Antibiomania

Quandt-Herrera, P.; Suarez-Jesus, J.; Yelmo-Cruz, S.

doi:10.1097/jcp.0000000000000380

Cited by 4 publications

(1 citation statement)

References 15 publications

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“…Conversely, the cipro-floxacin/fluoriquinolone-mediated inhibition of GABA-ergic signaling, partially driven via the production of mitochondrial ROS ( 86 ), has been shown to result in excitatory pro-convulsive neuronal activation as a putative contributing factor to the presentation of acute psychotic episodes ( 87 – 89 ). Subsequent case reports have observed acute psychotic/manic episodes following the administration of the nitroimidazole antibiotic, metronidazole ( 81 ), the mixed folate inhibitor/sulfonamide antibiotic cotrimoxazole ( 90 – 92 ), and the third generation cephalosporin derivatives ceftazidime ( 93 ) and ceftriaxone ( 94 ). Based on the diversity of the chemical structure and mode of action inherent to each class of antibiotic, a generalized downregulation of mitochondrial bioenergetics may account for the integrated psycho-affective behavioral effects observed in the string of case reports cited above.…”

Section: Antibiotic Usage and Acute Behavioral Disorders: Potentiamentioning

confidence: 99%

Dysregulated mitochondrial and chloroplast bioenergetics from a translational medical perspective (Review)

Stefano¹,

Kream²

2016

International Journal of Molecular Medicine

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Mitochondria and chloroplasts represent endosymbiotic models of complex organelle development, driven by intense evolutionary pressure to provide exponentially enhanced ATP-dependent energy production functionally linked to cellular respiration and photosynthesis. Within the realm of translational medicine, it has become compellingly evident that mitochondrial dysfunction, resulting in compromised cellular bioenergetics, represents a key causative factor in the etiology and persistence of major diseases afflicting human populations. As a pathophysiological consequence of enhanced oxygen utilization that is functionally uncoupled from the oxidative phosphorylation of ADP, significant levels of reactive oxygen species (ROS) may be generated within mitochondria and chloroplasts, which may effectively compromise cellular energy production following prolonged stress/inflammatory conditions. Empirically determined homologies in biochemical pathways, and their respective encoding gene sequences between chloroplasts and mitochondria, suggest common origins via entrapped primordial bacterial ancestors. From evolutionary and developmental perspectives, the elucidation of multiple biochemical and molecular relationships responsible for errorless bioenergetics within mitochondrial and plastid complexes will most certainly enhance the depth of translational approaches to ameliorate or even prevent the destructive effects of multiple disease states. The selective choice of discussion points contained within the present review is designed to provide theoretical bases and translational insights into the pathophysiology of human diseases from a perspective of dysregulated mitochondrial bioenergetics with special reference to chloroplast biology.

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