Sulthiame impairs mitochondrial function in vitro and may trigger onset of visual loss in Leber hereditary optic neuropathy - Reinert, Marie-Christine; Pacheu-Grau, David; Catarino, Claudia B.; Klopstock, Thomas; Ohlenbusch, Andreas; Schittkowski, Michael; Wilichowski, Ekkehard; Rehling, Peter; Brockmann, Knut; Reinert, Marie-Christine; Division of Pediatric Neurology, Department of Pediatrics and Adolescent Medicine, University Medical Center Göttingen, Göttingen, Germany; Pacheu-Grau, David; Department of Cellular Biochemistry, University Medical Center Göttingen, Göttingen, Germany; Catarino, Claudia B.; Department of Neurology, Friedrich-Baur-Institute, University Hospital, LMU Munich, Munich, Germany; et al. (Orphanet Journal of Rare Diseases, 2021)
Keywords: Adverse effects; Carbonic anhydrase inhibitor; Child; DNA, Mitochondrial; drug therapy [Optic Atrophy, Hereditary, Leber]; Female; Female [MeSH]; Mutation [MeSH]; Oxygen consumption rate; Adverse effects; DNA, Mitochondrial [MeSH]; Humans [MeSH]; Mitochondria [MeSH]; Optic Atrophy, Hereditary, Leber/drug therapy [MeSH]; Leber hereditary optic neuropathy; Pediatric neurology; Optic Atrophy, Hereditary, Leber/genetics [MeSH]; LHON; Smoking [MeSH]; Thiazines [MeSH]; Male [MeSH]; Research; Carbonic anhydrase inhibitor; Sulthiame; Child [MeSH]; genetics [Optic Atrophy, Hereditary, Leber]; Humans; Leber hereditary optic neuropathy; LHON; Male; Medicine; Mitochondria; Mutation; Optic Atrophy, Hereditary, Leber; Oxygen consumption rate; R; Smoking; sulthiame; Thiazines