Database : MEDLINE
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[PMID]: 29524682
[Au] Autor:Ghosh K; N I
[Ad] Address:Unit of Toxicology, Department of Zoology, School of Life Sciences, Bharathiar University, Coimbatore, 641046, Tamil Nadu, India; Department of Zoology, Annamalai University, Annamalainagar, Chidambaram, 608002, Tamil Nadu, India. Electronic address: kavisa9@gmail.com.
[Ti] Title:Cadmium treatment induces echinocytosis, DNA damage, inflammation, and apoptosis in cardiac tissue of albino Wistar rats.
[So] Source:Environ Toxicol Pharmacol;59:43-52, 2018 Feb 27.
[Is] ISSN:1872-7077
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Cadmium (Cd), a potent carcinogen present in almost all foods, poses a major health risk to humans. Major routes of exposure to Cd for humans are occupation, diet, and tobacco use. Cd elicits various deleterious effects on cellular molecules mainly by causing oxidant-antioxidant imbalance. Cd has been implicated in the pathogenesis of many cancers, Itai-itai disease, diabetic nephropathy, hypertension, peripheral artery disease, and myocardial infarction. This study was designed to investigate the effects of Cd intake on erythrocytes and cardiac tissue in male albino Wistar rats. We treated male albino Wistar rats with cadmium chloride (CdCl ) by intra-gastric administration for 30 days and examined Cd burden and changes in blood constituents and antioxidant status of blood and cardiac tissue. We also studied the structural alterations in the erthrocytes, elemental changes and Cd burden in cardiac tissue using scanning electron microscope (SEM/EDX). Inflammation and apoptosis were analysed in the cardiac tissue by polymerase chain reaction (PCR), western blotting, and DNA fragmentation assay. Cd treatment resulted in echinocytosis of erythrocytes and distorted myofibrils arrangement, vacuolization and congestion in the vessels. Cd administration has also induced inflammation and apoptosis in the cardiac tissue. At molecular level, Cd administration caused oxidative damage to DNA, lipids, and proteins and diminished the activities of various antioxidants. The present study provides a compelling evidence of Cd-induced imbalance in oxidant-antioxidant system with damage to erythrocytes and cardiac tissue that may contribute to various cardiac diseases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 391181 MEDLINE  
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[PMID]: 29524515
[Au] Autor:Feduccia AA; Mithoefer MC
[Ad] Address:MAPS Public Benefit Corporation, United States. Electronic address: alli@mapsbcorp.com.
[Ti] Title:MDMA-assisted psychotherapy for PTSD: Are memory reconsolidation and fear extinction underlying mechanisms?
[So] Source:Prog Neuropsychopharmacol Biol Psychiatry;, 2018 Mar 07.
[Is] ISSN:1878-4216
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:MDMA-assisted psychotherapy for treatment of PTSD has recently progressed to Phase 3 clinical trials and received Breakthrough Therapy designation by the FDA. MDMA used as an adjunct during psychotherapy sessions has demonstrated effectiveness and acceptable safety in reducing PTSD symptoms in Phase 2 trials, with durable remission of PTSD diagnosis in 68% of participants. The underlying psychological and neurological mechanisms for the robust effects in mitigating PTSD are being investigated in animal models and in studies of healthy volunteers. This review explores the potential role of memory reconsolidation and fear extinction during MDMA-assisted psychotherapy. MDMA enhances release of monoamines (serotonin, norepinephrine, dopamine), hormones (oxytocin, cortisol), and other downstream signaling molecules (BDNF) to dynamically modulate emotional memory circuits. By reducing activation in brain regions implicated in the expression of fear- and anxiety-related behaviors, namely the amygdala and insula, and increasing connectivity between the amygdala and hippocampus, MDMA may allow for reprocessing of traumatic memories and emotional engagement with therapeutic processes. Based on the pharmacology of MDMA and the available translational literature of memory reconsolidation, fear learning, and PTSD, this review suggests a neurobiological rationale to explain, at least in part, the large effect sizes demonstrated for MDMA in treating PTSD.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 391181 MEDLINE  
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[PMID]: 29524504
[Au] Autor:Qiu F; Dong C; Liu Y; Shao X; Huang D; Han Y; Wang B; Liu Y; Huo R; Paulo P; Zhang Z; Zhao D; Chu WF
[Ad] Address:Department of Pharmacology (the State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, PR China.
[Ti] Title:Pharmacological inhibition of SUMO-1 with ginkgolic acid alleviates cardiac fibrosis induced by myocardial infarction in mice.
[So] Source:Toxicol Appl Pharmacol;, 2018 Mar 07.
