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Yannopoulos, D., Matsuura, T., Schultz, J., Rudser, K., Halperin, H.R. and Lurie, K.G. (2011) Sodium nitrorprusside enhanced cardio-pulmonary resuscitation improves survival with good neurological function in a porcine model of prolonged cardiac arrest. Critical Care Medicine, 39, 1269-1274.

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• TITLE: Escherichia coli superoxide dismutase expression does not change in response to iron challenge during lag phase: Is the ferric uptake regulator to blame?

  AUTHORS: Robert L. Bertrand, Michael O. Eze

  KEYWORDS: Antioxidant Enzymes; Oxidative Stress; Iron Metabolism; Enzyme Expression

  JOURNAL NAME: Advances in Enzyme Research, Vol.1 No.4, December 10, 2013

  ABSTRACT: Intracellular iron levels and the expression of superoxide dismutase (SOD) and hydroperoxidase (HP) are regulated in Gram-negative bacteria by the iron(II)-activated ferric uptake regula- tor (Fur). We have previously observed that the expression of SOD in exponential phase Escherichia coli is dependent upon the redox state of iron in media, consistent with the ferrous specificity of Fur regulation (Bertrand et al., Med. Hypotheses 78: 130 - 133, 2012). Through the non-denaturing electrophoretic technique we have determined the Escherichia coli expression profiles of SOD and HP in response to iron challenge throughout lag, logarithmic, and stationary phases of replication. Lag phase SOD presented an unusual expression profile such that SOD expression was unresponsive to iron challenge, analogous to observations of mutant strains lacking Fur and of E. coli incubated in iron-deplete media. Challenging Escherichia coli with iron during logarithmic phase revealed that length of exposure to oxidants is unlikely to be the cause of SOD unresponsiveness in lag phase. HP activity was up-regulated two- or three-fold throughout all growth phases in response to iron challenge, but did not present redox- or growth phase-specific outcomes in a manner analogous to SOD. We hypothesize that low Fur levels during lag phase are responsible for unresponsive SOD.