Anaerobic Biomass from AnSBBR reactor treating synthetic sanitary sewage containing ibuprofen, diclofenac, and caffeine.
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PROVIDER: PRJNA1303184 | ENA |
REPOSITORIES: ENA
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Project description:Proteasomes hydrolyze most intracellular proteins. Immunoproteasome is a specific form of proteasome implicated in inflammation, cancer and autoimmune diseases. Modulation of immunoproteasome activity and content is a promising direction for the management of socially important pathologies. Using previously obtained reporter colorectal cancer cell lines, we tested how various commonly used compounds including ibuprofen, acetylsalicylic acid, vitamin C, caffeine and others, affect immunoproteasome expression. Methods: Immunoproteasome subunit expression was assessed by flow cytometry, qPCR and Western blot. Proteasome activity was tested using fluorogenic substrates and the activity probe. Transcriptome analysis was performed to identify patterns of gene expression changes. Results: Among the tested compounds caffeine was the only drug that revealed modest reduction in quantity of immunoproteasomes. The effect of caffeine on immunoproteasomes varied between cell lines and was stronger as a result of prolonged treatment. The reduction of immunoproteasome content in cells treated with caffeine coincided with decreased expression of immunoproteasome subunits and downregulation of Nrf3 transcription factor and a PAC4 proteasome assembly chaperone. Moreover, decreased expression of immunoproteasome subunits in cells treated with caffeine coincided with the reduction of oxidative stress levels. Caffeine did not affect the degradation of immunoproteasomes by autophagy. Conclusions: Modulation of immunoproteasome expression by caffeine might help to optimize existing and develop novel strategies for the treatment of colorectal cancer and several autoimmune diseases.
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Project description:The endocrine disrupting pharmaceuticals, non-steroidal anti-inflammatory drugs (NSAIDs) and 17α-ethinyl-estradiol (EE2), are among the most relevant molecules found in aquatic ecosystems, surface and drinking water due to their incomplete removal by wastewater treatment plants. Exposure to therapeutic doses has a negative impact on gonadal development and fertility in rodent models; however, the effects of their chronic exposure at lower doses are not known. In this study, we investigated the impact of chronic exposure to a mixture containing ibuprofen, 2hydroxy-ibuprofen, diclofenac, and EE2 at two environmentally relevant doses (added to the drinking water from fetal life, 8.5 dpc, until puberty) on the reproductive tract in F1 exposed mice and their F2 offspring. In F1 animals, exposure delayed male puberty and accelerated female puberty. In post-pubertal F1 testes and ovaries, differentiation/maturation of the different gonad cell types was altered, and some of these modifications were observed also in the non-exposed F2 generation. Transcriptomic analysis of post-pubertal testes and ovaries of F1 (exposed) and F2 animals revealed significant changes in gene expression profiles and enriched pathways, particularly the inflammasome, metabolism and extracellular matrix pathways, compared with controls (non-exposed). This suggested that exposure to these drug cocktails has an inter-generational impact (Int. J. Mol. Sci. 2023, 24, 5890. /doi: 10.3390/ijms24065890)
2024-09-01 | GSE235586 | GEO
Project description:The endocrine disrupting pharmaceuticals, non-steroidal anti-inflammatory drugs (NSAIDs) and 17α-ethinyl-estradiol (EE2), are among the most relevant molecules found in aquatic ecosystems, surface and drinking water due to their incomplete removal by wastewater treatment plants. Exposure to therapeutic doses has a negative impact on gonadal development and fertility in rodent models; however, the effects of their chronic exposure at lower doses are not known. In this study, we investigated the impact of chronic exposure to a mixture containing ibuprofen, 2hydroxy-ibuprofen, diclofenac, and EE2 at two environmentally relevant doses (added to the drinking water from fetal life, 8.5 dpc, until sexual maturity) on the reproductive tract in F1 exposed mice and their F2 offspring. In adult F1 and F2 animals, chronic exposure to low environmental doses of IBU, 2hydroxy-IBU, DCF, and EE2 mixtures, affected reproductive organ maturation, estrous cyclicity (in females), spermiogenesis (in males), and some sperm parameters in F2 males. Transcriptomics further revealed significant changes in gene expression patterns and associated pathways, underlying the modified mechanisms on testis and ovarian physiology and on germ cells, the precursors of gametes. Consequently, fertility of F1 male and female animals exposed to the higher dose of pharmaceuticals and that of their F2 offsprings, measured through the total number of pups and the time between litters, was affected after 5 months of age. This suggested that exposure to these drug cocktails has an inter-generational impact.
