Cholarmphenicol ototoxicity

Iqbal, Sohail; Srivatsav, C B

doi:10.1017/s0022215100147000

Cited by 10 publications

(4 citation statements)

References 6 publications

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“…Furthermore, inhibiting mitochondrial protein synthesis using chloramphenicol failed to elicit hair cell loss in our system, similar to an earlier study finding that chloramphenicol by itself is not ototoxic, but exacerbates the ototoxic effects of aminoglycosides (Hyde and Rubel, 1995). It needs to be noted, however, that chloramphenicol has occasionally been shown to cause hearing loss (Igbal and Srivatsav, 1984) and also caused hair cell death in zebrafish (Coffin et al, 2010). More detailed studies are needed to evaluate the contribution of mitochondrial and cytosolic translational inhibition in aminoglycoside ototoxicity.…”

Section: Discussionmentioning

confidence: 99%

A Novel Role of Cytosolic Protein Synthesis Inhibition in Aminoglycoside Ototoxicity

et al. 2013

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Ototoxicity is a main dose-limiting factor in the clinical application of aminoglycoside antibiotics. Despite longstanding research efforts, our understanding of the mechanisms underlying aminoglycoside ototoxicity remains limited. Here we report the discovery of a novel stress pathway that contributes to aminoglycoside-induced hair cell degeneration. Modifying the recently developed bioorthogonal noncanonical amino acid tagging (BONCAT) method, we used click-chemistry to study the role of protein synthesis activity in aminoglycoside-induced hair cell stress. We demonstrate that aminoglycosides inhibit protein synthesis in hair cells and activate a signaling pathway similar to ribotoxic stress response, contributing to hair cell degeneration. The ability of a particular aminoglycoside to inhibit protein synthesis and to activate the c-Jun N-terminal kinase (JNK) pathway correlated well with its ototoxic potential. Finally, we report that a FDA-approved drug known to inhibit ribotoxic stress response also prevents JNK activation and improves hair cell survival, opening up novel strategies to prevent and treat aminoglycoside ototoxicity.

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Section: Discussionmentioning

confidence: 99%

A Novel Role of Cytosolic Protein Synthesis Inhibition in Aminoglycoside Ototoxicity

et al. 2013

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“…Seven compounds were known ototoxins ( e.g ., neomycin, cisplatin), demonstrating proof-of-concept in our screening approach. The other 14 compounds were not identified ototoxins, although examination of the clinical literature revealed an occasional case report describing hearing loss in patients treated with a few of these drugs ( e.g ., chloramphenicol, estradiol valerate) 84,85. Two drugs, the anticholinergic compound propantheline bromine and the antiprotozoal pentamidine isethionate, were tested in vitro in cultures of mouse utricle (a vestibular end organ in the mammalian inner ear), and both compounds demonstrated ototoxicity in this mammalian model.…”

Section: Chemical Screening For Ototoxinsmentioning

confidence: 99%

Chemical Screening for Hair Cell Loss and Protection in the Zebrafish Lateral Line

et al. 2010

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In humans, most hearing loss results from death of hair cells, the mechanosensory receptors of the inner ear. Two goals of current hearing research are to protect hair cells from degeneration and to regenerate new hair cells, replacing those that are lost due to aging, disease, or environmental challenges. One limitation of research in the auditory field has been the relative inaccessibility of the mechanosensory systems in the inner ear. Zebrafish possess hair cells that are morphologically and functionally similar to human hair cells in both their inner ear and their lateral line system. The external location of the mechanosensory hair cells in the lateral line and the ease of in vivo labeling and imaging make the zebrafish lateral line a unique system for the study of hair cell toxicity, protection, and regeneration. This review focuses on the lateral line system as a model for understanding loss and protection of mechanosensory hair cells. We discuss chemical screens to identify compounds that induce hair cell loss and others that protect hair cells from known toxins and the potential application of these screens to human medicine.

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“…It began in one ear, but when the course of treatment was repeated, the second ear became involved. Hearing loss progressed to profound bilateral SNHL in this patient (90).…”

Section: Chloramphenicol Ototoxicity Clinical Reportsmentioning

confidence: 70%

Ototoxicity of Non-aminoglycoside Antibiotics

2021

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It is well-known that aminoglycoside antibiotics can cause significant hearing loss and vestibular deficits that have been described in animal studies and in clinical reports. The purpose of this review is to summarize relevant preclinical and clinical publications that discuss the ototoxicity of non-aminoglycoside antibiotics. The major classes of antibiotics other than aminoglycosides that have been associated with hearing loss in animal studies and in patients are discussed in this report. These antibiotics include: capreomycin, a polypeptide antibiotic that has been used to treat patients with drug-resistant tuberculosis, particularly in developing nations; the macrolides, including erythromycin, azithromycin and clarithromycin; and vancomycin. These antibiotics have been associated with ototoxicity, particularly in neonates. It is critical to be aware of the ototoxic potential of these antibiotics since so much attention has been given to the ototoxicity of aminoglycoside antibiotics in the literature.

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Cholarmphenicol ototoxicity

Cited by 10 publications

References 6 publications

A Novel Role of Cytosolic Protein Synthesis Inhibition in Aminoglycoside Ototoxicity

A Novel Role of Cytosolic Protein Synthesis Inhibition in Aminoglycoside Ototoxicity

Chemical Screening for Hair Cell Loss and Protection in the Zebrafish Lateral Line

Ototoxicity of Non-aminoglycoside Antibiotics

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