Oxazolidinones Inhibit Cellular Proliferation via Inhibition of Mitochondrial Protein Synthesis
نویسندگان
چکیده
منابع مشابه
Synthesis via Inhibition of Mitochondrial Protein Oxazolidinones Inhibit Cellular Proliferation
متن کامل
Inhibition of mammalian mitochondrial protein synthesis by oxazolidinones.
The effects of a variety of oxazolidinones, with different antibacterial potencies, including linezolid, on mitochondrial protein synthesis were determined in intact mitochondria isolated from rat heart and liver and rabbit heart and bone marrow. The results demonstrate that a general feature of the oxazolidinone class of antibiotics is the inhibition of mammalian mitochondrial protein synthesi...
متن کاملLinezolid-induced inhibition of mitochondrial protein synthesis.
BACKGROUND Linezolid is an oxazolidinone antibiotic that is increasingly used to treat drug-resistant, gram-positive pathogens. The mechanism of action is inhibition of bacterial protein synthesis. Optic and/or peripheral neuropathy and lactic acidosis are reported side effects, but the underlying pathophysiological mechanism has not been unravelled. METHODS We studied mitochondrial ultrastru...
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Adenovirus infection results in the suppression of cellular protein synthesis, but the mechanism has not been established. In this report we demonstrate that the shut-off of cellular protein synthesis by adenovirus is prevented in cells by treatment with the drug 2-aminopurine. Treatment with 2-aminopurine is shown to prevent suppression of cellular translation without disrupting the normal vir...
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Introduction: Cognitive dysfunction is the most common problem of patients with Alzheimer disease (AD). The pathological mechanism of cognitive impairment in AD may contribute to neuronal loss, synaptic dysfunction, and alteration in neurotransmitters receptors. Mitochondrial synapses dysfunction due to the accumulation of amyloid beta (Aβ) is one of the earliest pathological features of AD. Th...
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ژورنال
عنوان ژورنال: Antimicrobial Agents and Chemotherapy
سال: 2005
ISSN: 0066-4804,1098-6596
DOI: 10.1128/aac.49.9.3896-3902.2005