Ototoxic medication

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Ototoxicity is defined as the toxic effect on the functioning of the inner ear, which may lead to temporary or permanent hearing loss (cochleotoxic) and balancing problems (vestibulotoxic). [1] Drugs or pharmaceutical agents inducing ototoxicity are regarded as ototoxic medications.

Contents

Anatomy of the human ear Anatomy of the Human Ear.svg
Anatomy of the human ear

There is a wide range of ototoxic medications, for example, antibiotics, antimalarials, chemotherapeutic agents, non-steroidal anti-inflammatory drugs (NSAIDs) and loop diuretics. [2] While these drugs target on different body systems, they also trigger ototoxicity through different mechanisms, for example, destruction to cellular tissues of inner ear parts and disturbance on auditory nervous system. [2]

Onset of ototoxicity ranges from taking a single dose to long-term usage of the drugs. [3] Signs and symptoms of ototoxicity include tinnitus, hearing loss, dizziness and nausea and/or vomiting. [3] The diagnosis of medicine-induced ototoxicity is challenging as it usually shows only mild symptoms in early stages. Thus, prospective ototoxicity monitoring would be required when patients are using ototoxic medications. [1] Fortunately, the majority of ototoxicity cases are reversible by stopping the medication concerned.

Drugs

Alcohol is one of the leading substances known to have ototoxic effects. [4] A 2023 systematic review and meta-analysis found that alcohol consumption is associated with an increased risk of hearing loss. [5]

Antibiotics and chemotherapeutic agents

The most common classes of ototoxic medications include antibiotics (including aminoglycosides and glycopeptides) and chemotherapeutic agents. Aminoglycosides and some chemotherapeutic agents are associated with both cochleotoxicity and vestibulotoxicity. They are thought to damage the hair cells of the cochlea. Long-term exposure to these drugs may cause damage that progresses to the upper turn of the cochlea, impairing hearing or even causing deafness. [6] Glycopeptides, on the other hand, are rarely associated with ototoxicity.

Structures of ribosomes in prokaryotes and eukaryotes; Aminoglycosides binds to the 30S subunit at the bottom part of prokaryotic ribosomes Ribosome Structure.png
Structures of ribosomes in prokaryotes and eukaryotes; Aminoglycosides binds to the 30S subunit at the bottom part of prokaryotic ribosomes

Aminoglycosides

Aminoglycosides are a class of antibiotics. The most frequently used aminoglycosides include gentamicin, amikacin and streptomycin. These antibiotics are usually used in combination with other antimicrobial agents to treat drug-resistant organisms. For example, they are used with β-lactam for bacterial infections in pneumonia. [7] They are usually given either intravenously or intramuscularly due to their poor oral absorption.

Aminoglycosides irreversibly inhibit protein synthesis of bacteria, which specifically helps kill the gram-negative bacteria. The drug is first transported into the bacterial cell and it binds to the 30S ribosomal subunit. [8] This action interferes with the reading of codons during mRNA translation, causing misreading and premature termination of the process. This inhibits protein synthesis and ultimately leads to the death of bacterial cells. [9]

Events during protein synthesis Bacterial Protein synthesis.png
Events during protein synthesis

All aminoglycosides can cause either reversible or irreversible ototoxicity. Ototoxicity is more frequently observed in individuals who received the treatment for more than five days and those who have renal insufficiency. [7] The mechanism of aminoglycosides-induced ototoxicity is not well understood. It is thought that because cochlear cells are rich in mitochondria, these antibiotics may also target cochlear cells and cause their death. [10] Another hypothesis suggests that these drugs lead to the production of reactive oxygen species which generate oxidative stress and damage the inner ear. [11]

Glycopeptides

Cell wall components of gram-positive and gram-negative bacteria Bacterial cell walls.jpg
Cell wall components of gram-positive and gram-negative bacteria

