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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >On reversible H-2 loss upon N-2 binding to FeMo-cofactor of nitrogenase
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On reversible H-2 loss upon N-2 binding to FeMo-cofactor of nitrogenase

机译：On reversible H-2 loss upon N-2 binding to FeMo-cofactor of nitrogenase

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摘要

Nitrogenase is activated for N-2 reduction by the accumulation of four electrons/protons on its active site FeMo-cofactor, yielding a state, designated as E-4, which contains two iron-bridging hydrides Fe-H-Fe. A central puzzle of nitrogenase function is an apparently obligatory formation of one H-2 per N-2 reduced, which would "waste" two reducing equivalents and four ATP. We recently presented a draft mechanism for nitrogenase that provides an explanation for obligatory H-2 production. In this model, H-2 is produced by reductive elimination of the two bridging hydrides of E-4 during N-2 binding. This process releases H-2, yielding N-2 bound to FeMocofactor that is doubly reduced relative to the resting redox level, and thereby is activated to promptly generate bound diazene (HN=NH). This mechanism predicts that during turnover under D-2/N-2, the reverse reaction of D-2 with the N-2-bound product of reductive elimination would generate dideutero-E-4 E-4(D-2), which can relax with loss of HD to the state designated E-2, with a single deuteride bridge E-2(D). Neither of these deuterated intermediate states could otherwise form in H2O buffer. The predicted E-2(D) and E-4(D-2) states are here established by intercepting them with the nonphysiological substrate acetylene (C2H2) to generate deuterated ethylenes (C2H3D and C-2 H2D2). The demonstration that gaseous H-2/D-2 can reduce a substrate other than H+ with N-2 as a cocatalyst confirms the essential mechanistic role for H-2 formation, and hence a limiting stoichiometry for biological nitrogen fixation of eight electrons/protons, and provides direct experimental support for the reductive elimination mechanism.

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