Linezolid-Induced Inhibition of Mitochondrial Protein Synthesis

Vriese, An S. De; Coster, Rudy Van; Smet, J; Seneca, Sara; Lovering, Andrew; Haute, Lindsey Van; Vanopdenbosch, Ludo; Martin, Jean‐Jacques; Groote, Chantal Ceuterick‐de; Vandecasteele, Stefaan; Boelaert, Johan R.

doi:10.1086/501356

Cited by 275 publications

(187 citation statements)

References 23 publications

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“…The risk for linezolidinduced lactic acidosis is associated with duration of therapy [28], but early linezolid-induced lactic acidosis has also been reported [29]. Some studies using cell-culture experiments have suggested that linezolid toxicity is caused by inhibition of mitochondrial protein synthesis [30][31][32]. There is some evidence that polymorphisms in the mitochondrial 16S ribosomal RNA (rRNA) (e.g., A1036G) may contribute to severe linezolid-associated lactic acidosis in adults [33,34].…”

Section: Pathophysiologymentioning

confidence: 99%

Drug-induced acid-base disorders

et al. 2014

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The incidence of acid-base disorders (ABDs) is high, especially in hospitalized patients. ABDs are often indicators for severe systemic disorders. In everyday clinical practice, analysis of ABDs must be performed in a standardized manner. Highly sensitive diagnostic tools to distinguish the various ABDs include the anion gap and the serum osmolar gap. Drug-induced ABDs can be classified into five different categories in terms of their pathophysiology: (1) metabolic acidosis caused by acid overload, which may occur through accumulation of acids by endogenous (e.g., lactic acidosis by biguanides, propofol-related syndrome) or exogenous (e.g., glycol-dependant drugs, such as diazepam or salicylates) mechanisms or by decreased renal acid excretion (e.g., distal renal tubular acidosis by amphotericin B, nonsteroidal antiinflammatory drugs, vitamin D); (2) base loss: proximal renal tubular acidosis by drugs (e.g., ifosfamide, aminoglycosides, carbonic anhydrase inhibitors, antiretrovirals, oxaliplatin or cisplatin) in the context of Fanconi syndrome; (3) alkalosis resulting from acid and/or chloride loss by renal (e.g., diuretics, penicillins, aminoglycosides) or extrarenal (e.g., laxative drugs) mechanisms; (4) exogenous bicarbonate loads: milk-alkali syndrome, overshoot alkalosis after bicarbonate therapy or citrate administration; and (5) respiratory acidosis or alkalosis resulting from drug-induced depression of the respiratory center or neuromuscular impairment (e.g

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Section: Pathophysiologymentioning

confidence: 99%

Drug-induced acid-base disorders

et al. 2014

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“…In this way, the protein subunits within each OXPHOS complex were separated (Devreese et al 2002). The twodimensional (2D) gels were electro-blotted onto a nitrocellulose membrane using a tank blotting apparatus from Bio-Rad, as has been described previously (De Vriese et al 2006). The relative levels of the five OXPHOS complexes were evaluated by immunodetection, using the MS601 MitoProfile® human total OXPHOS complexes detection kit from MitoSciences in a 1/1000 dilution.…”

Section: Enzyme Assaysmentioning

confidence: 99%

Aberrant synthesis of ATP synthase resulting from a novel deletion in mitochondrial DNA in an African patient with progressive external ophthalmoplegia

Westhuizen

Smet

Levanets

et al. 2010

J of Inher Metab Disea

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“…Prolonged courses of linezolid have been associated with lactic acidosis and optic or peripheral neuropathy and appear to inhibit mitochondrial protein synthesis. 28,29,30 It would therefore be advisable not to co-administer other drugs, which suppress mitochondrial activity such as didanosine, stavudine, and to a lesser extent zidovudine. Clofazimine: Clofazimine is a substituted iminophenazine bright-red dye that inhibits mycobacterial growth and binds preferentially to mycobacterial DNA causing inhibition of transcription.…”

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confidence: 99%