Multinuclear copper enzymes such as tyrosinases, catechol oxidases, and multicopper oxidases reduce dioxygen exclusively at histidine-ligated coupled binuclear copper sites, which are conserved across aerobic life.1 While the first two-electron reduction of dioxygen is well-established (2Cu1+ + dioxygen → 2Cu2+ + peroxide), models for the second two-electron step are evolving rapidly; converging consensus suggests this step may present a first example of a biological system able to access copper(III).2-6 This talk will present synthetic precedent for a viable copper(III) intermediate that forms when deprotonation of ligating histidine can occur.2
The implications of histidine deprotonation can be challenging to probe directly in proteins but can be tested directly using appropriate synthetic systems. The effects are not subtle. We find that histidine deprotonation reduces dioxygen from peroxide to oxides, and oxidizes both copper centers to copper(III). This creates an electrophilic LUMO positioned appropriately to accept substrate electrons, and a deprotonated histidine positioned appropriately to act as a substrate-deprotonating base.2
A capacity for copper centers to switch from one-electron to two-electron shuttles through histidine hints at a provocative but simple alternative mechanism for tyrosinases, which finds theoretical support. Electrophilic aromatic substitution through a formal copper(III) intermediate accessed by even transient histidine deprotonation leads to only reasonable barriers, with deprotonation contributing to catalysis by up to 15 kcal•mol-1.
Given the conserved structures of binuclear copper sites, we suggest that copper(III) accessibility though histidine deprotonation may be more viable than generally appreciated.