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Toxics, Volume 7, Issue 2 (June 2019)

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Open AccessArticle
Antioxidant and Cytoprotective Effect of Piper aduncum L. against Sodium Fluoride (NaF)-Induced Toxicity in Albino Mice
Received: 7 April 2019 / Revised: 6 May 2019 / Accepted: 6 May 2019 / Published: 16 May 2019
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Abstract
Piper aduncum, commonly known as matico, is a plant that grows in the mountainous and coastal regions of Peru, and is studied for its antimicrobial properties and various ethnopharmacological uses. The main objective of this study was to determine the cytoprotective and [...] Read more.
Piper aduncum, commonly known as matico, is a plant that grows in the mountainous and coastal regions of Peru, and is studied for its antimicrobial properties and various ethnopharmacological uses. The main objective of this study was to determine the cytoprotective and antioxidant effects of the methanolic extract of Piper aduncum leaves in Mus musculus previously administered with sodium fluoride (NaF) using the Micronucleus test and the Comet assay. The extract was administrated orally in four different concentrations: 150, 300, 600, and 1200 mg/Kg for ten days. At the 11th day, a single dose of NaF was administrated via intraperitoneal at 20 mg/Kg. The genotoxicity study was performed with mice from the strain BALB/c, using the Micronucleus test on bone marrow and the Comet assay on peripheral blood according to OECD guidelines 474 and 489, respectively. The statistical analysis was performed by median analysis with ANOVA. Significant differences were found in Micronucleus frequency between the highest concentrations of Piper aduncum and NaF. The Comet assay showed significant reduction of NaF-induced damage on erythrocytes depending on the different concentrations of the extract which were evaluated in this study. It is concluded that the methanolic extract of P. aduncum leaves has cytoprotective and antioxidant activity against sodium fluoride. Full article
(This article belongs to the Section Toxicology and Public Health)
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Open AccessFeature PaperReview
Radiocarbon Tracers in Toxicology and Medicine: Recent Advances in Technology and Science
Received: 4 March 2019 / Revised: 30 April 2019 / Accepted: 6 May 2019 / Published: 9 May 2019
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Abstract
This review summarizes recent developments in radiocarbon tracer technology and applications. Technologies covered include accelerator mass spectrometry (AMS), including conversion of samples to graphite, and rapid combustion to carbon dioxide to enable direct liquid sample analysis, coupling to HPLC for real-time AMS analysis, [...] Read more.
This review summarizes recent developments in radiocarbon tracer technology and applications. Technologies covered include accelerator mass spectrometry (AMS), including conversion of samples to graphite, and rapid combustion to carbon dioxide to enable direct liquid sample analysis, coupling to HPLC for real-time AMS analysis, and combined molecular mass spectrometry and AMS for analyte identification and quantitation. Laser-based alternatives, such as cavity ring down spectrometry, are emerging to enable lower cost, higher throughput measurements of biological samples. Applications covered include radiocarbon dating, use of environmental atomic bomb pulse radiocarbon content for cell and protein age determination and turnover studies, and carbon source identification. Low dose toxicology applications reviewed include studies of naphthalene-DNA adduct formation, benzo[a]pyrene pharmacokinetics in humans, and triclocarban exposure and risk assessment. Cancer-related studies covered include the use of radiocarbon-labeled cells for better defining mechanisms of metastasis and the use of drug-DNA adducts as predictive biomarkers of response to chemotherapy. Full article
(This article belongs to the Special Issue Biomarkers of Environmental Toxicants)
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Open AccessArticle
The Associations between Immunological Reactivity to the Haptenation of Unconjugated Bisphenol A to Albumin and Protein Disulfide Isomerase with Alpha-Synuclein Antibodies
Received: 18 March 2019 / Revised: 30 April 2019 / Accepted: 2 May 2019 / Published: 6 May 2019
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Abstract
Patients with Parkinson’s disease (PD) have increased susceptibility to bisphenol A (BPA) exposure since they have an impaired biotransformation capacity to metabolize BPA. PD subjects have reduced levels of conjugated BPA compared to controls. Reduced ability to conjugate BPA provides increased opportunity for [...] Read more.