Glycopeptides are another class of antibiotics. Vancomycin is the class originator for the glycopeptides. Lipoglycopeptides are a subclass of glycopeptides and they are derived from the structure of vancomycin. Examples are telavancin and dalbavancin. [7]

Vancomycin and the lipoglycopeptides have slight differences in their mechanism of actions. Vancomycin inhibits cell wall synthesis of bacteria by preventing the cell wall component of bacteria, peptidoglycan, from elongating and cross-linking. With weakened peptidoglycan, the bacterial cell becomes susceptible to lysis. [9] Lipoglycopeptides, additionally, can increase the membrane permeability of the bacterial cell and disrupt the bacterial cell membrane potential. [9]

This class of antibiotics can be used to treat skin or joint infections, where gram-positive bacteria are the pathogens responsible. Vancomycin is also used as an initial empirical treatment agent of community-acquired bacterial meningitis in locations where penicillin-resistant S. pneumoniae is common. [12] This drug has other clinical uses, including endocarditis and respiratory tract infections caused by Methicillin-resistant Staphylococcus aureus (MRSA).

Case reports suggested that long-term use of vancomycin has been associated with ototoxicity. [13] However, there is no well-established causal link between vancomycin and ototoxicity. For instance, preclinical studies showed that vancomycin had a low risk of inducing ototoxicity. [2] Despite these findings, literature generally agreed that pre-existing hearing abnormalities, concomitant use of aminoglycosides and renal dysfunction are risk factors for vancomycin-induced ototoxicity. [14] [15]

Chemotherapeutic agents

Chemotherapeutic agents are drugs that are used in chemotherapy for the treatment of cancer. Many of these agents are known to have the potential to cause hearing loss. Such agents include cisplatin and bleomycin.

Cisplatin

Chemical structures of carboplatin and cisplatin Cau truc hoa hoc cua cisplatin va carboplatin.png
Chemical structures of carboplatin and cisplatin

Cisplatin is known as a platinum coordination complex. Carboplatin and oxaliplatin also belong to platinum coordination complexes, but they are less commonly associated with ototoxicity. These agents are used in the treatment of ovarian, head and neck, bladder, lung and colon cancers. Cisplatin and other platinum coordination complexes work by reacting with various sites on DNA in mainly cancer cells in order to form cross-links. The formed DNA-platinum complexes inhibit replication and transcription, leading to miscoding and cell death. [7]

The mechanism of cisplatin in inducing ototoxicity is believed to involve the accumulation of reactive oxygen species, which exert cytotoxic effect on cochlear cells. [16] Some pharmacogenetics research have opened up new perspectives on the contributing factors of cisplatin-induced ototoxicity. They investigated several cancer-inducing genes and genetic polymorphisms. Results showed that some genes are associated with protective effect on ototoxicity, while others may show no effect or even increased effect on ototoxicity. [10]

Bleomycin

Bleomycin is one of the antitumour antibiotics and is a fermentation product of Streptomyces verticillus . It has a unique mechanism of action, making it an important agent in treating Hodgkin disease and testicular cancer. This unique chemotherapeutic agent causes oxidative damage to the nucleotides and leads to single- and double-stranded breaks in DNA. Excess breaks in DNA eventually causes cell death. [9] Few case reports have identified the development of ototoxicity in some elderly patients who were administered with bleomycin. [17] Since such cases are rare, the mechanisms behind have yet to be discovered.

