Drug-induced diarrhea is a common adverse drug reaction, especially the one caused by the widespread use of antibiotics. The reduction of probiotics is one reason for intestinal disorders induced by an oral antibiotic. However, the intrinsic mechanism of drug-induced diarrhea is still unknown. In this study, we used metabolomics methods to explore the effects of the classic oral antibiotic, amoxicillin, on the growth and metabolism of Lactobacillus acidophilus, while scanning electron microscopy (SEM) and 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays were employed to evaluate changes in cell activity and morphology. The results showed that cell viability gradually decreased, while the degree of cell wall rupture increased, with increasing amoxicillin concentrations. A non-targeted metabolomics analysis identified 13 potential biomarkers associated with 9 metabolic pathways. The data showed that arginine and proline metabolism, nicotinate and nicotinamide metabolism, pyrimidine metabolism, glycine, serine and threonine metabolism, beta-alanine metabolism, glycerolipid metabolism, tryptophan metabolism, steroid hormone biosynthesis, and histidine metabolism may be involved in the different effects exerted by amoxicillin on L. acidophilus. This study provides potential targets for screening probiotics regulators and lays a theoretical foundation for the elucidation of their mechanisms.
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http://dx.doi.org/10.1038/s41429-022-00518-6 | DOI Listing |
Food Funct
January 2025
Acupuncture and Tuina School, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China.
Indole-3-propionic acid (IPA), a metabolite produced by gut microbiota through tryptophan metabolism, has recently been identified as playing a pivotal role in bone metabolism. IPA promotes osteoblast differentiation by upregulating mitochondrial transcription factor A (Tfam), contributing to increased bone density and supporting bone repair. Simultaneously, it inhibits the formation and activity of osteoclasts, reducing bone resorption, possibly through modulation of the nuclear factor-κB (NF-κB) pathway and downregulation of osteoclast-associated factors, thereby maintaining bone structural integrity.
View Article and Find Full Text PDFGenet Epidemiol
January 2025
Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston, Massachusetts, USA.
Large-scale gene-environment interaction (GxE) discovery efforts often involve analytical compromises for the sake of data harmonization and statistical power. Refinement of exposures, covariates, outcomes, and population subsets may be helpful to establish often-elusive replication and evaluate potential clinical utility. Here, we used additional datasets, an expanded set of statistical models, and interrogation of lipoprotein metabolism via nuclear magnetic resonance (NMR)-based lipoprotein subfractions to refine a previously discovered GxE modifying the relationship between physical activity (PA) and HDL-cholesterol (HDL-C).
View Article and Find Full Text PDFFree Radic Res
January 2025
Radiation Biology & Health Sciences Division, Bio-science Group, Bhabha Atomic Research Centre, Trombay, Mumbai-400085, India.
Free radicals have been implicated in the pathogenesis of cancer along with cardiovascular, neurodegenerative, pulmonary and inflammatory disorders. Further, the relationship between oxidative stress and disease is distinctively established. Clinical trials using anti-oxidants for the prevention of disease progression have indicated some beneficial effects.
View Article and Find Full Text PDFPer Med
January 2025
Department of Clinical Pharmacy, Zhejiang Provincial Key Laboratory for Drug Evaluation and Clinical Research, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Efforts have been made to leverage technology to accurately identify tumor characteristics and predict how each cancer patient may respond to medications. This involves collecting data from various sources such as genomic data, histological information, functional drug profiling, and drug metabolism using techniques like polymerase chain reaction, sanger sequencing, next-generation sequencing, fluorescence in situ hybridization, immunohistochemistry staining, patient-derived tumor xenograft models, patient-derived organoid models, and therapeutic drug monitoring. The utilization of diverse detection technologies in clinical practice has made "individualized treatment" possible, but the desired level of accuracy has not been fully attained yet.
View Article and Find Full Text PDFNMR Biomed
February 2025
Department of Biomedical Engineering, Yale University, New Haven, Connecticut, USA.
Cellular metabolism is inextricably linked to transmembrane levels of proton (H), sodium (Na), and potassium (K) ions. Although reduced sodium-potassium pump (Na-K ATPase) activity in tumors directly disturbs transmembrane Na and K levels, this dysfunction is a result of upregulated aerobic glycolysis generating excessive cytosolic H (and lactate) which are extruded to acidify the interstitial space. These oncogene-directed metabolic changes, affecting intracellular Na and H, can be further exacerbated by upregulation of ion exchangers/transporters.
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