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First published online December 20, 2006
In this issue |
The signalling molecule nitric oxide (NO) helps to regulate blood flow, nerve transmission and cellular defence. It might also regulate cellular respiration by inhibiting cytochrome c oxidase (CcO) - a component of the mitochondrial electron transport chain. On p. 160, Salvador Moncada and co-authors report that CcO can maintain mitochondrial respiration even when partly inhibited by NO by increasing its electron turnover. The authors use a visible-light spectroscopy system to measure O2 and NO concentrations, mitochondrial respiration, and cytochrome redox states in cells genetically modified to produce NO when treated with arginine. Their results show that although endogenously generated NO affects the redox state of cytochromes - it increases their reduction by inhibiting CcO - respiration is not inhibited until this reaches a critical point. Respiration continues unabated until then, they report, because of an increased flux of electrons through uninhibited NO-free CcO. This physiological mechanism, the authors suggest, enables cells to maintain their respiration without compromising their bioenergetic state when the cellular O2:NO ratio changes in response to different types of stress - for example, hypoxia.
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