Other examples of ototoxic medications

Non-steroidal anti-inflammatory drugs

A simplified mechanism of action of COX inhibitors Cyclooxygenase.png
A simplified mechanism of action of COX inhibitors

Non-steroidal anti-inflammatory drugs (NSAIDs) are one of the most recurrently used classes of drug clinically, indicated for anti-inflammatory, analgesic and antipyretic effects. [18] Examples include high-dose aspirin, ibuprofen and naproxen. Its therapeutic effect is achieved by inhibiting the activity of cyclooxygenase (COX), an enzyme mediating the biosynthesis of prostaglandins (PGs) and thromboxanes (TXAs). As this enzyme is inhibited, prostaglandin and thromboxane production is reduced, hence inhibiting the inflammatory response of pain and swelling caused by prostaglandin. [19]

Studies have proven that high-dose usage of aspirin can be associated with ototoxicity, manifesting reversible hearing loss and tinnitus. [20] The underlying mechanism is associated with a change in isolated cochlear outer hair cells (OHCs). Due to the COX inhibition, there is an increasing amount of leukotrienes in the inner ear. This leukotriene elevation leads to an alteration in the shape of isolated OHCs, thus disrupting their functions. Cochlear blood flow is eventually reduced, causing hearing impairment. [21]

Phosphodiesterase-5 inhibitors

Phosphodiesterase-5 (PDE-5) inhibitors are the first-line drugs indicated for erectile dysfunction (ED), implying the sustained impairment of erectile functioning, which may lead to unsatisfactory sexual performance. [22] Specific PDE-5 inhibitors are also approved for the treatment of benign prostatic hyperplasia, pulmonary hypertension and lower urinary tract symptoms. [23] Common drug examples include sildenafil, vardenafil and tadalafil. The enzyme PDE-5, found in the corpus cavernosum smooth muscle, is responsible for degrading cyclic guanosine monophosphate (cGMP) to 5-GMP. Inhibitors of this enzyme compete with cGMP for binding sites, which in turn increases the level of cGMP in smooth muscles. Through this mechanism, penis erection in male is eventually prolonged, resulting in a correction of ED. These drugs are known to cause headache, flushing and abnormal vision as their adverse effects.

PDE-5 inhibitors are also known for inducing sudden sensorineural hearing loss. It is mainly related to the obstruction and dysfunction of eustachian tubes which affects middle-ear pressure. Due to the high similarity in structure between the penile corpus cavernosum and nasal erectile tissue, PDE-5 inhibitors targeting on corpus cavernosum smooth muscle will also act on nasal erectile tissues, which are mainly located at the inferior turbinate, the middle turbinate and nasal septum. Hence, specific nasal areas may become congested. This mediates inflammatory responses in the eustachian tube which connects to the middle ear, causing an impact on middle ear pressure. Such events will eventually lead to sudden hearing loss. [24]

Antimalarials

Chemical structure of quinine Quinine.svg
Chemical structure of quinine

Antimalarial drugs can be classified into several classes based on different mechanisms of action and effects, including quinoline-type drugs, naphthoquinone, antifolates, guanidine derived drugs, sesquiterpene lactones, etc. In particular, quinoline-type drugs are known to be ototoxic. Examples include chloroquine and hydroxychloroquine which are quinine-like. Apart from antimalarial effects, these drugs are also used in the treatment of other diseases such as dermatological, immunological, rheumatological, and severe infectious diseases. [25]

Various ototoxic effects are manifested by using antimalarial drugs, with dizziness being one of the most common one. Other effects include vestibular symptoms, hearing loss and tinnitus, which can appear to be both temporary or permanent. [25] Nonetheless, the underlying mechanisms of antimalarial-induced ototoxicity are still poorly understood. Studies have suggested that high doses of quinine have an impact on the central auditory pathway and auditory periphery, which leads to elongation and subsequent contraction of isolated OHCs in the cochlea. This structural alteration affects their functions and results in cochlear blood flow reduction.

Loop diuretics

The vestibular system in the inner ear Inner ear's cupula transmitting indication of acceleration.jpg
The vestibular system in the inner ear

Loop diuretics is a major class of diuretic drugs indicated for oedema due to heart failure, liver disease and kidney disease. It is also used for treating hypertension. [26] Common examples include furosemide, bumetanide and ethacrynic acid. Loop diuretics act on the thick ascending limb of the loop of Henle in the kidney nephrons. The major mechanism of ion reabsorption in the thick ascending limb is the active transport of ions through Na+-K+-2Cl− co-transporters (NKCCs). By binding to and inhibiting NKCCs at the apical membrane of the loop of Henle, the reabsorption of Na+, K+ and Cl- is impaired, contributing to a higher ion concentration in the lumen. [26] Hence, the ultimate effect of loop diuretics is a reduction in salt reabsorption and an increase in water excretion.

