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Cellular and Molecular Mechanisms of Ischemic Acute Renal Failure and Repair
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Joseph V. Bonventre, Ralph Witzgall
Some bacteria are well suited to a hypoxic environment, and it is likely that some of the genetic features characterizing their response to hypoxia will have homologs in higher organisms. Escherichia coli, as a facultative anaerobic bacterium, can use O2 as electron acceptor, but can also use other substrates such as fumarate or nitrate (see Haddock and Jones, 1977, for a review). FNR, the product of the fnr-gene, is essential for the bacteria to grow under anaerobic conditions (Shaw and Guest, 1982a). The gene has been cloned and sequenced and was shown to exhibit homologies with other E. coli transcriptional regulator proteins (Shaw and Guest, 1982b). Organisms overexpressing this gene overproduce fumarate reductase. Thus the gene product functions as a positive regulator for expression of anaerobic energy-generating systems.
An Overview of Helminthiasis
Published in Venkatesan Jayaprakash, Daniele Castagnolo, Yusuf Özkay, Medicinal Chemistry of Neglected and Tropical Diseases, 2019
Leyla Yurttaș, Betül Kaya Çavușoğlu, Derya Osmaniye, Ulviye Acar Çevik
Thiabendazole (3) was the first broad spectrum benzimidazole anthelmintic drug and it was introduced in the market 1961. Thiabendazole inhibits the helminth-specific mitochondrial fumarate reductase. The other effect of thiabendazole is to bind selectively to parasite β-tubulin and prevent microtubule formation. Thiabendazole is an effective oral drug and it is generally used in the treatment of strongyloidiasis, trichinosis, visceral larva migrans and cutaneous larva migrans (Martin et al. 1997, Köhler 2001, Finch et al. 2010).
Thiabendazole and Flubendazole
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
Although the exact mechanism of anthelmintic activity of thiabendazole has not been fully elucidated, it is likely that its mode of action is similar to that of other benzimidazole drugs, namely inhibition of polymerization of parasite beta-tubulin (see Chapter 200, Albendazole). The drug has been shown to inhibit the helminth-specific enzyme fumarate reductase (Criado et al., 1987). In animals, thiabendazole has anti-inflammatory, antipyretic, and analgesic effects, which may explain its usefulness in dracunculiasis and trichinosis.
Identification of a growth factor required for culturing specific fastidious oral bacteria
Published in Journal of Oral Microbiology, 2023
Pallavi Murugkar, Eric Dimise, Eric Stewart, Stéphane N. Viala, Jon Clardy, Floyd E. Dewhirst, Kim Lewis
The role of quinones in an electron transport chain is most well known in aerobic organisms where electrons and hydrogen are transferred to O2, producing H2O. The role of menaquinones in anaerobic bacteria is also important so that they can respire using other electron acceptors such as nitrate, sulfate FeIII, or fumarate. A key role of menaquinone in Porphyromonas is the reduction of fumarate to succinate using the enzyme fumarate reductase (quinol) flavoprotein [34]. P. pasteri strains KLE1280, F0450 and JCM 30531 all possess fumarate reductase (quinol) flavoprotein (frdA) proteins KDU78448, EJU17319, and GGM57237, respectively. The gene appears to be present in all P. gingivalis strains and Porphyromonas species examined. The pool of fumarate available for reduction likely comes from the action of aspartate ammonia-lyase on the intracellular pool of aspartate as the Porphyromonas species are proteolytic rather than saccharolytic.
Intestinal accumulation of microbiota-produced succinate caused by loss of microRNAs leads to diarrhea in weanling piglets
Published in Gut Microbes, 2022
Xihong Zhou, Yonghui Liu, Xia Xiong, Jingqing Chen, Wenjie Tang, Liuqin He, Zhigang Zhang, Yulong Yin, Fengna Li
Recently, numerous studies have found that the intestinal contents and feces contain abundant microRNAs (miRNAs).10–13 These miRNAs are critical for regulating microbial homeostasis. Importantly, we and others have found that the feces of diseased subjects or subjects who have recovered from disease might be enriched with miRNAs having therapeutic or preventive effects.14,15 These miRNAs exert beneficial effects in a microbiome-dependent manner, including affecting the growth of specific microbes and their metabolism. To explore whether and how fecal miRNAs and microbes might be involved in the regulation of stress-induced diarrhea in weaning piglets, we examined the gut microbiome composition and miRNA richness in weaned piglets with or without diarrhea in this study. We found alterations in the fecal microbiome and their metabolites in piglets with diarrhea. Importantly, we found that loss of ssc-miRNA-425-5p and ssc-miRNA-423-3p, which inhibit the gene expression of fumarate reductase (frd) in Prevotella genus, caused succinate accumulation in piglets, which resulted in diarrhea. Our findings enrich the mechanistic basis of diarrhea and suggest that miRNAs inhibit colonic accumulation of microbiota-produced succinate to suppress diarrhea in weanling piglets.
Efflux pump inhibitors as a promising adjunct therapy against drug resistant tuberculosis: a new strategy to revisit mycobacterial targets and repurpose old drugs
Published in Expert Review of Anti-infective Therapy, 2020
Liliana Rodrigues, Pedro Cravo, Miguel Viveiros
Thiabendazole is a fungicide and parasiticide mostly used for the treatment of strongyloidiasis, cutaneous larva migrans, visceral larva migrans, and trichinosis. Thiabendazole is a known inhibitor of tubulin polymerization. It selectively binds to nematode ß-tubulin, inhibiting polymerization, thus preventing the formation of microtubules and preventing cell division [127,128]. Thiabendazole has also been shown to inhibit the helminth-specific enzyme, fumarate reductase [129]. Previous studies examined the effect of thiabendazole in M. tuberculosis and demonstrated that this drug prevented FtsZ polymerization, causing septum formation inhibition and, thus, abolishing cell division [130,131]. Our strategy identified a probable succinate dehydrogenase (Rv0248c) and a probable fumarate reductase (Rv1552) as potential targets of thiabendazole in M. tuberculosis. These enzymes are involved in interconversion of fumarate and succinate in aerobic respiration. Experimental studies are now needed in order to determine if these proteins are indeed targets of thiabendazole.