The comparative effects of sodium thiosulfate, diethyldithiocarbamate, fosfomycin and WR-2721 on ameliorating cisplatin-induced ototoxicity

Church, Michael W.; Kaltenbach, James A.; Blakley, Brian W.; Burgio, Don L.

doi:10.1016/0378-5955(95)00066-d

Cited by 80 publications

(68 citation statements)

References 20 publications

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“…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). 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).…”

Section: Introductionmentioning

confidence: 99%

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

Gopal

Shrestha

et al. 2012

Neurotoxicology and Teratology

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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.

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Section: Introductionmentioning

confidence: 99%

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

Gopal

Shrestha

et al. 2012

Neurotoxicology and Teratology

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“…The hamster was chosen as the animal model because it has proven to be an excellent model of CIS-induced hearing loss. Moreover, the present study was designed to be a followup and extension of our previous studies that used hamsters (Church et al 1995;Kaltenbach et al 1997).…”

Section: Introductionmentioning

confidence: 99%

“…In two previous studies using hamsters, we found that STS and DDTC ameliorated CIS's ototoxicity and mortality, but WR did not (Church et al 1995;Kaltenbach et al 1997). Our WR dose selection (18 mg/ kg) was extrapolated from human studies (Glover et al 1986(Glover et al , 1987.…”

Section: Introductionmentioning

confidence: 99%

“…The ABR was chosen as the dependent measure because of its proven sensitivity in assessing CISinduced hearing loss and the efficacy of chemoprotective drugs (e.g., Campbell et al 2003aCampbell et al , 2003bChurch et al 1995;Schweitzer 1993;Schweitzer et al 1986). The hamster was chosen as the animal model because it has proven to be an excellent model of CIS-induced hearing loss.…”

Section: Introductionmentioning

confidence: 99%

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WR-2721 (Amifostine) Ameliorates Cisplatin-Induced Hearing Loss But Causes Neurotoxicity In Hamsters: Dose-Dependent Effects

Church

Blakley

Burgio

et al. 2004

JARO

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Chemoprotective agents reduce the toxic side effects of chemotherapy agents such as cisplatin. The conventional belief is that the chemoprotective agent WR-2721 (Amifostine), while protecting against most cisplatin-induced side effects, does not protect against cisplatin-induced ototoxicity (i.e., hearing loss). There is no knowledge, however, about the efficacy of high doses of WR-2721 (WR) in possibly protecting against cisplatin-induced ototoxicity. Thus, the dose-dependent effects of WR in possibly ameliorating cisplatin-induced ototoxicity were investigated. Hamsters were given a series of 5 cisplatin injections (3 mg/kg/injection once every other day, i.p.) either alone or in combination with 18, 40, 80, or 400 mg/kg/injection of the rescue agent WR (n = 5 or 10/group). Other groups received either 80 mg/kg/injection WR alone (n = 5) or were untreated (n = 14). Ototoxicity was assessed by auditory brain stem responses (ABR). WR provided dose-dependent rescue from cisplatin's ototoxicity with no protection at the low dose of 18 mg/ kg, moderate protection at 40 mg/kg, and nearly complete protection at 80 and 400 mg/kg. However, WR doses of 40 mg/kg or higher caused neurotoxicity as evidenced by prolongations in the ABR's interpeak latencies. Thus, high doses of WR provided the beneficial effect of protecting against cisplatininduced ototoxicity, but had the harmful side effect of neurotoxicity. Previous failures to find chemoprotection from cisplatin-induced ototoxicity were likely due to the use of WR doses that were too small. The clinical implications of the beneficial and harmful effects of high doses of WR are discussed.

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“…A similar result was observed by Rebert et al 28 , as well as by Freitas 23 . However, in hamsters, Church et al 29 reported prolongation of the I-IV interval with the 15 mg/kg dose of CDDP, suggesting retrocochlear damage by this drug.…”

Section: ■ Discussionmentioning

confidence: 99%

Study of the protective effect of dexamethasone on cisplatin-induced ototoxicity in rats

Capelo

Batista²,

Brito³

et al. 2017

Acta Cir. Bras.

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Study of the protective effect of dexamethasone on cisplatininduced ototoxicity in rats 1 9-Experimental SurgeryActa Cir Bras. 2017;32(10):873-880 AbstractPurpose: To evaluate the ability of dexamethasone to protect against cisplatin (CDDP)-induced ototoxicity. Methods: Male Wistar rats were divided into the following three groups: 1) Control (C): 6 animals received intraperitoneal (IP) saline solution, 8 ml/kg/day for four days; 2) C + CDDP: 11 animals received 8 ml/kg/day of IP saline and, 90 min after saline administration, 8 mg/kg/ day of IP CDDP for four days; and 3) DEXA15 + CDDP: 11 animals received IP dexamethasone 15 mg/kg/day and, 90 min after dexamethasone administration, received 8 mg/kg/day of IP CDDP for four days.Results: It was found that dexamethasone did not protect against weight loss in CDDPexposed animals. The mortality rate was comparable with that previously reported in the literature. The auditory threshold of animals in the DEXA15 + CDDP group was not significantly altered after exposure to CDDP. The stria vascularis of animals in the DEXA15 + CDDP group was partially preserved after CDDP exposure. Conclusions: Dexamethasone at the dose of 15 mg/kg/day partially protected against CDDPinduced ototoxicity, based on functional evaluation by brainstem evoked response audiontry (BERA) and morphological evaluation by optical microscopy. However, dexamethasone did not protect against systemic toxicity. 873Study of the protective effect of dexamethasone on cisplatin-induced ototoxicity in rats Capelo IOJ et al. Acta Cir Bras. 2017;32(10):873-880 874 kept in cages with free access to food and water and natural sleep and wake cycles.The animals were divided into three groups:Group 1 (n = 6) (Control; C): rats were treated on four consecutive days with saline solution at 8 ml/kg/day (total of 32 ml/kg). The animals were evaluated by brainstem evoked response audiometry (BERA) one day before (D0) and four days after (D4) treatment initiation.Group 2 (n = 11) (C + CDDP): rats were treated on four consecutive days with saline solution at 8 ml/kg/day (total of 32 ml/kg) and with CDDP at 8 mg/kg (total of 32 mg/kg) 90 min after saline administration. The animals were evaluated by BERA on D0 and D4.Group 3 (n = 11) (DEXA15 + CDDP): rats were treated on four consecutive days with dexamethasone at 15 mg/kg/day (total of 60 mg/kg) and with CDDP at 8 mg/kg/day (total of 32 mg/kg) 90 min after dexamethasone administration. The animals were evaluated by BERA on D0 and D4.Wistar rats underwent deep anesthesia with 80 mg/kg ketamine combined with 10 mg/kg xylazine. A previous otoscopy was performed, and animals with external and middle ear alterations were excluded from the study. Those with normal otoscopy received auditory evaluation (BERA) just prior to drug administration (D0). In all groups, the medications were injected intraperitoneally. In groups 2 and 3, the chemotherapy injection was performed 90 minutes after the initial injection of dexamethasone or saline solution. On the subsequent three days...

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The comparative effects of sodium thiosulfate, diethyldithiocarbamate, fosfomycin and WR-2721 on ameliorating cisplatin-induced ototoxicity

Cited by 80 publications

References 20 publications

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

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

WR-2721 (Amifostine) Ameliorates Cisplatin-Induced Hearing Loss But Causes Neurotoxicity In Hamsters: Dose-Dependent Effects

Study of the protective effect of dexamethasone on cisplatin-induced ototoxicity in rats

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