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Metronidazole
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Metronidazole is a prodrug that diffuses into the cell and in the low oxidation–reduction (redox) potential environments of anaerobic bacteria and protozoa, it is activated by reduction of (i.e. acceptance of electrons by) its nitro group. This process occurs as a single reduction step and involves the transfer of one electon. The source of electrons is the pyruvate oxidase or POR complex, which decarboxylates pyruvate, generating electrons that are passed onto ferredoxin and flavodoxin (Edwards, 1993b; Reysset, 1996). This biochemical reaction probably creates a gradient which promotes further uptake of the drug into anaerobic organisms. A product of metronidazole reduction is the anionic nitro radical, which is toxic. It binds to DNA, producing DNA strand breakage and thus cell death (Edwards, 1979; Edwards, 1993b). Sigeti et al. (1983) showed that metronidazole was rapidly bactericidal against B. fragilis by an immediate inhibition of DNA synthesis.
Growth of Porphyromonas gingivalis on human serum albumin triggers programmed cell death
Published in Journal of Oral Microbiology, 2023
Shirin Ghods, M. Fata Moradali, Danielle Duryea, Alejandro R. Walker, Mary E. Davey
As shown in Supplemental Table S2, asRNAs corresponding to the two iron-related gene products involved in oxidative stress discussed above [ferredoxin (PG1421) and rubrerythrin (PG0195)], along with PG1615 and PG1617 (putatively involved in succinate metabolism) and PG0537 (aminoacyl-histidine dipeptidase) were found to be highly expressed (up to 10.5-fold; q-value <0.01) during the exponential phase of W83 when compared with the same growth time-point of W50 cells and the corresponding genes (PG1421, PG0195, PG1615, PG1617, and PG0537) were also detected at higher levels, suggesting that the asRNA may support stability of these transcripts. In contrast, the initiation of W83 cell lysis in comparison to its late exponential phase was concomitant with more than twofold lower expression levels of a suite of asRNAs (27 transcripts) (Supplemental Table S2). Importantly, asRNAs detected at the lowest levels (by up to 10 times, q-value <0.01) in the early lysis phase of W83 cells correspond to the genes encoding HmuY (PG1551; heme-binding and iron acquisition), flavodoxin (PG1858; electron transport system), a predicted subunit K of v-type ATPase (PG1807; bioenergetics), aminoacyl-histidine dipeptidase/carnosinase PepD (PG0137), FabD (PG0138; fatty acid and phospholipid biosynthesis), and the arginine-specific gingipain RgpB (PG0506; nutrient acquisition).
Antiviral drugs and plasma therapy used for Covid-19 treatment: a nationwide Turkish algorithm
Published in Drug Metabolism Reviews, 2020
The mechanism of action of the drug Nitazoxanide is believed to be due to the interaction with the pyruvate: ferredoxin oxidoreductase (PFOR) enzyme-dependent electron transfer reaction, which is necessary for anaerobic energy metabolism. The most accepted hypothesis in the mechanism of action of the drug Nitazoxanide is that pyruvate: ferredoxin/flavodoxin oxidoreductase (PFOR) disrupts the energy metabolism in the cycle and inactivates anaerobic microorganisms (Broekhuysen et al. 2000). Nitazoxanide drug is active in vitro against both facultatively anaerobic gram positive and gram negative bacteria. It is also active against Mycobacterium tuberculosis replica and non-replicated strains (Dubreuil et al. 1996). It has been suggested to act on parasitic-protozoa and anaerobic bacteria by inducing lesions in Nitazoxanide cell membranes and by storing the mitochondrial membrane while inhibiting the enzymes of quinone oxidoreductase (NQO1), nitroreductase-1 and protein disulfide isomerase enzymes (Dubreuil et al. 1996). Nitazoxanide stops viral replication by activating the eukaryotic translation initiation factor 2a by inhibiting it in the first phase of the viral transcription factor. In addition, its effectiveness has been determined on tumor cells (Shakya et al. 2018).
Multidrug resistance in Helicobacter pylori: current state and future directions
Published in Expert Review of Clinical Pharmacology, 2019
Lyudmila Boyanova, Petyo Hadzhiyski, Nayden Kandilarov, Rumyana Markovska, Ivan Mitov
So far, no eradication therapy can provide high (>90%) eradiation rates. The most effective treatment regimen appropriate against MDR strains has been bismuth-containing quadruple therapy, however bismuth preparations are not available everywhere. New antibiotics with high anti-H. pylori activity should be developed and studies on sitafloxacin-based therapy should be continued. Evaluation of newer antibiotics such as delafloxacin as well as anti-H. pylori activity of flavodoxin inhibitors merit both in vitro and clinical evaluation. Dual and triple vonoprazan-based regimens have successfully been used in Japan; nevertheless, their benefits should be determined in more countries. Studies on antibiotic adjuvants such as bacteriocin-producing probiotics, N-acetylcysteine and plant extracts should continue and combination of some non-antibiotic agents may be useful.