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In vitro transcriptomic responses to thioacetamide-S-oxide exposure in Sprague-Dawley rat primary hepatocytes, renal tube epithelial, and cardiomyocytes

ABSTRACT: In this study we tested the ability to predict organ injury endpoints from in vitro transcriptomics responses at early time points (9 and 24 hours) after to thioacetamide-S-oxide treatment, the toxic metabolite of thioacetamide. Thioacetamide, an organosulfur compound, have been extensively used in animal studies as a hepatotoxin and carcinogen for its ability to cause acute liver damage.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE134569 | GEO | 2019/11/19

REPOSITORIES: GEO

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In vitro transcriptomic responses to thioacetamide-S-oxide exposure in human primary hepatocytes, renal tube epithelial, and cardiomyocytes

Project description:In this study we tested the ability to predict organ injury endpoints from in vitro transcriptomics responses at early time points (9 and 24 hours) after to thioacetamide-S-oxide treatment, the toxic metabolite of thioacetamide. Thioacetamide, an organosulfur compound, have been extensively used in animal studies as a hepatotoxin and carcinogen for its ability to cause acute liver damage.

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In vitro transcriptomic responses to thioacetamide-S-oxide exposure in Sprague-Dawley rat primary hepatocytes, renal tube epithelial, and cardiomyocytes

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Pulmonary toxicity of inhaled nano-sized cerium oxide aerosols in Sprague-Dawley rats.

Project description:Cerium oxide nanoparticles (CeO2NPs), used in some diesel fuel additives to improve fuel combustion efficiency and exhaust filter operation, have been detected in ambient air and concerns have been raised about their potential human health impact. The majority of CeO2NP inhalation studies undertaken to date have used aerosol particles of larger sizes than the evidence suggests are emitted from vehicles using such fuel additives. Hence, the objective of this study was to investigate the effects of inhaled CeO2NP aerosols of a more environmentally relevant size, utilizing a combination of methods, including untargeted multi-omics to enable the broadest possible survey of molecular responses and synchrotron X-ray spectroscopy to investigate cerium speciation. Male Sprague-Dawley rats were exposed by nose-only inhalation to aerosolized CeO2NPs (mass concentration 1.8 mg/m3, aerosol count median diameter 40 nm) for 3 h/d for 4 d/week, for 1 or 2 weeks and sacrificed at 3 and 7 d post-exposure. Markers of inflammation changed significantly in a dose- and time-dependent manner, which, combined with results from lung histopathology and gene expression analyses suggest an inflammatory response greater than that seen in studies using micron-sized ceria aerosols. Lipidomics of lung tissue revealed changes to minor lipid species, implying specific rather than general cellular effects. Cerium speciation analysis indicated a change in Ce3+/Ce4+ ratio within lung tissue. Collectively, these results in conjunction with earlier studies emphasize the importance of aerosol particle size on toxicity determination. Furthermore, the limited effect resolution within 7 d suggested the possibility of longer-term effects.

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The identification of putative circulating miRNA biomarkers of Thioacetamide-induced hepatotoxicity.

Project description:The Thioacetamide-treated rat was first identified as a model of hepatotoxicity by Gupta in 1956 and is now well-established, not least because the histopathogical output closely mimics that seen in humans with chronic liver disease. Acute treatment of rats with Thioacetamide causes pronounced necrosis and inflammation. Animals received intraperitoneal (ip) doses of vehicle-only (0.9% (v/v) saline) (n=3), or 100 mg/kg Thioacetamide (n=3) and were sacrificed after 24 hours. Blood was withdrawn via the descending vena cava and immediately transferred into potassium/EDTA tubes. Following centrifugation (16,100g, 4M-BM-0C, 5 min) the plasma was collected and stored at -80M-BM-0C. miRNA microarray profiling of RNA extracted from the plasma of rats treated with Thioacetamide revealed that a subset of miRNAs were differentially expressed following treatment. These miRNAs appeared to mediate pathways involved in hepatic fibrosis and stellate cell activation, suggesting that they might function as predictive biomarkers following compound-induced hepatotoxicity. The changes correlated well with increases in ALT levels, which are the current gold standard method for determining the extent of liver injury. Furthermore, it is hypothesised that particular aetiologies of liver damage might cause differing expression profiles of miRNAs, thus certain miRNAs could be implemented in a panel-type expression study to distinguish between different types of hepatic injury. Single channel miRNA microarrays were performed on n= 3 samples, 2 treatment groups; control and test. Control animals received vehicle-only (0.9% (v/v) saline) via the ip route. Test animals received 100 mg/kg Thioacetamide dissolved in 0.9% (v/v) saline, via the ip route. 24 h after dosing animals were sacrificed using decapitation under terminal anaesthesia.

