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Mitochondrion. 2019 May;46:270-277. doi: 10.1016/j.mito.2018.07.007. Epub 2018 Aug 4.

Toxic medications in Leber's hereditary optic neuropathy.

Author information

1
Doheny Eye Institute, 1355 San Pablo Street, Los Angeles, CA 90033, USA. Electronic address: kaitlin9210@gmail.com.
2
Doheny Eye Institute, 1355 San Pablo Street, Los Angeles, CA 90033, USA.
3
Doheny Eye Institute, 1355 San Pablo Street, Los Angeles, CA 90033, USA; Doheny Eye Center, Department of Ophthalmology, David Geffen School of Medicine at UCLA, 800 South Fairmount Avenue, Suite 215, Pasadena, CA 91105, USA.
4
Doheny Eye Institute, 1355 San Pablo Street, Los Angeles, CA 90033, USA; Doheny Eye Center, Department of Ophthalmology, David Geffen School of Medicine at UCLA, 800 South Fairmount Avenue, Suite 215, Pasadena, CA 91105, USA; The Ottawa Eye Institute, University of Ottawa, 501 Smyth Rd, Ottawa, ON K1H 8M2, Canada; Ottawa Hospital Research Institute, 1053 Carling Avenue, Ottawa, ON K1Y 4E9, Canada.

Abstract

Leber's hereditary optic neuropathy (LHON) is a maternally inherited mitochondrial disorder characterized by acute bilateral vision loss. The pathophysiology involves reactive oxygen species (ROS), which can be affected by medications. This article reviews the evidence for medications with demonstrated and theoretical effects on mitochondrial function, specifically in relation to increased ROS production. The data reviewed provides guidance when selecting medications for individuals with LHON mutations (carriers) and are susceptible to conversion to affected. However, as with all medications, the proven benefits of these therapies must be weighed against, in some cases, purely theoretical risks for this unique patient population.

KEYWORDS:

Antimicrobials; Leber's hereditary optic neuropathy; Medications; Mitochondrial toxicity

PMID:
30081212
DOI:
10.1016/j.mito.2018.07.007
[Indexed for MEDLINE]

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