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An enzyme called tyrosinase is the key driver of this process

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This effect is partly achieved through the inhibition of calcium influx in presynaptic channels, which reduces noradrenaline release in the ciliary body and subsequently decreases AH production (48)

Further complicating this picture, elevated lipid peroxidation and amino acid imbalances contribute to ferroptosis, as well as reduced nitric oxide availability, exacerbating tissue damage and delaying repair