Patients with Parkinson’s disease (PD) have increased susceptibility to bisphenol A (BPA) exposure since they have an impaired biotransformation capacity to metabolize BPA. PD subjects have reduced levels of conjugated BPA compared to controls. Reduced ability to conjugate BPA provides increased opportunity for unconjugated BPA to bind to albumin in human serum and protein disulfide isomerase on neurons. Once unconjugated BPA binds to proteins, it changes the allosteric structure of the newly configured protein leading to protein misfolding and the ability of the newly configured protein to act as a neoantigen. Once this neoantigen is formed, the immune system produces antibodies against it. The goal of our research was to investigate associations between unconjugated BPA bound to human serum albumin (BPA–HSA) antibodies and alpha-synuclein antibodies and between Protein Disulfide Isomerase (PDI) antibodies and alpha-synuclein antibodies. Enzyme–linked immunosorbent assay was used to determine the occurrences of alpha-synuclein antibodies, antibodies to BPA–HSA adducts, and PDI antibodies in the sera of blood donors. Subjects that exhibited high levels of unconjugated BPA–HSA antibodies or PDI antibodies had correlations and substantial risk for also exhibiting high levels of alpha-synuclein antibodies (p < 0.0001). We conclude that there are significant associations and risks between antibodies to BPA–HSA adducts and PDI antibodies for developing alpha-synuclein antibodies. Full article
(This article belongs to the Special Issue Dietary Toxicants and Neurological Disease)
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Open AccessEditorial
Cadmium Sources and Toxicity
Received: 2 May 2019 / Accepted: 4 May 2019 / Published: 6 May 2019
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Abstract
This special issue of Toxics, Cadmium (Cd) sources and toxicity, consists of one comprehensive review [...] Full article
(This article belongs to the Special Issue Cadmium Sources and Toxicity)
Open AccessArticle
A Neurodevelopmental Model of Combined Pyrethroid and Chronic Stress Exposure
Received: 1 March 2019 / Revised: 26 April 2019 / Accepted: 30 April 2019 / Published: 2 May 2019
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Abstract
Attention-deficit hyperactivity disorder (ADHD) is one of the most common neurodevelopmental disorders of childhood and previous studies indicate the dopamine system plays a major role in ADHD pathogenesis. Two environmental exposures independently associated with dopaminergic dysfunction and ADHD risk include exposure to deltamethrin, [...] Read more.
Attention-deficit hyperactivity disorder (ADHD) is one of the most common neurodevelopmental disorders of childhood and previous studies indicate the dopamine system plays a major role in ADHD pathogenesis. Two environmental exposures independently associated with dopaminergic dysfunction and ADHD risk include exposure to deltamethrin, a pyrethroid insecticide, and chronic stress. We hypothesized that combined neurodevelopmental exposure to both deltamethrin and corticosterone (CORT), the major stress hormone in rodents, would result in additive changes within the dopamine system. To study this, we developed a novel dual exposure paradigm and exposed pregnant C57BL/6 dams to 3 mg/kg deltamethrin through gestation and weaning, and their offspring to 25 μg/mL CORT dissolved in the drinking water through adulthood. Midbrain RNA expression as well as striatal and cortical protein expression of key dopaminergic components were investigated, in addition to ADHD-like behavioral tasks and electrochemical dopamine dynamics via fast-scan cyclic voltammetry. Given the well-described sexual dimorphism of ADHD, males and females were assessed separately. Males exposed to deltamethrin had significantly decreased midbrain Pitx3 expression, decreased cortical tyrosine hydroxylase (TH) expression, increased activity in the Y maze, and increased dopamine uptake rate in the dorsal striatum. These effects did not occur in males exposed to CORT only, or in males exposed to both deltamethrin and CORT, suggesting that CORT may attenuate these effects. Additionally, deltamethrin- and CORT-exposed females did not display these dopaminergic features, which indicates these changes are sex-specific. Our results show dopaminergic changes from the RNA through the functional level. Moreover, these data illustrate the importance of testing multiple environmental exposures together to better understand how combined exposures that occur in certain vulnerable populations could affect similar neurodevelopmental systems, as well as the importance of studying sex differences of these alterations. Full article
(This article belongs to the collection Xenobiotics in Developmental Neurotoxicity)
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Open AccessArticle
Comparison of the Respiratory Toxicity and Total Cholinesterase Activities in Dimethyl Versus Diethyl Paraoxon-Poisoned Rats
Received: 26 February 2019 / Revised: 11 April 2019 / Accepted: 13 April 2019 / Published: 16 April 2019
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Abstract
The chemical structure of organophosphate compounds (OPs) is a well-known factor which modifies the acute toxicity of these compounds. We compared ventilation at rest and cholinesterase activities in male Sprague-Dawley rats poisoned with dimethyl paraoxon (DMPO) and diethyl paraoxon (DEPO) at a subcutaneous [...] Read more.
