Cochlear damage due to germanium-induced mitochondrial dysfunction in guinea pigs.

Area of Science:

• Ototoxicology
• Mitochondrial Biology
• Toxicology

Background:

• Germanium dioxide (GeO(2)) is a compound with potential toxic effects.
• Mitochondrial dysfunction is implicated in various cellular pathologies.
• Hearing impairment can result from damage to the cochlea's delicate structures.

Purpose of the Study:

• To investigate the impact of GeO(2) exposure on hearing acuity.
• To determine if GeO(2) induces mitochondrial dysfunction.
• To identify the specific cellular targets of GeO(2) toxicity in the auditory system.

Main Methods:

• Guinea pigs were administered diets containing 0%, 0.15%, or 0.5% GeO(2) for two months.
• Hearing acuity was assessed using standard audiological tests.
• Auditory organs (cochlea, stria vascularis, supporting cells) and other tissues were examined for pathological changes and mitochondrial inclusions using electron microscopy.
• Cytochrome c oxidase activity was measured in skeletal muscle and kidney tissue.

Main Results:

• Guinea pigs fed 0.5% GeO(2) developed significant hearing impairment.
• Pathological changes, including degeneration of stria vascularis and cochlear supporting cells with electron-dense mitochondrial inclusions, were observed in the high-dose group.
• Decreased cytochrome c oxidase activity and mitochondrial inclusions were also noted in the skeletal muscles and kidneys of the 0.5% GeO(2) group.
• No hearing impairment or significant pathological changes were found in untreated animals or those receiving 0.15% GeO(2).

Conclusions:

• Oral administration of 0.5% GeO(2) induces mitochondrial dysfunction in the cochlea, leading to hearing impairment.
• The stria vascularis and cochlear supporting cells are primary targets of GeO(2)-induced ototoxicity.
• GeO(2) toxicity affects mitochondria in multiple organs, including skeletal muscle and kidney, suggesting a systemic effect.