Loop diuretics-induced ototoxicity is suggested to be associated with their action on stria vascularis located on the lateral wall of the cochlea. This area is responsible for maintaining the balance of ions of endolymph. A high potassium concentration as well as a low sodium concentration should be maintained in the endolymph to allow cochlear hair cells to function normally. [27] As the inhibitory actions of loop diuretics will also target on NKCCs existing on membrane surfaces of stria vascularis marginal cells, there will be a disturbance on the ionic composition of endolymph. [28] Once the endocochlear potential cannot be maintained, hearing is temporarily impaired. It is noticed that the risk of ototoxicity caused by furosemide is much higher than that of bumetanide.

Monitoring and management of ototoxicity

Several approaches can be considered in managing patients who developed ototoxicity as an adverse reaction to the medications. One approach to managing ototoxicity is the use of otoprotective agents. An example is sodium thiosulfate, which the US FDA approved in 2022 to minimise the risk of ototoxicity and hearing loss in newborn, child, and adolescent cancer patients receiving cisplatin. [29] [30] [31] Other agents being investigated for their potential to reduce ototoxicity include D-methionine and L-N-acetylcysteine. [3] The use of D-methionine to protect against hearing loss induced by drugs like cisplatin and aminoglycosides is preliminarily supported by animal studies. [32] NMDA antagonists are also shown to limit aminoglycoside-induced ototoxicity. [33]

Illustration of a cochlear implant Cochlear Implant.png
Illustration of a cochlear implant

Restorative care, which aims to regenerate hair cells that are damaged by ototoxic drugs, can also be considered. For example, the infusion of neurotrophic factors (neurotrophin-3) was shown to produce otoprotective effects. [34] This protective agent was also found to be associated with the survival of cochlear spiral ganglion neurones after hearing loss or deafness. [35]

Audiological management can be implemented, for example, by providing hearing aids. In more seriously affected patients, cochlear implantation may be considered and discussed with the patient. It is also important for the healthcare team to educate affected patients and their family members on communication skills in order to minimise the impact on patients’ daily life. [3]

Related Research Articles

<span class="mw-page-title-main">Vancomycin</span> Antibiotic medication

Vancomycin is a glycopeptide antibiotic medication used to treat a number of bacterial infections. It is used intravenously as a treatment for complicated skin infections, bloodstream infections, endocarditis, bone and joint infections, and meningitis caused by methicillin-resistant Staphylococcus aureus. Blood levels may be measured to determine the correct dose. Vancomycin is also taken orally as a treatment for severe Clostridium difficile colitis. When taken orally it is poorly absorbed.

<span class="mw-page-title-main">Minocycline</span> Antibiotic medication

Minocycline, sold under the brand name Minocin among others, is a tetracycline antibiotic medication used to treat a number of bacterial infections such as some occurring in certain forms of pneumonia. It is generally less preferred than the tetracycline doxycycline. Minocycline is also used for the treatment of acne and rheumatoid arthritis. It is taken by mouth or applied to the skin.

<span class="mw-page-title-main">Gentamicin</span> Antibiotic medication

Gentamicin is an aminoglycoside antibiotic used to treat several types of bacterial infections. This may include bone infections, endocarditis, pelvic inflammatory disease, meningitis, pneumonia, urinary tract infections, and sepsis among others. It is not effective for gonorrhea or chlamydia infections. It can be given intravenously, by intramuscular injection, or topically. Topical formulations may be used in burns or for infections of the outside of the eye. It is often only used for two days until bacterial cultures determine what specific antibiotics the infection is sensitive to. The dose required should be monitored by blood testing.