The chemical structure of organophosphate compounds (OPs) is a well-known factor which modifies the acute toxicity of these compounds. We compared ventilation at rest and cholinesterase activities in male Sprague-Dawley rats poisoned with dimethyl paraoxon (DMPO) and diethyl paraoxon (DEPO) at a subcutaneous dose corresponding to 50% of the median lethal dose (MLD). Ventilation at rest was recorded by whole body plethysmography. Total cholinesterase activities were determined by radiometric assay. Both organophosphates decreased significantly the respiratory rate, resulting from an increase in expiratory time. Dimethyl-induced respiratory toxicity spontaneously reversed within 120 min post-injection. Diethyl-induced respiratory toxicity was long-lasting, more than 180 min post-injection. Both organophosphates decreased cholinesterase activities from 10 to 180 min post-injection with the same degree of inhibition of total cholinesterase within an onset at the same times after injection. There were no significant differences in residual cholinesterase activities between dimethyl and diethyl paraoxon groups at any time. The structure of the alkoxy-group is a determinant factor of the late phase of poisoning, conditioning duration of toxicity without significant effects on the magnitude of alteration of respiratory parameters. For same duration and magnitude of cholinesterase inhibition, there was a strong discrepancy in the time-course of effects between the two compounds. Full article
(This article belongs to the Special Issue Toxicity of Chemical Mixtures)
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Open AccessCorrection
Correction: Takaoka, S., et al. Survey of the Extent of the Persisting Effects of Methylmercury Pollution on the Inhabitants around the Shiranui Sea, Japan. Toxics 2018, 6, 39
Received: 19 March 2019 / Accepted: 22 March 2019 / Published: 11 April 2019
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Abstract
The authors wish to make the following corrections to this paper [...] Full article
(This article belongs to the Special Issue Mercury and Methylmercury Toxicology and Risk Assessment)
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Open AccessReview
A Review of Biomonitoring of Phthalate Exposures
Received: 31 January 2019 / Revised: 27 March 2019 / Accepted: 29 March 2019 / Published: 5 April 2019
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Abstract
Phthalates (diesters of phthalic acid) are widely used as plasticizers and additives in many consumer products. Laboratory animal studies have reported the endocrine-disrupting and reproductive effects of phthalates, and human exposure to this class of chemicals is a concern. Several phthalates have been [...] Read more.
