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RDX (121-82-4)

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219 References Were Found:

Data/Software
Data/ Software

Hazardous Chemical Information System (HCIS). Exposure standard documentation: Cyclonite

Author: Safe Work Australia (2018) [Database] HERO ID: 4287214

[Less] Direct Link to RDX Entry: http://hcis.safeworkaustralia.gov.au/ExposureStandards/Details?exposureSta . . . [More] Direct Link to RDX Entry: http://hcis.safeworkaustralia.gov.au/ExposureStandards/Details?exposureStandardID=174

Data/Software
Data/ Software

ChemIDplus - a TOXNET database

Author: ChemIDplus (2018) National Institutes of Health, U.S. Library of Medicine. HERO ID: 4235826


Data/Software
Data/ Software

ChemIDplus - a TOXNET database

Author: NLM (2016) Bethesda, MD: National Institutes of Health, U.S. Library of Medicine. HERO ID: 2991424


Technical Report
Technical Report

Memorandum for National Center for Environmental Assessment (8101R/Dr. Louis D'Amico), U.S. EPA - Office of Research and Development, 1200 Pennsylvania Ave., NW, Washington, DC 20460. Subject: Additional data from the oral subchronic toxicity of RDX in rats, 2006. (Toxicology study no. 85-XC-5131-03), U.S. Army Center for Health Promotion and Preventative Medicine, Aberdeen Proving Ground, Maryland; Incidence of seizure relative to mortality events

Author: Johnson, MS (2015) (MCHB-IP-T). Aberdeen Proving Ground, MD: Department of the Army, US Army Institute of Public Health. HERO ID: 2804501


Technical Report
Technical Report

Memorandum for Office of Research and Development (NCEA/Dr. Louis D’Amico), National Center for Environmental Assessment, U.S. Environmental Protection Agency, Two Potomac Yard, 2733 South Crystal Drive, Arlington, VA 22202. Subject: Lack of evidence for GABAa receptor-mediated MOA of RDX-induced prostatitis

Author: Johnson, MS (2015) Aberdeen Proving Ground, MD: Department of the Armyu, U.S. Army Institute of Public Health. HERO ID: 2849970


Technical Report
Technical Report

RDX PBPK files in acsIX format

Author: U.S. EPA (2014) [PBPK] HERO ID: 2347176


The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
Peer Reviewed Journal Article

MicroRNA and messenger RNA profiling reveals new biomarkers and mechanisms for RDX induced neurotoxicity

Authors: Deng, Y; Ai, J; Guan, X; Wang, Z; Yan, B; Zhang, D; Liu, C; Wilbanks, MS; Escalon, BL; Meyers, SA; Yang, MQ; Perkins, EJ (2014) BMC Genomics 15 Suppl 11:S1. HERO ID: 2770411

[Less] BACKGROUND: RDX is a well-known pollutant to induce neurotoxicity. MicroRNAs (miRNA) and messenger RNA . . . [More] BACKGROUND: RDX is a well-known pollutant to induce neurotoxicity. MicroRNAs (miRNA) and messenger RNA (mRNA) profiles are useful tools for toxicogenomics studies. It is worthy to integrate MiRNA and mRNA expression data to understand RDX-induced neurotoxicity. RESULTS: Rats were treated with or without RDX for 48 h. Both miRNA and mRNA profiles were conducted using brain tissues. Nine miRNAs were significantly regulated by RDX. Of these, 6 and 3 miRNAs were up- and down-regulated respectively. The putative target genes of RDX-regulated miRNAs were highly nervous system function genes and pathways enriched. Fifteen differentially genes altered by RDX from mRNA profiles were the putative targets of regulated miRNAs. The induction of miR-71, miR-27ab, miR-98, and miR-135a expression by RDX, could reduce the expression of the genes POLE4, C5ORF13, SULF1 and ROCK2, and eventually induce neurotoxicity. Over-expression of miR-27ab, or reduction of the expression of unknown miRNAs by RDX, could up-regulate HMGCR expression and contribute to neurotoxicity. RDX regulated immune and inflammation response miRNAs and genes could contribute to RDX- induced neurotoxicity and other toxicities as well as animal defending reaction response to RDX exposure. CONCLUSIONS: Our results demonstrate that integrating miRNA and mRNA profiles is valuable to indentify novel biomarkers and molecular mechanisms for RDX-induced neurological disorder and neurotoxicity.

