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      Antibiotic use and abuse: A threat to mitochondria and chloroplasts with impact on research, health, and environment

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          Recently, several studies have demonstrated that tetracyclines, the antibiotics most intensively used in livestock and that are also widely applied in biomedical research, interrupt mitochondrial proteostasis and physiology in animals ranging from round worms, fruit flies, and mice to human cell lines. Importantly, plant chloroplasts, like their mitochondria, are also under certain conditions vulnerable to these and other antibiotics that are leached into our environment. Together these endosymbiotic organelles are not only essential for cellular and organismal homeostasis stricto sensu, but also have an important role to play in the sustainability of our ecosystem as they maintain the delicate balance between autotrophs and heterotrophs, which fix and utilize energy, respectively. Therefore, stricter policies on antibiotic usage are absolutely required as their use in research confounds experimental outcomes, and their uncontrolled applications in medicine and agriculture pose a significant threat to a balanced ecosystem and the well‐being of these endosymbionts that are essential to sustain health.

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          Most cited references 63

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          Mitochondria and apoptosis.

          A variety of key events in apoptosis focus on mitochondria, including the release of caspase activators (such as cytochrome c), changes in electron transport, loss of mitochondrial transmembrane potential, altered cellular oxidation-reduction, and participation of pro- and antiapoptotic Bcl-2 family proteins. The different signals that converge on mitochondria to trigger or inhibit these events and their downstream effects delineate several major pathways in physiological cell death.
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            A common mechanism of cellular death induced by bactericidal antibiotics.

            Antibiotic mode-of-action classification is based upon drug-target interaction and whether the resultant inhibition of cellular function is lethal to bacteria. Here we show that the three major classes of bactericidal antibiotics, regardless of drug-target interaction, stimulate the production of highly deleterious hydroxyl radicals in Gram-negative and Gram-positive bacteria, which ultimately contribute to cell death. We also show, in contrast, that bacteriostatic drugs do not produce hydroxyl radicals. We demonstrate that the mechanism of hydroxyl radical formation induced by bactericidal antibiotics is the end product of an oxidative damage cellular death pathway involving the tricarboxylic acid cycle, a transient depletion of NADH, destabilization of iron-sulfur clusters, and stimulation of the Fenton reaction. Our results suggest that all three major classes of bactericidal drugs can be potentiated by targeting bacterial systems that remediate hydroxyl radical damage, including proteins involved in triggering the DNA damage response, e.g., RecA.
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              Mitochondrial diseases in man and mouse.

               D C Wallace (1999)
              Over the past 10 years, mitochondrial defects have been implicated in a wide variety of degenerative diseases, aging, and cancer. Studies on patients with these diseases have revealed much about the complexities of mitochondrial genetics, which involves an interplay between mutations in the mitochondrial and nuclear genomes. However, the pathophysiology of mitochondrial diseases has remained perplexing. The essential role of mitochondrial oxidative phosphorylation in cellular energy production, the generation of reactive oxygen species, and the initiation of apoptosis has suggested a number of novel mechanisms for mitochondrial pathology. The importance and interrelationship of these functions are now being studied in mouse models of mitochondrial disease.

                Author and article information

                John Wiley and Sons Inc. (Hoboken )
                08 September 2015
                October 2015
                : 37
                : 10 ( doiID: 10.1002/bies.v37.10 )
                : 1045-1053
                [ 1 ] Laboratory of Integrative and Systems PhysiologyÉcole Polytechnique Fédérale de Lausanne LausanneSwitzerland
                [ 2 ] Laboratory Genetic Metabolic DiseasesAcademic Medical Center AmsterdamThe Netherlands
                Author notes
                [* ] Corresponding authors:

                Riekelt Houtkooper

                E‐mail: r.h.houtkooper@

                Johan Auwerx

                E‐mail: admin.auwerx@


                These authors contributed equally to this work.

                © 2015 The Authors. Bioessays published by WILEY Periodicals, Inc.

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                Page count
                Pages: 9
                Funded by: ERC
                Award ID: 638290
                Funded by: ZonMw
                Award ID: 91613050
                Funded by: EPFL
                Funded by: NIH
                Award ID: R01AG043930
                Funded by: Krebsforschung Schweiz/Swiss Cancer League
                Award ID: KFS‐3082‐02‐2013
                Funded by: Systems X
                Award ID: 2013/153
                Funded by: SNSF
                Award ID: 31003A‐140780
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                October 2015
                Converter:WILEY_ML3GV2_TO_NLMPMC version:4.9.4 mode:remove_FC converted:06.10.2016


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