Quinolones and coumarins eliminate chloroplasts from Euglena gracilis

Krajčovič, Juraj; Ebringer, L.; Polónyi, J

doi:10.1128/aac.33.11.1883

Cited by 37 publications

(14 citation statements)

References 24 publications

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“…Thereafter, he demonstrated (Ebringer et al, 1969;Ebringer, 1972) that practically all inhibitors of bacterial protein-and DNA-synthesis caused bleaching in E. gracilis. Several antibacterial substances have been studied extensively and their mode of action has been well described in Euglena (for review see Ebringer, 1972;Gillham, 1978; see also Hashimoto and Murakami, 1982;Heizmann et al, 1982;Krajčovič et al, 1989). Bleaching in Euglena provide a rapid screening method for identification of agents which specifically inhibit prokaryotic biochemical and molecular biological pathways while having no effect on eukaryotic metabolic activities.…”

Section: Euglena As a Model Organism For Mutagen And Antimutagen Scrementioning

confidence: 99%

Euglenoid flagellates: A multifaceted biotechnology platform

Krajčovič

Vesteg

Schwartzbach

2015

Journal of Biotechnology

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Section: Euglena As a Model Organism For Mutagen And Antimutagen Scrementioning

confidence: 99%

Euglenoid flagellates: A multifaceted biotechnology platform

Krajčovič

Vesteg

Schwartzbach

2015

Journal of Biotechnology

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“…Other interests have been focused on mitochondria. Because quinolones have been reported to damage mitochondria of the flagellate Euglena gracilis (Krajcovic et al, 1989;Polonyi et al, 1990) and the yeast Saccharomyces cerevisiae (Obernauerova et al, 1992), interest is focused on mammalian mitochondria. Hildebrand et al (1993) reported a reduction of mitochondrial dehydrogenase activity in chondrocytes in vitro under the action of different quinolones.…”

Section: Chondrotoxicitymentioning

confidence: 99%

Toxicity of quinolone antimicrobial agents

Takayama¹,

Hirohashi²,

Kato³

et al. 1995

Journal of Toxicology and Environmental Health

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An approach to minimization of toxicity of a new compound is to elucidate the mechanisms of toxicity of analogous compounds and to clarify their structure-toxicity relationships. A problem with this approach, however, is that such elucidation remains difficult. For quinolones, some improvements in this mechanistic approach have been achieved in the central nervous system (CNS), particularly with regard to their interaction with non-steroidal anti-inflammatory drugs (NSAIDs), and in genotoxicity and phototoxicity studies, particularly in comparison with other toxicities, such as to the cardiovascular, gastrointestinal, bone, reproductive, and developmental systems. This review concentrates on a description of the known effects of quinolones on various organ systems in experimental animals and humans. Given the logarithmic increase in the synthesis of new quinolones, it is questionable whether these drugs share similar safety and efficacy. Nevertheless, this mechanistic approach to the investigation and minimization of toxicity has produced satisfactory results to date and deserves to be continued.

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“…Mammalian mitochondria resemble bacteria in numerous ways and are thought to possess their own DNA topoisomerases, independent from nucleus-originated ones (6,11,12). The function of these putative mammalian enzymes has been tested as a potential target of DNA gyrase inhibitors, with no convincing result (7,37 (23,33) and the yeast Saccharomyces cerevisiae (29).…”

mentioning

confidence: 99%

Cytofluorometric analysis of chondrotoxicity of fluoroquinolone antimicrobial agents

Hayem

Petit

Levacher

et al. 1994

Antimicrob Agents Chemother

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To better understand quinolone-related arthropathy, we conceived an experimental ex vivo model using cell cultures of articular chondrocytes issued from pretreated New Zealand White rabbits (NZW). Juvenile (4-to 5-week-old) NZW were orally dosed with ofloxacin or pefloxacin (300 mg/kg of body weight for 1 day) or with pefloxacin (300 mg/kg for 7 days). Adult (5-month-old) NZW were treated with pefloxacin (300 mg/kg for 1 day). Chondrocytes were enzymatically recovered from cartilage and were analyzed by cytofluorometry using 2',7'-dichlorofluorescein diacetate (DCFH-DA) and dihydrorhodamine 123 (DHR), reflecting cellular respiratory-burst activity, and rhodamine 123 (Rh123) and 10-N-nonyl-acridine orange (NAO), specific for the mitochondrial activity and mass, respectively. A significant increase in the respiratory burst was detected by DCFH-DA and DHR in all treated groups of young animals, compared with untreated control groups. No significant increase of respiratory burst was noted in older treated rabbits. The 7-day treatment resulted in a decrease in mitochondrial uptake of Rh123 and an increase in NAO uptake. Fluoroquinolone arthrotoxicity seems to involve in its early phase the respiratory burst of immature articular chondrocytes.

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Quinolones and coumarins eliminate chloroplasts from Euglena gracilis

Cited by 37 publications

References 24 publications

Euglenoid flagellates: A multifaceted biotechnology platform

Euglenoid flagellates: A multifaceted biotechnology platform

Toxicity of quinolone antimicrobial agents

Cytofluorometric analysis of chondrotoxicity of fluoroquinolone antimicrobial agents

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