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Ototoxicity. Amelioration by protective agents.

L P Rybak1, S Somani

  • 1Department of Surgery, Southern Illinois University, School of Medicine, Springfield 62794-9638, USA.

Annals of the New York Academy of Sciences
|June 8, 2000
PubMed
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Four chemoprotective agents effectively prevented cisplatin-induced hearing loss and cochlear damage in rats. These agents protected the antioxidant defense system, mitigating ototoxicity and lipid peroxidation.

Area of Science:

  • Ototoxicity research
  • Biochemistry
  • Pharmacology

Background:

  • Cisplatin is a widely used chemotherapy agent.
  • Cisplatin administration can lead to ototoxicity, manifesting as hearing loss and cochlear damage.
  • The underlying mechanisms of cisplatin-induced ototoxicity involve oxidative stress and biochemical alterations in the cochlea.

Purpose of the Study:

  • To evaluate the efficacy of four chemoprotective agents in preventing cisplatin-induced ototoxicity in a rat model.
  • To compare the protective effects of DDTC, MTBA, ebselen, and alpha-lipoic acid against cisplatin's damaging effects on the cochlea.
  • To investigate the impact of these agents on cochlear glutathione levels, antioxidant enzyme activities, and lipid peroxidation.

Main Methods:

  • Wistar rats were used, with auditory brainstem response (ABR) testing to assess hearing thresholds before and after treatment.

Related Experiment Videos

  • Cisplatin was administered at a dosage of 16 mg/kg intraperitoneally (i.p.).
  • Protective agents (DDTC, MTBA, ebselen, alpha-lipoic acid) were administered at specific dosages and timings relative to cisplatin.
  • Cochlear tissues were analyzed for glutathione (GSH), antioxidant enzyme activities (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase), and malondialdehyde levels.

    • Main Results:

    • Cisplatin treatment resulted in significant ABR threshold shifts (27-40 dB), indicating hearing loss.
    • Rats co-treated with chemoprotective agents and cisplatin exhibited minimal ABR threshold shifts (<10 dB).
    • Cisplatin significantly depleted cochlear glutathione and reduced antioxidant enzyme activities, while increasing malondialdehyde levels.
    • The chemoprotective agents largely prevented these biochemical changes, preserving the antioxidant defense system.

    Conclusions:

    • Cisplatin-induced ototoxicity is strongly linked to lipid peroxidation and oxidative stress within the cochlea.
    • The evaluated chemoprotective agents (DDTC, MTBA, ebselen, alpha-lipoic acid) demonstrate significant efficacy in preventing cisplatin-induced hearing loss and cochlear damage.
    • These agents protect the cochlea by preserving the endogenous antioxidant defense system and inhibiting lipid peroxidation, offering a promising strategy for mitigating chemotherapy-induced ototoxicity.