<span class="mw-page-title-main">Linezolid</span> Antibiotic medication

Linezolid is an antibiotic used for the treatment of infections caused by Gram-positive bacteria that are resistant to other antibiotics. Linezolid is active against most Gram-positive bacteria that cause disease, including streptococci, vancomycin-resistant enterococci (VRE), and methicillin-resistant Staphylococcus aureus (MRSA). The main uses are infections of the skin and pneumonia although it may be used for a variety of other infections including drug-resistant tuberculosis. It is used either by injection into a vein or by mouth.

<span class="mw-page-title-main">Furosemide</span> Loop diuretic medication

Furosemide is a loop diuretic medication used to treat edema due to heart failure, liver scarring, or kidney disease. It has had many trade names including Discoid, Frusemide, Lasix and Uremide. Furosemide may also be used for the treatment of high blood pressure. It can be taken intravenously or orally. When given intravenously, furosemide typically takes effect within five minutes; when taken orally, it typically metabolizes within an hour.

<span class="mw-page-title-main">Aminoglycoside</span> Antibacterial drug

Aminoglycoside is a medicinal and bacteriologic category of traditional Gram-negative antibacterial medications that inhibit protein synthesis and contain as a portion of the molecule an amino-modified glycoside (sugar). The term can also refer more generally to any organic molecule that contains amino sugar substructures. Aminoglycoside antibiotics display bactericidal activity against Gram-negative aerobes and some anaerobic bacilli where resistance has not yet arisen but generally not against Gram-positive and anaerobic Gram-negative bacteria.

Ototoxicity is the property of being toxic to the ear (oto-), specifically the cochlea or auditory nerve and sometimes the vestibular system, for example, as a side effect of a drug. The effects of ototoxicity can be reversible and temporary, or irreversible and permanent. It has been recognized since the 19th century. There are many well-known ototoxic drugs used in clinical situations, and they are prescribed, despite the risk of hearing disorders, for very serious health conditions. Ototoxic drugs include antibiotics, loop diuretics, and platinum-based chemotherapy agents. A number of nonsteroidal anti-inflammatory drugs (NSAIDS) have also been shown to be ototoxic. This can result in sensorineural hearing loss, dysequilibrium, or both. Some environmental and occupational chemicals have also been shown to affect the auditory system and interact with noise.

<span class="mw-page-title-main">Clindamycin</span> Antibiotic

Clindamycin is a lincosamide antibiotic medication used for the treatment of a number of bacterial infections, including osteomyelitis (bone) or joint infections, pelvic inflammatory disease, strep throat, pneumonia, acute otitis media, and endocarditis. It can also be used to treat acne, and some cases of methicillin-resistant Staphylococcus aureus (MRSA). In combination with quinine, it can be used to treat malaria. It is available by mouth, by injection into a vein, and as a cream or a gel to be applied to the skin or in the vagina.

<span class="mw-page-title-main">Loop diuretic</span> Diuretics that act along the loop of Henle in the kidneys

Loop diuretics are pharmacological agents that primarily inhibit the Na-K-Cl cotransporter located on the luminal membrane of cells along the thick ascending limb of the loop of Henle. They are often used for the treatment of hypertension and edema secondary to congestive heart failure, liver cirrhosis, or chronic kidney disease. While thiazide diuretics are more effective in patients with normal kidney function, loop diuretics are more effective in patients with impaired kidney function.

