D-Methionine protects against cisplatin damage to the stria vascularis

Campbell, Kathleen C.M.; Meech, Robert P.; Rybak, Leonard P.; Hughes, Larry F.

doi:10.1016/s0378-5955(99)00142-2

Cited by 111 publications

(96 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…D-Met has been shown to prevent or ameliorate peripheral cisplatininduced hearing threshold shifts, outer hair cell loss, loss of hair cell function, loss of spiral ganglion cell neurons, and damage to the stria vascularis in animals (Campbell et al, 1996(Campbell et al, , 1999(Campbell et al, , 2007Gabaizadeh et al, 1997;Wimmer et al, 2004). However, to our knowledge, this investigation is the first evidence of direct cisplatin damage to the cortical neurons, in vitro, and the amelioration of this damage by an over-thecounter supplement -D-Met.…”

Section: Discussionmentioning

confidence: 70%

“…Studies of cisplatin-induced hearing loss have generally focused on damage to the peripheral auditory system, with morphological alterations in the organ of Corti of the cochlea, loss of and damage of cochlear hair cells, damage to the stria vascularis and degeneration of spiral ganglion neurons (Campbell et al, 1996(Campbell et al, , 1999Meech et al, 1998;Hoistad et al, 1998). Cisplatin has been shown to enhance the formation of reactive oxygen species, and the free radicalinduced cell damage is thought to play an important role in cisplatin neurotoxicity (Dehne et al, 2001;Poirrier et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

“…These adverse effects from cisplatin exposure have led to the search for preventative treatments (Campbell et al, 1996(Campbell et al, , 1999Rybak et al, 2007). Sulfur containing compounds such as sodium thiosulfate (STS) and diethyl-dithiocarbamate (DDTC) were reported to provide good otoprotection against cisplatin (Otto et al, 1988), but had significant side effects and/or interference with antitumor activity (Jones et al, 1991;Church et al, 1995;Gandara et al, 1995;Muldoon et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

“…D-Methionine (D-Met), also a sulfur-containing nucleophilic antioxidant, has shown to provide effective nephroprotection against cisplatin without interfering with antitumor action (Jones and Basinger, 1989). Cisplatin-induced hearing loss, and subsequent outer hair cell loss and stria vascularis damage, is protected by D-Met (Campbell et al, 1996(Campbell et al, , 1999. In the cochlea, D-Met partially protected cisplatin-induced decreases in antioxidant enzymes such as superoxide dismutase (SOD), catalase, and glutathione a reductase (GR), and prevented increases in malondialdehyde levels, a measure of lipid peroxidation (Campbell et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

d-Methionine protects against cisplatin-induced neurotoxicity in cortical networks

Gopal

Shrestha

et al. 2012

Neurotoxicology and Teratology

Self Cite

View full text Add to dashboard Cite

Cisplatin is a platinum-based chemotherapeutic agent widely used for the treatment of various types of cancer. Patients undergoing cisplatin treatment often suffer from a condition known as "chemobrain", ototoxicity, peripheral neuropathy, weight loss, nausea, vomiting, nephrotoxicity, seizures, hearing loss and tinnitus.D-Methionine (D-Met), a sulfur-containing nucleophilic antioxidant, has been shown to prevent cisplatininduced side effects in animals without antitumor interference. In this study, we have used an in vitro model of cortical networks (CNs), enriched in auditory cortex cells; to quantify cisplatin neurotoxicity and the protective effects of D-Met. Dissociated neurons from auditory cortices of mouse embryos were grown on microelectrode arrays with 64 transparent indium-tin oxide electrodes, which enabled continuous optical and electrophysiological monitoring of network neurons. Cisplatin at 0.10-0.25 mM induced up to a 200% increase in spontaneous spiking activity, while concentrations at or above 0.5 mM caused irreversible loss of neuronal activity, accompanied by cell death. Pretreatment with D-Met, at a concentration of 1.0 mM, prevented the cisplatin-induced excitation at 0.10-0.25 mM, caused sustained excitation without occurrence of cell death at 0.5 mM, and delayed cell death at 0.75 mM cisplatin. L-Methionine, the optical isomer, showed lower potency and less efficacy than D-Met, was less protective against 0.1 mM cisplatin, and proved ineffective at a concentration of 0.5 mM cisplatin. Pre-exposure time of D-Met was associated with the protective effects at 0.1 and 0.5 mM cisplatin, with longer pre-exposure times exhibiting better protection. This study quantifies as a function of concentration and time that D-Met protects central nervous system tissue from acute cisplatin toxicity.

show abstract

Section: Discussionmentioning

confidence: 70%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

d-Methionine protects against cisplatin-induced neurotoxicity in cortical networks

Gopal

Shrestha

et al. 2012

Neurotoxicology and Teratology

Self Cite

View full text Add to dashboard Cite

show abstract

“…PBN is able to form adducts with ROS thereby reducing the likelihood of oxidative stress. The role of oxidative stress in cochlear injury has also been underscored as a consequence of aminoglycoside antibiotic (Garetz et al 1994;Hester et al 1998;Lautermann et al 1997) and cisplatin (Rybak et al 1995Campbell et al 1996Campbell et al , 1999Kopke et al 1997;Dehne et al 2001). Both of these agents are widely recognized as promoting NIHL (e.g., Bone and Ryan 1978;Brown et al 1980;Bhattacharyya and Dayal 1991;Gratton et al 1990).…”

Section: Introductionmentioning

confidence: 99%

Acrylonitrile Potentiates Noise-Induced Hearing Loss in Rat

Fechter

Gearhart

Shirwany

2004

JARO - Journal of the Association for Research in Otolaryngolog

View full text Add to dashboard Cite

Acrylonitrile, one of the 50 most commonly produced industrial chemicals, has recently been identified as a promoter of noise-induced hearing loss (NIHL). This agent has the potential to produce oxidative stress through multiple pathways. We hypothesize that acrylonitrile potentiates NIHL as a consequence of oxidative stress. The objectives of this study were to characterize acrylonitrile exposure conditions that promote permanent NIHL in rats and determine the ability of this nitrile to produce auditory dysfunction by itself. Additionally, we sought to determine whether a spin-trap agent that can form adducts with ROS would protect against the effects of acrylonitrile. Acrylonitrile administration produced significant elevation in NIHL detected as a loss in compound action potential sensitivity. The effect was particularly robust for high-frequency tones and particularly when acrylonitrile and noise were given on repeated occasions. Acrylonitrile by itself did not disrupt threshold sensitivity. Administration of the spin-trap agent phenyl-N-tert-butylnitrone (PBN), given to rats prior to acrylonitrile and noise, did block the elevation of NIHL by acrylonitrile. However, PBN at the dose and time interval given was ineffective in protecting auditory function in subjects exposed to noise alone. The results suggest that oxidative stress may play a role in the promotion of NIHL by acrylonitrile.

show abstract