Ascorbic acid prevents chloroquine-induced toxicity in inner glial cells

Area of Science:

• Oto-neuroscience
• Cellular toxicology

Background:

• Ototoxicity is a known side effect of chloroquine, an antimalarial and anti-lupus drug.
• Inner ear glial cells maintain auditory system homeostasis.
• The precise mechanism of chloroquine-induced ototoxicity on glial cells is not fully understood.

Purpose of the Study:

• To investigate chloroquine's toxicity on mouse inner ear Schwann glial cells.
• To evaluate the protective effects of ascorbic acid against chloroquine-induced ototoxicity.
• To explore the role of reactive oxygen species (ROS) in chloroquine's ototoxicity.

Main Methods:

• Schwann glial cells were cultured from mouse cochlear organ of Corti.
• Cell viability was assessed after chloroquine treatment.
• Glutamate uptake and ROS production were measured using HPLC and DCFH-DA fluorescence, respectively.
• Co-treatment with ascorbic acid was performed.

Main Results:

• Chloroquine induced concentration- and time-dependent toxicity in glial cells (LC50 = 70 μM).
• Chloroquine significantly decreased glutamate uptake and increased ROS production.
• Ascorbic acid co-treatment effectively prevented chloroquine-induced ROS production and cell toxicity.

Conclusions:

• Chloroquine induces ototoxicity via ROS production in inner ear glial cells.
• Ascorbic acid demonstrates a protective effect against chloroquine-induced ototoxicity.
• This study provides a preclinical basis for understanding and potentially mitigating chloroquine's ototoxic effects.