Vancomycin-resistant <i>Staphylococcus aureus</i> Antibiotica resistant bacteria

Vancomycin-resistant Staphylococcus aureus (VRSA) are strains of Staphylococcus aureus that have acquired resistance to the glycopeptide antibiotic vancomycin. Bacteria can acquire resistant genes either by random mutation or through the transfer of DNA from one bacterium to another. Resistance genes interfere with the normal antibiotic function and allow bacteria to grow in the presence of the antibiotic. Resistance in VRSA is conferred by the plasmid-mediated vanA gene and operon. Although VRSA infections are uncommon, VRSA is often resistant to other types of antibiotics and a potential threat to public health because treatment options are limited. VRSA is resistant to many of the standard drugs used to treat S. aureus infections. Furthermore, resistance can be transferred from one bacterium to another.

<span class="mw-page-title-main">Sensorineural hearing loss</span> Hearing loss caused by an inner ear or vestibulocochlear nerve defect

Sensorineural hearing loss (SNHL) is a type of hearing loss in which the root cause lies in the inner ear, sensory organ, or the vestibulocochlear nerve. SNHL accounts for about 90% of reported hearing loss. SNHL is usually permanent and can be mild, moderate, severe, profound, or total. Various other descriptors can be used depending on the shape of the audiogram, such as high frequency, low frequency, U-shaped, notched, peaked, or flat.

<span class="mw-page-title-main">Cisplatin</span> Chemical compound and pharmaceutical drug

Cisplatin is a chemical compound with formula cis-[Pt(NH3)2Cl2]. It is a coordination complex of platinum that is used as a chemotherapy medication used to treat a number of cancers. These include testicular cancer, ovarian cancer, cervical cancer, bladder cancer, head and neck cancer, esophageal cancer, lung cancer, mesothelioma, brain tumors and neuroblastoma. It is given by injection into a vein.

Nephrotoxicity is toxicity in the kidneys. It is a poisonous effect of some substances, both toxic chemicals and medications, on kidney function. There are various forms, and some drugs may affect kidney function in more than one way. Nephrotoxins are substances displaying nephrotoxicity.

<span class="mw-page-title-main">Glycopeptide antibiotic</span> Class of antibiotic drugs

Glycopeptide antibiotics are a class of drugs of microbial origin that are composed of glycosylated cyclic or polycyclic nonribosomal peptides. Significant glycopeptide antibiotics include the anti-infective antibiotics vancomycin, teicoplanin, telavancin, ramoplanin and decaplanin, corbomycin, complestatin and the antitumor antibiotic bleomycin. Vancomycin is used if infection with methicillin-resistant Staphylococcus aureus (MRSA) is suspected.

<span class="mw-page-title-main">Tobramycin</span> Chemical compound

Tobramycin is an aminoglycoside antibiotic derived from Streptomyces tenebrarius that is used to treat various types of bacterial infections, particularly Gram-negative infections. It is especially effective against species of Pseudomonas.

<span class="mw-page-title-main">Amikacin</span> Antibiotic medication

Amikacin is an antibiotic medication used for a number of bacterial infections. This includes joint infections, intra-abdominal infections, meningitis, pneumonia, sepsis, and urinary tract infections. It is also used for the treatment of multidrug-resistant tuberculosis. It is used by injection into a vein using an IV or into a muscle.

Antimicrobial pharmacodynamics is the relationship between the concentration of an antibiotic and its ability to inhibit vital processes of endo- or ectoparasites and microbial organisms. This branch of pharmacodynamics relates the concentration of an anti-infective agent to its effect, specifically to its antimicrobial effect.

<span class="mw-page-title-main">Dalbavancin</span> Antibiotic used to treat MRSA

Dalbavancin, sold under the brand names Dalvance in the US and Xydalba in the EU among others, is a second-generation lipoglycopeptide antibiotic medication. It belongs to the same class as vancomycin, the most widely used and one of the treatments available to people infected with methicillin-resistant Staphylococcus aureus (MRSA).

