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Description
Tyrosine hydroxylase is inactivated by catechol-quinones and converted to a redox-cycling quinoprotein
Notably, these developmental outcomes correlate with adverse effects on offspring mitochondrial function, including impaired complex I activity, shifts in the NADH/NAD + ratio, and disrupted cellular metabolism that persist into adulthood and correlate with accelerated biological aging
The addition of fluorophores can affect the distribution of the Pt species due to interactions of the conjugates with biological macromolecules 3
Modulation of oxidative stress as an anticancer strategy