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Project description:Diclofenac is a widely used analgesic drug that can cause serious adverse drug reactions. We used Saccharomyces cerevisiae as model eukaryote to elucidate the molecular mechanisms of diclofenac toxicity and resistance. Although most yeast cells died during initial diclofenac treatment, some survived and started growing again. Microarray analysis of the adapted cells identified three major processes involved in diclofenac detoxification and tolerance. Especially pleiotropic drug resistance genes and genes under control of Rlm1p, a transcription factor in the protein kinase C (PKC) pathway, were upregulated in diclofenac-adapted cells. Genes involved in ribosome biogenesis and rRNA processing were downregulated, as well as zinc-responsive genes.
2011-05-17 | GSE29331 | GEO
Project description:Diclofenac is widely used as nonsteroidal anti-inflammatory drug leaving residues in the environment. To investigate effects on terrestrial ecosystems, we measured dissipation rate in soil and investigated ecotoxicological and transcriptome-wide responses in Folsomia candida. Exposure for 4 weeks to diclofenac reduced both survival and reproduction of F. candida in a dose-dependent manner. At concentrations ≥200 mg/kg soil diclofenac remained stable in the soil during a 21-day incubation period. Microarrays examined transcriptional changes at low and high diclofenac exposure concentrations. The results indicated that development and growth were severely hampered and immunity-related genes, mainly directed against bacteria and fungi, were significantly up-regulated. Furthermore, neural metabolic processes were significantly affected only at the high concentration. We conclude that diclofenac is toxic to non-target soil invertebrates, although its mode of action is different from the mammalian toxicity. The genetic markers proposed in this study may be promising early markers for diclofenac ecotoxicity.
2014-10-01 | GSE59589 | GEO
Project description:Ibuprofen is one of the most commonly detected pharmaceuticals in wastewater effluent; however the effects of ibuprofen on aquatic organisms are poorly understood. This study presents the transcriptome-wide response of the inland silverside, Menidia beryllina, to chronic 14 d exposures to ibuprofen.
2015-09-01 | GSE64967 | GEO
Project description:Transcriptional profiling of small intestinal explants cultured in the absence or in the presence of Ibuprofen (100 µM). Two-condition experiment, control intestinal explants vs Ibuprofen intestinal explants
2019-01-07 | GSE108369 | GEO
Project description:Gene expression analysis of diclofenac-treated rat cardiomyocytes vs non-treated rat cardiomyocytes. Goal of study is to identify changes on genes expression induced by diclofenac. The data analysis focused on genes that might be related to cardiotoxicity; genes expression ion channels and pathways.
2016-02-13 | GSE77880 | GEO
Project description:Ibuprofen is one of the most commonly detected pharmaceuticals in wastewater effluent; however the effects of ibuprofen on aquatic organisms are poorly understood. This study presents the transcriptome-wide response of the inland silverside, Menidia beryllina, to chronic 14 d exposures to ibuprofen. Twenty-four samples were run on twenty-four arrays, there were six replicates for each of three ibuprofen exposure concentrations and a control group.
2015-09-01 | E-GEOD-64967 | biostudies-arrayexpress
Project description:Diclofenac is a widely used analgesic drug that can cause serious adverse drug reactions. We used Saccharomyces cerevisiae as model eukaryote to elucidate the molecular mechanisms of diclofenac toxicity and resistance. Although most yeast cells died during initial diclofenac treatment, some survived and started growing again. Microarray analysis of the adapted cells identified three major processes involved in diclofenac detoxification and tolerance. Especially pleiotropic drug resistance genes and genes under control of Rlm1p, a transcription factor in the protein kinase C (PKC) pathway, were upregulated in diclofenac-adapted cells. Genes involved in ribosome biogenesis and rRNA processing were downregulated, as well as zinc-responsive genes. Five independent yeast cultures were incubated with 100 µM diclofenac for 75 hours. Every 24h, cultures were diluted to OD600 ~0.1 in YNB containing 100 µM diclofenac. Five independent control cultures were grown in the absence of diclofenac.
2011-05-17 | E-GEOD-29331 | biostudies-arrayexpress