In vitro Analysis of the Impact of Enrofloxacin Residues on the Human Intestinal Microbiota Using 1H-NMR Spectroscopy

2012 ◽  
Vol 22 (5) ◽  
pp. 317-325
Author(s):  
Youngbeom Ahn ◽  
Ji Young Jung ◽  
Yong Hyun Chung ◽  
Minho Chae ◽  
Che Ok Jeon ◽  
...  
Antibiotics ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 886
Author(s):  
Youngbeom Ahn ◽  
Ji Young Jung ◽  
Ohgew Kweon ◽  
Brian T. Veach ◽  
Sangeeta Khare ◽  
...  

Studying potential dietary exposure to antimicrobial drug residues via meat and dairy products is essential to ensure human health and consumer safety. When studying how antimicrobial residues in food impact the development of antimicrobial drug resistance and disrupt normal bacteria community structure in the intestine, there are diverse methodological challenges to overcome. In this study, traditional cultures and molecular analysis techniques were used to determine the effects of tetracycline at chronic subinhibitory exposure levels on human intestinal microbiota using an in vitro continuous flow bioreactor. Six bioreactor culture vessels containing human fecal suspensions were maintained at 37 °C for 7 days. After a steady state was achieved, the suspensions were dosed with 0, 0.015, 0.15, 1.5, 15, or 150 µg/mL tetracycline, respectively. Exposure to 150 µg/mL tetracycline resulted in a decrease of total anaerobic bacteria from 1.9 × 107 ± 0.3 × 107 down to 2 × 106 ± 0.8 × 106 CFU/mL. Dose-dependent effects of tetracycline were noted for perturbations of tetB and tetD gene expression and changes in acetate and propionate concentrations. Although no-observed-adverse-effect concentrations differed, depending on the traditional cultures and the molecular analysis techniques used, this in vitro continuous flow bioreactor study contributes to the knowledge base regarding the impact of chronic exposure of tetracycline on human intestinal microbiota.


Author(s):  
Spencer B. Chambers ◽  
Clare E. Padmore ◽  
Stacy Fan ◽  
Ruby Grewal ◽  
James Johnson ◽  
...  

1977 ◽  
Vol 66 (11) ◽  
pp. 1660-1662 ◽  
Author(s):  
H.L. Johnson ◽  
D.W. Thomas ◽  
M. Ellis ◽  
L. Cary ◽  
J.I. DeGraw

2002 ◽  
Vol 63 (4) ◽  
pp. 1538-1543 ◽  
Author(s):  
Jussi-Pekka Usenius ◽  
Pauli Vainio ◽  
Juha Hernesniemi ◽  
Risto A. Kauppinen

2018 ◽  
Vol 22 (2) ◽  
pp. 235-239
Author(s):  
O. B. Shevelev ◽  
M. P. Moshkin

Deviations in brain metabolism are the result of longterm pathological processes, which finally are manifested as symptoms of Parkinson’s or Alzheimer’s diseases or multiple sclerosis and other neuropathologies, as for example diabetic neuropathy. A deficiency of available energy for brain cells under neurodegenerative diseases is either developed due to age-dependent underexpression of genes that encode glycolytic enzymes or induced due to the uncoupling of oxidation and phosphorylation that could be mediated by inflammatory cytokines. Since the activity of many enzymes is under the control of adenosine triphosphate (ATP) or cofactors, such as nicotinamide adenine dinucleotide (NADH) and nicotinamide adenine dinucleotide phosphate (NADPH), energy deficiency can cause metabolic changes in brain tissue. Some clinical studies using proton nuclear magnetic resonance spectroscopy (1H NMR spectroscopy) revealed metabolic changes in brain tissue in patients with neurodegenerative diseases. However, data from different authors are quite contradictory, probably because of the complex genesis of metabolic disorders. In the present study, we tested the hypothesis of multidirectional changes in metabolism under the impact of the oxidation and phosphorylation uncoupler 2,4-dinitrophenol (2,4-DNP) and under the impact of 2-deoxy-Dglucose (2-DG), blocking the access of glucose to the brain cells. 1H NMR spectroscopy showed that 2-DG leads to the predominance of excitatory (glutamine + glutamate) neurotransmitters over inhibitory ones (gamma-aminobutyric acid), and 2,4 DNP causes opposite effects. The biochemical mechanisms of the observed changes require a special study, but it can be noted that the ATP deficiency caused by inhibition of glycolysis and the ATP deficiency caused by the uncouplers are accompanied by differently directed changes in the intensity of the tricarboxylic acid cycle. These changes in the intensity of the Krebs cycle are correlated with differently directed changes in the balance of the exciting and inhibitory neurotransmitters. The obtained results show that 1H NMR spectroscopy can be an effective method of differentiated lifetime assessment of the available energy deficit caused by a general suppression of energy exchange in nerve cells or oxidation and phosphorylation uncoupling.


1999 ◽  
Vol 45 (4) ◽  
pp. 459-464 ◽  
Author(s):  
Sytske H Moolenaar ◽  
Jo Poggi-Bach ◽  
Udo FH Engelke ◽  
Jacqueline MB Corstiaensen ◽  
Arend Heerschap ◽  
...  

Abstract Background: A38-year-old man presented with a history of fish odor (since age 5) and unusual muscle fatigue with increased serum creatine kinase. Our aim was to identify the metabolic error in this new condition. Methods: We used 1H NMR spectroscopy to study serum and urine from the patient. Results: The concentration of N,N-dimethylglycine (DMG) was increased ∼100-fold in the serum and ∼20-fold in the urine. The presence of DMG as a storage product was confirmed by use of 13C NMR spectroscopy and gas chromatography–mass spectrometry. The high concentration of DMG was caused by a deficiency of the enzyme dimethylglycine dehydrogenase (DMGDH). A homozygous missense mutation was found in the DMGDH gene of the patient. Conclusions: DMGDH deficiency must be added to the differential diagnosis of patients complaining of a fish odor. This deficiency is the first inborn error of metabolism discovered by use of in vitro 1H NMR spectroscopy of body fluids.


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