Phthalates (diesters of phthalic acid) are widely used as plasticizers and additives in many consumer products. Laboratory animal studies have reported the endocrine-disrupting and reproductive effects of phthalates, and human exposure to this class of chemicals is a concern. Several phthalates have been recognized as substances of high concern. Human exposure to phthalates occurs mainly via dietary sources, dermal absorption, and air inhalation. Phthalates are excreted as conjugated monoesters in urine, and some phthalates, such as di-2-ethylhexyl phthalate (DEHP), undergo secondary metabolism, including oxidative transformation, prior to urinary excretion. The occurrence of phthalates and their metabolites in urine, serum, breast milk, and semen has been widely reported. Urine has been the preferred matrix in human biomonitoring studies, and concentrations on the order of several tens to hundreds of nanograms per milliliter have been reported for several phthalate metabolites. Metabolites of diethyl phthalate (DEP), dibutyl- (DBP) and diisobutyl- (DiBP) phthalates, and DEHP were the most abundant compounds measured in urine. Temporal trends in phthalate exposures varied among countries. In the United States (US), DEHP exposure has declined since 2005, whereas DiNP exposure has increased. In China, DEHP exposure has increased since 2000. For many phthalates, exposures in children are higher than those in adults. Human epidemiological studies have shown a significant association between phthalate exposures and adverse reproductive outcomes in women and men, type II diabetes and insulin resistance, overweight/obesity, allergy, and asthma. This review compiles biomonitoring studies of phthalates and exposure doses to assess health risks from phthalate exposures in populations across the globe. Full article
(This article belongs to the Special Issue Biomarkers of Environmental Toxicants)
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Open AccessEditorial
Advances in Methylmercury Toxicology and Risk Assessment
Received: 19 March 2019 / Accepted: 22 March 2019 / Published: 1 April 2019
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Abstract
Mercury (Hg) is a global pollutant that affects the health of both humans and ecosystems [...] Full article
(This article belongs to the Special Issue Mercury and Methylmercury Toxicology and Risk Assessment)
Open AccessArticle
Protective Effects of Centella asiatica on Cognitive Deficits Induced by D-gal/AlCl3 via Inhibition of Oxidative Stress and Attenuation of Acetylcholinesterase Level
Received: 19 January 2019 / Revised: 6 March 2019 / Accepted: 8 March 2019 / Published: 30 March 2019
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Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder with cholinergic dysfunctions and impaired redox homeostasis. The plant Centella asiatica (CA) is renowned for its nutritional benefits and herbal formulas for promoting health, enhancing cognition, and its neuroprotective effects. The present study aims to [...] Read more.
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder with cholinergic dysfunctions and impaired redox homeostasis. The plant Centella asiatica (CA) is renowned for its nutritional benefits and herbal formulas for promoting health, enhancing cognition, and its neuroprotective effects. The present study aims to investigate the protective role of CA on D-gal/AlCl3-induced cognitive deficits in rats. The rats were divided into six groups and administered with donepezil 1 mg/kg/day, CA (200, 400, and 800 mg/kg/day) and D-gal 60 mg/kg/day + AlCl3 200 mg/kg/day for 10 weeks. The ethology of the rats was evaluated by the Morris water maze test. The levels of acetylcholinesterase (AChE), phosphorylated tau (P-tau), malondialdehyde (MDA) and activities of superoxide dismutase (SOD), in the hippocampus and cerebral cortex were estimated by enzyme-linked immunosorbent assay (ELISA). Additionally, the ultrastructure of the prefrontal cortex of the rats’ was observed using transmission electron microscopy (TEM). Rats administered with D-gal/AlCl3 exhibited cognitive deficits, decreased activities of SOD, and marked increase in AChE and MDA levels. Further, prominent alterations in the ultrastructure of the prefrontal cortex were observed. Conversely, co-administration of CA with D-gal/AlCl3 improved cognitive impairment, decreased AChE levels, attenuated the oxidative stress in hippocampus and cerebral cortex, and prevented ultrastructural alteration of neurons in the prefrontal cortex. Irrespective of the dose of CA administered, the protective effects were comparable to donepezil. In conclusion, this study suggests that CA attenuated the cognitive deficits in rats by restoring cholinergic function, attenuating oxidative stress, and preventing the morphological aberrations. Full article
(This article belongs to the Special Issue Toxicity of Chemical Mixtures)
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