Data/Software
Data/ Software

Hazardous substances information system (HSIS). Exposure standard documentation: Cyclonite

Author: Safe Work Australia (2014) [Database] HERO ID: 3102203


The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
Peer Reviewed Journal Article

Role of GABAergic activity of sodium valproate against ischemia-reperfusion-induced acute kidney injury in rats

Authors: Brar, R; Singh, J; Kaur, T; Arora, S; Singh, A (2014) Naunyn-Schmiedeberg's Archives of Pharmacology 387:143-151. HERO ID: 2279439

[Less] Gamma amino butyric acid (GABA) has been reported to be renoprotective in various preclinical studies. . . . [More] Gamma amino butyric acid (GABA) has been reported to be renoprotective in various preclinical studies. Sodium valproate (SVP) is documented to protect against renal injury through its histone deacetylase-inhibiting activity. The present study investigated the involvement of GABAA receptors and the role of GABAergic activity of SVP against ischemia-reperfusion-induced acute kidney injury (AKI) in rats. The rats were subjected to bilateral renal ischemia for 40 min followed by reperfusion for 24 h to induce AKI. The creatinine clearance, serum urea, uric acid, lactate dehydrogenase, potassium, fractional excretion of sodium, and microproteinuria were measured to assess kidney injury. The thiobarbituric acid-reactive substances, reduced glutathione level, myeloperoxidase, and catalase activity were assayed to assess oxidative stress in renal tissues along with hematoxylin-eosin staining to observe histopathological changes. The ischemia-reperfusion-induced AKI witnessed an increase in serum parameters, microproteinuria, oxidative stress, and histopathological changes in renal tissues. Picrotoxin aggravated ischemia-reperfusion injury-induced AKI confirming the role of GABAA receptors in AKI. The SVP treatment afforded protection against AKI that was blocked by concurrent treatment with picrotoxin. Hence, it is concluded that regulation of GABAA receptors is important for management of AKI. Moreover, the GABAergic activity of SVP is important for its renoprotective effect.

The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
Peer Reviewed Journal Article

The relationship between chemical-induced kidney weight increases and kidney histopathology in rats

Authors: Craig, EA; Yan, Z; Zhao, QJ (2014) Journal of Applied Toxicology. HERO ID: 2823545

[Less] The kidney is a major site of chemical excretion, which results in its propensity to exhibit chemically-induced . . . [More] The kidney is a major site of chemical excretion, which results in its propensity to exhibit chemically-induced toxicological effects at a higher rate than most other organs. Although the kidneys are often weighed in animal toxicity studies, the manner in which these kidney weight measurements are interpreted and the value of this information in predicting renal damage remains controversial. In this study we sought to determine whether a relationship exists between chemically-induced kidney weight changes and renal histopathological alterations. We also examined the relative utility of absolute and relative (kidney-to-body weight ratio) kidney weight in the prediction of renal toxicity. For this, data extracted from oral chemical exposure studies in rats performed by the National Toxicology Program were qualitatively and quantitatively evaluated. Our analysis showed a statistically significant correlation between absolute, but not relative, kidney weight and renal histopathology in chemically-treated rats. This positive correlation between absolute kidney weight and histopathology was observed even with compounds that statistically decreased terminal body weight. Also, changes in absolute kidney weight, which occurred at subchronic exposures, were able to predict the presence or absence of kidney histopathology at both subchronic and chronic exposures. Furthermore, most increases in absolute kidney weight reaching statistical significance (irrespective of the magnitude of change) were found to be relevant for the prediction of histopathological changes. Hence, our findings demonstrate that the evaluation of absolute kidney weight is a useful method for identifying potential renal toxicants.