<span class="mw-page-title-main">Polypeptide antibiotic</span> Class of antibiotics

Polypeptide antibiotics are a chemically diverse class of anti-infective and antitumor antibiotics containing non-protein polypeptide chains. Examples of this class include actinomycin, bacitracin, colistin, and polymyxin B. Actinomycin-D has found use in cancer chemotherapy. Most other polypeptide antibiotics are too toxic for systemic administration, but can safely be administered topically to the skin as an antiseptic for shallow cuts and abrasions.

<span class="mw-page-title-main">Arbekacin</span> Antibiotic

Arbekacin (INN) is a semisynthetic aminoglycoside antibiotic which was derived from kanamycin. It is primarily used for the treatment of infections caused by multi-resistant bacteria including methicillin-resistant Staphylococcus aureus (MRSA). Arbekacin was originally synthesized from dibekacin in 1973 by Hamao Umezawa and collaborators. It has been registered and marketed in Japan since 1990 under the trade name Habekacin. Arbekacin is no longer covered by patent and generic versions of the drug are also available under such trade names as Decontasin and Blubatosine.

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  25. 1 2 Jozefowicz-Korczynska, Magdalena; Pajor, Anna; Lucas Grzelczyk, Weronika (2021). "The Ototoxicity of Antimalarial Drugs-A State of the Art Review". Frontiers in Neurology. 12: 661740. doi: 10.3389/fneur.2021.661740 . ISSN   1664-2295. PMC   8093564 . PMID   33959089.
  26. 1 2 Sarafidis, Pantelis A; Georgianos, Panagiotis I; Lasaridis, Anastasios N (2010). "Diuretics in clinical practice. Part I: mechanisms of action, pharmacological effects and clinical indications of diuretic compounds". Expert Opinion on Drug Safety. 9 (2): 243–257. doi:10.1517/14740330903499240. ISSN   1474-0338. PMID   20095917. S2CID   7303716.
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  30. ↑ Winstead, Edward (October 6, 2022). "Sodium Thiosulfate Reduces Hearing Loss in Kids with Cancer". National Cancer Institute. Archived from the original on March 9, 2023. Retrieved March 9, 2023.
  31. ↑ "FDA approves sodium thiosulfate to reduce the risk of ototoxicity associated with cisplatin in pediatric patients with localized, non-metastatic solid tumors". U.S. Food and Drug Administration. 20 September 2022. Archived from the original on 9 March 2023. Retrieved 9 March 2023.
  32. ↑ Campbell, Kathleen C.M.; Meech, Robert P.; Klemens, James J.; Gerberi, Michael T.; Dyrstad, Sara S.W.; Larsen, Deb L.; Mitchell, Diana L.; El-Azizi, Mohammed; Verhulst, Steven J.; Hughes, Larry F. (2007). "Prevention of noise- and drug-induced hearing loss with d-methionine". Hearing Research. 226 (1–2): 92–103. doi:10.1016/j.heares.2006.11.012. PMID   17224251. S2CID   24953862.
  33. ↑ Basile, Anthony S.; Huang, Jer-Min; Xie, Chen; Webster, Douglas; Berlin, Charles; Skolnick, Phil (1996). "N–Methyl–D–aspartate antagonists limit aminoglycoside antibiotic–induced hearing loss". Nature Medicine. 2 (12): 1338–1343. doi:10.1038/nm1296-1338. ISSN   1078-8956. PMID   8946832. S2CID   30861122.
  34. ↑ Ernfors, Patrik; Li Duan, Mao; Elshamy, Wael M.; Canlon, Barbara (1996). "Protection of auditory neurons from aminoglycoside toxicity by neurotrophin-3". Nature Medicine. 2 (4): 463–467. doi:10.1038/nm0496-463. ISSN   1078-8956. PMID   8597959. S2CID   22927156.
  35. ↑ Leake, Patricia A.; Akil, Omar; Lang, Hainan (2020). "Neurotrophin gene therapy to promote survival of spiral ganglion neurons after deafness". Hearing Research. 394: 107955. doi:10.1016/j.heares.2020.107955. PMC   7660539 . PMID   32331858.
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