences)
Source: Toxicological Sciences - August 30, 2016 Category: Toxicology Authors: Valente, M. J., Araujo, A. M., Bastos, M. d. L., Fernandes, E., Carvalho, F., Guedes de Pinho, P., Carvalho, M. Tags: Cathinone Designer Drugs and Liver Toxicity Source Type: research
Vesicular Monoamine Transporter 2 (VMAT2) Level Regulates MPTP Vulnerability and Clearance of Excess Dopamine in Mouse Striatal Terminals
The vesicular monoamine transporter 2 (VMAT2) packages neurotransmitters for release during neurotransmission and sequesters toxicants into vesicles to prevent neuronal damage. In mice, low VMAT2 levels causes catecholaminergic cell loss and behaviors resembling Parkinson’s disease, while high levels of VMAT2 increase dopamine release and protect against dopaminergic toxicants. However, comparisons across these VMAT2 mouse genotypes were impossible due to the differing genetic background strains of the animals. Following back-crossing to a C57BL/6 line, we confirmed that mice with approximately 95% lower VMAT2 levels...
Source: Toxicological Sciences - August 30, 2016 Category: Toxicology Authors: Lohr, K. M., Chen, M., Hoffman, C. A., McDaniel, M. J., Stout, K. A., Dunn, A. R., Wang, M., Bernstein, A. I., Miller, G. W. Tags: Vesicular Transport and Dopamine Toxicity Source Type: research
Prolonged Particulate Hexavalent Chromium Exposure Suppresses Homologous Recombination Repair in Human Lung Cells
Genomic instability is one of the primary models of carcinogenesis and a feature of almost all cancers. Homologous recombination (HR) repair protects against genomic instability by maintaining high genomic fidelity during the repair of DNA double strand breaks. The defining step of HR repair is the formation of the Rad51 nucleofilament, which facilitates the search for a homologous sequence and invasion of the template DNA strand. Particulate hexavalent chromium (Cr(VI)), a human lung carcinogen, induces DNA double strand breaks and chromosome instability. Since the loss of HR repair increases Cr(VI)-induced chromosome ins...
Source: Toxicological Sciences - August 30, 2016 Category: Toxicology Authors: Browning, C. L., Qin, Q., Kelly, D. F., Prakash, R., Vanoli, F., Jasin, M., Wise, J. P. Tags: Hexavalent Chromium Exposure and DNA Repair in Lung Cells Source Type: research
From the Cover: Thirdhand Cigarette Smoke Causes Stress-Induced Mitochondrial Hyperfusion and Alters the Transcriptional Profile of Stem Cells
Thirdhand cigarette smoke (THS) was recently recognized as an environmental health hazard; however, little is known about it effects on cells. Mitochondria are sensitive monitors of cell health and report on environmentally induced stress. We tested the effects of low levels of THS extracted from terry cloth on mitochondrial morphology and function using stem cells with well-defined mitochondria. Concentrations of THS that did not kill cells caused stress-induced mitochondrial hyperfusion (SIMH), which was characterized by changes in mitochondrial morphology indicative of fusion, increased mitochondrial membrane potential ...
Source: Toxicological Sciences - August 30, 2016 Category: Toxicology Authors: Bahl, V., Johnson, K., Phandthong, R., Zahedi, A., Schick, S. F., Talbot, P. Tags: Mitochondrial Effects of Thirdhand Cigarette Smoke Source Type: research
Histone Deacetylase Inhibitors Prolong Cardiac Repolarization through Transcriptional Mechanisms
Histone deacetylase (HDAC) inhibitors are an emerging class of anticancer agents that modify gene expression by altering the acetylation status of lysine residues of histone proteins, thereby inducing transcription, cell cycle arrest, differentiation, and cell death or apoptosis of cancer cells. In the clinical setting, treatment with HDAC inhibitors has been associated with delayed cardiac repolarization and in rare instances a lethal ventricular tachyarrhythmia known as torsades de pointes. The mechanism(s) of HDAC inhibitor-induced effects on cardiac repolarization is unknown. We demonstrate that administration of struc...
Source: Toxicological Sciences - August 30, 2016 Category: Toxicology Authors: Spence, S., Deurinck, M., Ju, H., Traebert, M., McLean, L., Marlowe, J., Emotte, C., Tritto, E., Tseng, M., Shultz, M., Friedrichs, G. S. Tags: HDAC Inhibitor and Cardiac Repolarization Source Type: research
The Role of Lipin-1 in the Regulation of Fibrogenesis and TGF-{beta} Signaling in Hepatic Stellate Cells
The adipogenic transcriptional regulation was reported to inhibit transdifferentiation of hepatic stellate cells (HSCs), which constitute the main fibrogenic cell type in the liver. Lipin-1 exhibits a dual function: an enzyme that catalyzes the conversion of phosphatidate to diacylglycerol and a transcriptional regulator. However, the involvement of Lipin-1 in the regulation of transforming growth factor-β (TGF-β) signaling and fibrogenesis in HSCs is not fully understood. Here, we showed that Lipin-1 was downregulated in activated primary HSCs and TGF-β-treated LX-2 cells, immortalized human HSC cell lines....
Source: Toxicological Sciences - August 30, 2016 Category: Toxicology Authors: Jang, C. H., Kim, K. M., Yang, J. H., Cho, S. S., Kim, S. J., Shin, S. M., Cho, I. J., Ki, S. H. Tags: Lipin-1 and Fibrogenesis in Hepatic Stellate Cells Source Type: research
Generalized Concentration Addition Modeling Predicts Mixture Effects of Environmental PPAR{gamma} Agonists
The vast array of potential environmental toxicant combinations necessitates the development of efficient strategies for predicting toxic effects of mixtures. Current practices emphasize the use of concentration addition to predict joint effects of endocrine disrupting chemicals in coexposures. Generalized concentration addition (GCA) is one such method for predicting joint effects of coexposures to chemicals and has the advantage of allowing for mixture components to have differences in efficacy (ie, dose-response curve maxima). Peroxisome proliferator–activated receptor gamma (PPAR) is a nuclear receptor that plays...
Source: Toxicological Sciences - August 30, 2016 Category: Toxicology Authors: Watt, J., Webster, T. F., Schlezinger, J. J. Tags: Predicting Mixture Effects of PPAR[gamma ] Agonists Source Type: research
Table of Contents
(Source: Toxicological Sciences)
Source: Toxicological Sciences - August 30, 2016 Category: Toxicology Tags: Standing Material Source Type: research
Editor's Highlight: Abrasion of Artificial Stones as a New Cause of an Ancient Disease. Physicochemical Features and Cellular Responses
New outbursts of silicosis were recently reported among workers manufacturing an engineered material known as "artificial stone," composed by high percentages of quartz (up to 98%) agglomerated with pigments and polymeric resins. Dusts released by abrasion during artificial stone polishing were characterized for particle size, morphology, and elemental composition and studied for (1) ability to catalyze free radical generation in acellular tests, (2) membranolytic potential on human erythrocytes, (3) cytotoxic activity (lactate dehydrogenase release) on murine alveolar macrophages (MH-S) and human bronchial epithelial (BEA...
Source: Toxicological Sciences - August 30, 2016 Category: Toxicology Authors: Pavan, C., Polimeni, M., Tomatis, M., Corazzari, I., Turci, F., Ghigo, D., Fubini, B. Tags: Occupational Exposure to Synthetic Stone and Pulmonary Dysfunction Source Type: research
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(Source: Toxicological Sciences)
Source: Toxicological Sciences - August 30, 2016 Category: Toxicology Tags: Standing Material Source Type: research