[Is] ISSN:1096-0333
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND AND PURPOSE: Protein modification by small ubiquitin-like modifier (SUMO) plays a critical role in the pathogenesis of heart diseases. The present study was designed to determine whether ginkgolic acid (GA) as a SUMO-1 inhibitor exerts an inhibitory effect on cardiac fibrosis induced by myocardial infarction (MI). EXPERIMENTAL APPROACH: GA was delivered by osmotic pumps in MI mice. Masson staining, electron microscopy (EM) and echocardiography were used to assess cardiac fibrosis, ultrastructure and function. Expression of SUMO-1, PML, TGF-ß1 and Pin1 was measured with Western blot or Real-time PCR. Collagen content, cell viability and myofibroblast transformation were measured in neonatal mouse cardiac fibroblasts (NMCFs). Promyelocytic leukemia (PML) protein was over-expressed by plasmid transfection. KEY RESULTS: GA improved cardiac fibrosis and dysfunction, and decreased SUMO-1 expression in MI mice. GA (>20 µM) inhibited NMCF viability in a dose-dependent manner. Nontoxic GA (10 µM) restrained angiotensin II (Ang II)-induced myofibroblast transformation and collagen production. GA also inhibited expression of TGF-ß1 mRNA and protein in vitro and in vivo. GA suppressed PML SUMOylation and PML nuclear body (PML-NB) organization, and disrupted expression and recruitment of Pin1 (a positive regulator of TGF-ß1 mRNA), whereas over-expression of PML reversed that. CONCLUSIONS AND IMPLICATIONS: Inhibition of SUMO-1 by GA alleviated MI-induced heart dysfunction and fibrosis, and the SUMOylated PML/Pin1/TGF-ß1 pathway is crucial for GA-inhibited cardiac fibrosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524503
[Au] Autor:Huang H; Liu L; Li J; Zhu C; Xie X; Ao Y; Wang H
[Ad] Address:Department of Pharmacology, School of Basic Medical Sciences, Wuhan University, Wuhan 430071, China; Department of Pharmacy, Wuhan No. 1 Hospital, Wuhan 430022, China.
[Ti] Title:Autophagy as a compensation mechanism participates in ethanol-induced fetal adrenal dysfunction in female rats.
[So] Source:Toxicol Appl Pharmacol;, 2018 Mar 07.
[Is] ISSN:1096-0333
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Autophagy plays a vital role in embryonic development and cell differentiation. Our previous study demonstrated that prenatal ethanol exposure (PEE) resulted in intrauterine growth retardation (IUGR) and adrenal developmental toxicities in rat offspring. The present study focused on PEE-induced autophagy as an underlying mechanism and its biological significance in female fetal rats. Female fetuses in the PEE group exhibited lower body weights and suffered adrenal structural abnormalities compared to the controls. Cell proliferation was inhibited, the insulin-like growth factor 1 (IGF1) pathway was reduced, and autophagy was activated in the glands of female fetal rats. Ethanol increased the ratio of microtubule-associated protein light chain 3 beta-II (LC3ß-II) to LC3ß-I in vitro, and it reduced cortisol levels in time- and concentration-dependent manners in human adrenocortical carcinoma cells (NCI-H295A). Bafilomycin A1 inhibited autophagy, steroidogenic factor 1 (SF1) protein and steroidogenesis in the present study. Rapamycin with ethanol up-regulated autophagy and SF1 expression and activated steroidogenesis when compared with ethanol alone. In addition, ethanol inhibited IGF1 receptor (IGF1R) and phospho-mTOR (Ser2448) expression in a concentration-dependent manner. These results demonstrate that PEE activated autophagy in fetal adrenal glands, and the underlying mechanism may be associated with inhibition of the IGF1R/phospho-mTOR (Ser2448) pathway. Autophagy may be a compensatory mechanism for the PEE-induced inhibition of fetal adrenal steroidogenesis to maintain fetal adrenal development.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 391181 MEDLINE  
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[PMID]: 29524502
[Au] Autor:Nakagawa M; Uno S; Iriyama N; Matsunawa M; Makishima M; Takeuchi J; Tsuboi I; Hatta Y; Takei M
[Ad] Address:Division of Hematology and Rheumatology, Department of Medicine, Nihon University School of Medicine, 30-1 Oyaguchi-kamicho, Itabashi-ku, Tokyo 173-8610, Japan.
[Ti] Title:Combined treatment with benzo[a]pyrene and 1α,25-dihydroxyvitamin D induces expression of plasminogen activator inhibitor 1 in monocyte/macrophage-derived cells.
[So] Source:Toxicol Appl Pharmacol;, 2018 Mar 07.
