Mitochondrial Toxicity of Antiviral Drugs: A Challenge to Accurate Diagnosis

Baar, Michel P. de; Ronde, Anthony de

doi:10.1002/9780470372531.ch20

Cited by 3 publications

(2 citation statements)

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“…This leads to reduced mtDNA levels and hence to depletion of the 13 polypeptides encoded by mtDNA. In vitro studies show that the NRTIs impair mtDNA replication with a rank order of Zalcitabine (ddC) > Didanosine (ddI) > Stavudine > Lamivudine > Abacavir, Tenofovir (de Baar and de Ronde, ). These in vitro findings correlate well with the observed clinical adverse events related to mitochondrial toxicity (Benbrik et al, ).…”

Section: Drug‐induced Mitochondrial Toxicitymentioning

confidence: 99%

Current Concepts in Drug‐Induced Mitochondrial Toxicity

Nadanaciva

Will

2009

CP Toxicology

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Mitochondria generate most of the cell's ATP and play key roles in fatty acid oxidation, steroid synthesis, heme synthesis, thermogenesis, calcium homeostasis, and apoptosis. With the development of new methods to study mitochondrial function, it is becoming clear that drug-induced mitochondrial dysfunction is one of the causes of drug toxicity. Mitochondria can be impaired by drugs in a variety of ways. These include inhibition of oxidative phosphorylation, uncoupling of electron transport from ATP synthesis, irreversible opening of the mitochondrial permeability transition pore, inhibition of transporters within the mitochondrial inner membrane, increased oxidative stress, inhibition of the citric acid cycle, inhibition of fatty acid oxidation, and impairment of either mtDNA replication or mtDNA-encoded protein synthesis. This unit provides an overview on the physiological roles of mitochondria and the mechanisms by which they can be adversely affected by drugs.

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Section: Drug‐induced Mitochondrial Toxicitymentioning

confidence: 99%

Current Concepts in Drug‐Induced Mitochondrial Toxicity

Nadanaciva

Will

2009

CP Toxicology

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“…8 Upon withdrawal of mitochondrial toxicants, mitochondria can successfully regenerate over one to several weeks. 14,15 The likelihood of DILI is significantly increased in patients exhibiting polymorphisms of mitochondrial DNA polymerase gamma, 16,17 superoxide dismutase 2 (which scavenges mitochondrial superoxide), 18 or specific human leukocyte antigen (HLA) markers associated with immunoallergic injury. [19][20][21][22][23] Immunoallergic injury or hypersensitivity is associated with fever, rash, eosinophilia, and antidrug antibodies and occurs rapidly on rechallenge (sometimes within hours).…”

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confidence: 99%