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In Oxidative Stress Induced by Fluoroquinolones on Treatment for Complicated Urinary Tract Infections in Indian Patients it was found that, for human patients with urinary tract infections and treated with various fluoroquinolones, There was substantial depletion in both SOD and glutathione levels particularly with ciprofloxacin. Without sufficient SOD, as noted above, superoxide cannot cross the inner mitochondrial membrane and can oxidize. Oxidization within the mitochondrial membrane is harmful because it damages mitochondrial DNA (mtDNA) and starts the vicious cycle of oxidative damage to mitochondria

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Recent studies have revealed the elevation of SIRT1 in a rat model of status epilepticus, a common neurological emergency which is defined as a prolonged seizure with at least five minutes or multiple seizures with incomplete recovery of consciousness [117] and its neuroprotection is conducted via deacetylation of proliferator-activated receptors and coactivator 1 (PGC-1), an important regulator for mitochondrial biogenesis [118, 119]

The hepatotoxicity differences between the KO and WT mice were in a time and dose dependent manner

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