[Is] ISSN:1096-0333
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Benzo[a]pyrene (BaP) is an environmental pollutant found in cigarette smoke and is implicated as a causative agent of tobacco-related diseases, such as arteriosclerosis. In contrast, vitamin D signaling, which is principally mediated by conversion of vitamin D to the active form, 1α,25-dihydroxyvitamin D [1,25(OH) D ], decreases cardiovascular disease risk. However, combined treatment with BaP and 1,25(OH) D enhances BaP toxicity, including BaP-DNA adduct formation. We further investigated the cross-talk between BaP and 1,25(OH) D signaling pathways, and found that combined treatment with these compounds induces mRNA and protein expression of plasminogen activator inhibitor 1 (PAI-1) in monocyte/macrophage-derived THP-1 and U937 cells. Protein synthesis inhibitor treatment did not inhibit induction of the PAI-1 gene (SERPINE1) in these cells. BaP plus 1,25(OH) D induced differentiation markers, inhibited cellular proliferation, and induced apoptosis and oxidative stress in these cells. Reactive oxygen species scavenger treatment suppressed apoptosis but not SERPINE1 induction in cells treated with BaP plus 1,25(OH) D . Thus, combined treatment with BaP and 1,25(OH) D induced SERPINE1 mRNA expression in these cells through a mechanism that does not require de novo protein synthesis or reactive oxygen species production. These findings suggest that induction of the proinflammatory factor PAI-1 plays a role in BaP toxicity. Interestingly, PAI-1 knockdown decreased expression of the cell surface antigen CD14, a monocytic differentiation marker, in THP-1 cells treated with BaP plus 1,25(OH) D . PAI-1 induction may also be related to a function of monocytes/macrophages in response to xenobiotic and vitamin D signaling.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 391181 MEDLINE  
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[PMID]: 29524501
[Au] Autor:Sachana M; Rolaki A; Bal-Price A
[Ad] Address:European Commission, Joint Research Centre, Ispra, Italy; Environment Health and Safety Division, Environment Directorate, Organisation for Economic Co-operation and Development (OECD), 2 rue André Pascal, 75775 Paris Cedex 16, France.
[Ti] Title:Development of the Adverse Outcome Pathway (AOP): Chronic binding of antagonist to N-methyl-d-aspartate receptors (NMDARs) during brain development induces impairment of learning and memory abilities of children.
[So] Source:Toxicol Appl Pharmacol;, 2018 Mar 07.
[Is] ISSN:1096-0333
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The Adverse Outcome Pathways (AOPs) are designed to provide mechanistic understanding of complex biological systems and pathways of toxicity that result in adverse outcomes (AOs) relevant to regulatory endpoints. AOP concept captures in a structured way the causal relationships resulting from initial chemical interaction with biological target(s) (molecular initiating event) to an AO manifested in individual organisms and/or populations through a sequential series of key events (KEs), which are cellular, anatomical and/or functional changes in biological processes. An AOP provides the mechanistic detail required to support chemical safety assessment, the development of alternative methods and the implementation of an integrated testing strategy. An example of the AOP relevant to developmental neurotoxicity (DNT) is described here following the requirements of information defined by the OECD Users' Handbook Supplement to the Guidance Document for developing and assessing AOPs. In this AOP, the binding of an antagonist to glutamate receptor N-methyl-d-aspartate (NMDAR) receptor is defined as MIE. This MIE triggers a cascade of cellular KEs including reduction of intracellular calcium levels, reduction of brain derived neurotrophic factor release, neuronal cell death, decreased glutamate presynaptic release and aberrant dendritic morphology. At organ level, the above mentioned KEs lead to decreased synaptogenesis and decreased neuronal network formation and function causing learning and memory deficit at organism level, which is defined as the AO. There are in vitro, in vivo and epidemiological data that support the described KEs and their causative relationships rendering this AOP relevant to DNT evaluation in the context of regulatory purposes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 391181 MEDLINE  
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[PMID]: 29524465
[Au] Autor:Chang S; Yang Z; Han N; Liu Z; Yin J
[Ad] Address:Development and Utilization Key Laboratory of Northeast Plant Materials, School of Traditional Chinese Materia, Shenyang Pharmaceutical University, Wenhua Road 103, Shenyang 110016, China.
[Ti] Title:The antithrombotic, anticoagulant activity and toxicity research of ambinine, an alkaloid from the tuber of Corydalis ambigua var. amurensis.
[So] Source:Regul Toxicol Pharmacol;, 2018 Mar 07.