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Pulmonary Responses of Sprague-Dawley Rats in Single Inhalation Exposure to Graphene Oxide Nanomaterials.

Project description:Graphene is receiving increased attention due to its potential widespread applications in future. However, the health effects of graphene have not yet been well studied. Therefore, this study examined the pulmonary effects of graphene oxide using male Sprague-Dawley rats and a single 6-hour nose-only inhalation technique. Following the exposure, the rats were allowed to recover for 1 day, 7 days, or 14 days. A total of three groups were compared: control (fresh air), low concentration (0.46 ± 0.06 mg/m(3)), and high concentration (3.76 ± 0.24 mg/m(3)). The exposure to graphene oxide did not induce significant changes in the body weights, organ weights, and food consumption during the 14 days of recovery time. The microalbumin and lactate dehydrogenase levels in the bronchoalveolar lavage (BAL) fluid were not significantly changed due to the exposure. Similarly, total cell count, macrophages, polymorphonuclear leukocytes, and lymphocytes were not significantly altered in the BAL fluid. Plus, the histopathological examination of the rat lungs only showed an uptake of graphene oxide in the alveolar macrophages of the high-concentration group. Therefore, these results demonstrate that the single inhalation exposure to graphene oxide induce minimal toxic responses in rat lungs at the concentrations and time points used in the present study.

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Project description:The aim is to characterize rat liver fibrosis induced by thioacetamide (TAA). To induce hepatic fibrosis, Male Sprague Dawley rats (9-12 weeks of age and 380-420 g of weight upon arrival, supplied by Beijing Vital River laboratory animal Co., Ltd.) were treated with thioacetamide (TAA). Rat liver samples were collected from five groups of rats at week 1, 2, 4, 8 and 13 after TAA (300 mg/kg) administration three times per week while five control groups receive the same volume of 0.9% normal saline. Four biological replicates were used for each group.

2021-09-29 | E-MTAB-10547 | biostudies-arrayexpress

Spleen data: Cerium oxide nanoparticles attenuate polymicrobial sepsis induced spenic damage in male Sprague Dawley rats.

Project description:Sepsis is a serious life threatening medical emergency which, if not treated properly, oftentimes results in organ failure and death. Current sepsis treatment protocols are largely centered on the use of antibiotics and supportive care. Recent studies have suggested that antibiotics fail to be effective for sepsis treatment when administered during hypo-dynamic phase of sepsis that is usually characterized by the presence of a cytokine storm. As such, there is an urgent need to develop novel therapeutic drugs that target the inflammatory cytokines that are secreted as a result of increased reactive oxygen species. Cerium oxide nanoparticles (CeO2) have been shown to act as anti-inflammatory and anti-oxidant agent. More recently, they have been shown to attenuate polymicrobial insult-induced mortality in Sprague Dawley rats. Here, we investigated whether CeO2 nanoparticles can attenuate splenic damage in this animal model of sepsis. A single intravenous dose (0.5 mg/kg) of CeO2 nanoparticles attenuated the sepsis-induced loss in splenic cell structural integrity. These improvements in splenic structure were accompanied by a decrease in expression of late phase pro-inflammatory cytokine high mobility group box 1 (HMGB1) along with reduced bacterial load in the blood and peritoneal fluid of septic animals. Taken together these findings suggest that CeO2 nanoparticles can be used to attenuate polymicrobial insult-induced splenic damage in Sprague dawley rats.

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