eprintid: 98 rev_number: 9 eprint_status: archive userid: 2 importid: 0 dir: disk0/00/00/00/98 datestamp: 2021-11-08 15:59:16 lastmod: 2022-03-02 23:55:09 status_changed: 2021-11-08 15:59:16 type: article succeeds: 0 commentary: 0 metadata_visibility: show item_issues_count: 0 sword_depositor: 0 creators_name: Bullón, Pedro creators_name: Román-Malo, Lourdes creators_name: Marín-Aguilar, Fabiola creators_name: Alvarez-Suarez, José Miguel creators_name: Giampieri, Francesca creators_name: Battino, Maurizio creators_name: Cordero, Mario D. creators_id: creators_id: creators_id: creators_id: josemanuel.alvarez@unini.edu.mx creators_id: creators_id: maurizio.battino@uneatlantico.es creators_id: title: Lipophilic antioxidants prevent lipopolysaccharide-induced mitochondrial dysfunction through mitochondrial biogenesis improvement ispublished: pub subjects: uneat_sn divisions: uneatlantico_produccion_cientifica divisions: uninimx_produccion_cientifica full_text_status: none keywords: Porphyromonas gingivalis; Lipopolysaccharide; Coenzyme Q10; N-acetylcysteine; Mitochondria abstract: Oxidative stress is implicated in several infectious diseases. In this regard, lipopolysaccharide (LPS), an endotoxic component, induces mitochondrial dysfunction and oxidative stress in several pathological events such as periodontal disease or sepsis. In our experiments, LPS-treated fibroblasts provoked increased oxidative stress, mitochondrial dysfunction, reduced oxygen consumption and mitochondrial biogenesis. After comparing coenzyme Q10 (CoQ10) and N-acetylcysteine (NAC), we observed a more significant protection of CoQ10 than of NAC, which was comparable with other lipophilic and hydrophilic antioxidants such as vitamin E or BHA respectively. CoQ10 improved mitochondrial biogenesis by activating PGC-1α and TFAM. This lipophilic antioxidant protection was observed in mice after LPS injection. These results show that mitochondria-targeted lipophilic antioxidants could be a possible specific therapeutic strategy in pharmacology in the treatment of infectious diseases and their complications. date: 2015 date_type: published publication: Pharmacological Research volume: 91 pagerange: 1-8 pages: 0 id_number: doi:10.1016/j.phrs.2014.10.007 refereed: TRUE issn: 10436618 official_url: http://doi.org/10.1016/j.phrs.2014.10.007 num_pieces: 0 gscholar_impact: 0 gscholar_datestamp: 0000-00-00 00:00:00 access: close language: en citation: Artículo Materias > Alimentación Universidad Europea del Atlántico > Investigación > Producción Científica Universidad Internacional Iberoamericana México > Investigación > Producción Científica Cerrado Inglés Oxidative stress is implicated in several infectious diseases. In this regard, lipopolysaccharide (LPS), an endotoxic component, induces mitochondrial dysfunction and oxidative stress in several pathological events such as periodontal disease or sepsis. In our experiments, LPS-treated fibroblasts provoked increased oxidative stress, mitochondrial dysfunction, reduced oxygen consumption and mitochondrial biogenesis. After comparing coenzyme Q10 (CoQ10) and N-acetylcysteine (NAC), we observed a more significant protection of CoQ10 than of NAC, which was comparable with other lipophilic and hydrophilic antioxidants such as vitamin E or BHA respectively. CoQ10 improved mitochondrial biogenesis by activating PGC-1α and TFAM. This lipophilic antioxidant protection was observed in mice after LPS injection. These results show that mitochondria-targeted lipophilic antioxidants could be a possible specific therapeutic strategy in pharmacology in the treatment of infectious diseases and their complications. metadata Bullón, Pedro; Román-Malo, Lourdes; Marín-Aguilar, Fabiola; Alvarez-Suarez, José Miguel; Giampieri, Francesca; Battino, Maurizio y Cordero, Mario D. mail SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, josemanuel.alvarez@unini.edu.mx, SIN ESPECIFICAR, maurizio.battino@uneatlantico.es, SIN ESPECIFICAR (2015) Lipophilic antioxidants prevent lipopolysaccharide-induced mitochondrial dysfunction through mitochondrial biogenesis improvement. Pharmacological Research, 91. pp. 1-8. ISSN 10436618