[Is] ISSN:1096-0295
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Ambinine, the major alkaloid of the tuber of Corydalis ambigua var. amurensis, has protective effects on H C myocardial cells. In the present paper, we observed that ambinine demonstrates activities of both anticoagulation and thrombolysis in vitro by significantly degrading the blood clot and delaying the plasma recalcification time (PRT) in a dose-dependent manner (0.5-2 mg/mL). We further studied its safety profile of acute and subacute toxicity by repeated-dose intravenous injection. The median lethal dosage (LD ) of mice given by oral and intravenous administration of ambinine were approximate 800, 41.60 mg/kg, respectively. The acute toxicity research results suggested that compared with an intravenous administration, the oral route is safer to administer ambinine as the promising lead compound for thrombosis. In subacute toxicity research, when mice were given ambinine at doses of 1.40 and 2.10 mg/kg for 7 days by injection, significant alteration of the relative kidney weight, the relative liver weight and serum biochemistry parameters and marked histopathological changes of them were found.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  8 / 391181 MEDLINE  
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[PMID]: 29524394
[Au] Autor:Bairam AF; Rasool MI; Alherz FA; Abunnaja MS; El Daibani AA; Gohal SA; Kurogi K; Sakakibara Y; Suiko M; Liu MC
[Ad] Address:Department of Pharmacology, College of Pharmacy and Pharmaceutical Sciences, University of Toledo Health Science Campus, Toledo, OH 43614 USA; Department of Pharmacology, College of Pharmacy, University of Kufa, Najaf, Iraq.
[Ti] Title:Sulfation of Catecholamines and Serotonin by SULT1A3 Allozymes.
[So] Source:Biochem Pharmacol;, 2018 Mar 07.
[Is] ISSN:1873-2968
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Previous studies have demonstrated the involvement of sulfoconjugation in the metabolism of catecholamines and serotonin. The current study aimed to clarify the effects of single nucleotide polymorphisms (SNPs) of human SULT1A3 and SULT1A4 genes on the enzymatic characteristics of the sulfation of dopamine, epinephrine, norepinephrine and serotonin by SULT1A3 allozymes. Following a comprehensive search of different SULT1A3 and SULT1A4 genotypes, twelve non-synonymous (missense) coding SNPs (cSNPs) of SULT1A3/SULT1A4 were identified. cDNAs encoding the corresponding SULT1A3 allozymes, packaged in pGEX-2T vector were generated by site-directed mutagenesis. SULT1A3 allozymes were expressed, and purified. Purified SULT1A3 allozymes exhibited differential sulfating activity toward catecholamines and serotonin. Kinetic analyses demonstrated differences in both substrate affinity and catalytic efficiency of the SULT1A3 allozymes. Collectively, these findings provide useful information relevant to the differential metabolism of dopamine, epinephrine, norepinephrine and serotonin through sulfoconjugation in individuals having different SULT1A3/SULT1A4 genotypes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
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  9 / 391181 MEDLINE  
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[PMID]: 29524393
[Ti] Title:Preface for the "Diamond Jubilee Special Issue: Celebrating 60 Years of Excellence".
[So] Source:Biochem Pharmacol;, 2018 Mar 07.
[Is] ISSN:1873-2968
[Cp] Country of publication:England
[La] Language:eng
[Pt] Publication type:EDITORIAL
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  10 / 391181 MEDLINE  
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[PMID]: 29524386
[Au] Autor:Mohanty I; Parija SC; Suklabaidya S; Rattan S
[Ad] Address:Department of Medicine, Division of Gastroenterology and Hepatology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania; Department of Pharmacology and Toxicology, College of Veterinary Sciences and Animal Husbandry, Orissa University of Agriculture and Technology, Bh
[Ti] Title:Acidosis potentiates endothelium-dependent vasorelaxation and gap junction communication in the superior mesenteric artery.
[So] Source:Eur J Pharmacol;, 2018 Mar 07.
[Is] ISSN:1879-0712
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Extracellular pH is an important physiological determinant of vascular tone that is normally maintained within 7.35-7.45. Any change outside this range leads to severe pathological repercussions. We investigated the unknown effects of extracellular acidosis on relaxation in the superior mesenteric artery (SMA) of goat. SMA rings were employed to maintain isometric contractions at extracellular pH (pH ) 7.4 and 6.8. We analyzed the effect of acidosis (pH 6.8) compared to physiological pH (pH 7.4) on three signaling mediators of endothelium-dependent hyperpolarization: nitric oxide (NO), prostaglandin I (PGI ), and myoendothelial gap junctions (MEGJ). NO and cyclic guanosine monophosphate (cGMP) levels were compared between normal and acidic pH. Quantitative real-time PCR (qPCR) studies determined the change in expression of vascular connexin (Cx), Cx37, Cx40, and Cx43. Under acidosis, acetyl choline-induced relaxation was augmented in an endothelium-dependent manner via eNOS-NO-cGMP signaling. Conversely, at normal pH, acetyl choline-induced vasorelaxation was mediated primarily via COX-PGI pathway. The functional activity of MEGJ was increased under acidosis as evident from increased sensitivity of connexin blockers and upregulated gene and protein expression of connexins. In conclusion, acetyl choline-induced augmented vasorelaxation under acidosis is mediated by NOS-NO-cGMP, with a partial role of MEGJ as EDH mediators in the SMA. Present data suggest a novel role of connexin as therapeutic targets to attenuate the detrimental effect of acidosis on vascular tone.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher


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