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Abstract
Cobalt exposure is associated with impairments in learning and memory functions even at low concentrations.
- Cobalt can act as an epigenetic hazard, potentially leading to neurodegenerative damage.
- Ferroptosis, a form of cell death, may be induced by cobalt exposure through specific mechanisms.
- N6-methyladenosine demethylase ALKBH5 is implicated in the regulation of cobalt-induced ferroptosis.
- Heme oxygenase-1 (HO-1) is identified as a direct target of ALKBH5, crucial for mitigating cobalt-induced effects.
- Deficiency in ALKBH5 alters the regulation of HO-1 mRNA, affecting its stability and splicing, which could increase susceptibility to ferroptosis.
- The role of heterogeneous nuclear ribonucleoprotein M (hnRNPM) in HO-1 mRNA splicing may be influenced by mA modifications.
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