ABSTRACT: Chemical Proportionality Experiment of B.subtilis with antibiotics & pesticides such as Sulfamethoxazole, sulfadimethoxine and asulam to look for potential biotransformation
Project description:Chemical Proportionality Experiment of B.subtilis with antibiotics & pesticides such as Sulfamethoxazole, sulfadimethoxine and asulam to look for potential biotransformation
Project description:Chemical Proportionality Experiment of B.subtilis and E.coli added with pooled antibiotics (Sulfamethoxazole, sulfadimethoxine, cyproconazole and asulam) to look for potential biotransformation.
Project description:Chemical Proportionality Experiment of B.subtilis and E.coli added with pooled antibiotics (Sulfamethoxazole, sulfadimethoxine, cyproconazole and asulam) to look for potential biotransformation.
Project description:RNA sequencing was performed on E. coli K12 MG1655 on three media (M9, CA-MHB, R10LB) treated with four antibiotics (Ciprofloxacin, Trimethoprim-sulfamethoxazole, Ceftriaxone, Meropenem) at their media-specific MIC90s
Project description:To assay every gene in the E. coli genome to identify those that contribute to increased or decreased susceptibility to the antibiotics trimethoprim and sulfamethoxazole. This will help to define more accurately those bacterial cell mechanisms that contribute to these phenomena and provide information that will contribute to the development of new antibiotics, or compounds or known antibiotics that synergise with those already in clinical use. Thus, this set of experiments confirmed that AZT, widely known for its antiviral activity, acts synergistically with trimehoprim.
Project description:Cell–cell junctions, including tight and adherens junctions, are critical for maintaining placental barrier integrity and ensuring proper maternal–fetal exchange. To investigate the impact of co-trimoxazole (CTX) as well as sulfamethoxazole (SMA) and trimethoprim (TMP) on these junctional networks, RNA sequencing was performed on BeWo placental cells exposed to non-cytotoxic concentrations of these three antibiotics for 24 h. Transcriptomic profiling revealed significant differential gene expression in sulfamethoxazole, trimethoprim and co-trimoxazole-treated cells compared to controls, with enrichment of ERK pathway that might be related to tight junctions, adherens junctions, and cell–cell adhesion. These alterations suggested disruption of placental barrier integrity. In addition, co-trimoxazole exposure was associated with activation of the ERK1/2 signaling cascade, reflected by downregulation of multiple dual-specificity phosphatase (DUSP) genes that normally suppress MAPK activity. Together, the RNA-seq findings indicate that CTX interferes with barrier-related gene networks and promotes ERK pathway activation, supporting its potential to compromise placental barrier function.
Project description:Xenobiotics are ubiquitous in the environment and modified abundantly in the human body by phase I and II metabolism. Liquid chromatography coupled to high resolution mass spectrometry is a powerful tool to investigate these biotransformation products. Here, we present a workflow based on stable isotope-assisted metabolomics and the bioinformatics tool MetExtract II for deciphering all measureable xenobiotic metabolites produced by human cells in vitro in an untargeted manner. The value of this workflow is demonstrated by the detailed investigation of the metabolism of deoxynivalenol (DON), an abundant food contaminant, in two cell models (HepG2, HT29). Detected known metabolites included DON-3-sulfate, DON-10-sulfonate, and DON-10-glutathione as well as DON-cysteine. Conjugation with amino acids and antibiotics was observed and confirmed for the first time. The approach allows for the generic and untargeted elucidation of human xenobiotic products in tissue culture. It may be easily applied to other fields of research including drug metabolism, personalized medicine and systems biology and serves to better understand the relevance of in vitro experiments.
Project description:Animals have developed extensive mechanisms of response to xenobiotic chemical attacks. Although recent genome surveys have suggested a broad conservation of the chemical defensome across metazoans, global gene expression responses to xenobiotics are not known in most invertebrates. Here, using high density tiling arrays with over 2 million probes, we explored genome-wide gene expression in the tunicate Oikopleura dioica in response to two model xenobiotic chemicals – the carcinogenic polycyclic aromatic hydrocarbon benzo[a]pyrene (BaP) the pharmaceutical compound Clofibrate (Clo). The genotoxic compound BaP induced xenobiotic biotransformation and oxidative stress responsive genes, as in vertebrates. Notable exceptions were genes of the aryl hydrocarbon receptor (AhR) signaling pathway. Clo also affected the expression of many biotransformation genes and markedly repressed genes involved in energy metabolism and muscle contraction pathways. Oikopleura appears to have basic defensome toolkit consisting of phase I, phase II and phase III biotransformation genes.
Project description:The response of antibiotic adapted resistant mutants of B. cenocepacia J2315 to antibiotic stress was investigated using expression profiling of three biological replicates and comparing the profiles to the J2315 parent control grown without antibiotics.<br>A reference design was used with Cy3 labeled genomic DNA of B. cenocepacia J2315 as common reference. Three test conditions with three biological replicates each were compared to three replicates of the control condition.<br>Test conditions: J2315-A grown in the presence of 250 ug per ml amikacin, J2315-M grown in the presence of 8 ug per ml meropenem and J2315-T grown in the presence of 60 ug per ml trimethoprim and 300 ug per ml sulfamethoxazole.<br>Control condition: J2315 parent strain grown without antibiotics.