A stable model for an unstable target

Researchers use a new technique to explore how light-activated singlet oxygen modifies target molecules

2014-04-14

(Press-News.org) A study in The Journal of General Physiology provides new insights about singlet oxygen and sets the stage for better understanding of this highly reactive and challenging substance.

Singlet oxygen is an electronically excited state of oxygen that is less stable than normal oxygen. Its high reactivity has enabled its use in photodynamic therapy, in which light is used in combination with a photosensitizing drug to generate large amounts of singlet oxygen to kill cancer cells or various pathogens.

Light-generated singlet oxygen also plays a role in a range of biological processes. It is produced during photosynthesis in plants, for example, and its production in skin cells has been linked to aging and cancer development. Moreover, small amounts of singlet oxygen produced during metabolic reactions can act as a local signaling factor that oxidizes and modifies target molecules, but the underlying mechanisms are poorly understood.

Lei Zhou and colleagues from Virginia Commonwealth University unveil a new technique to show how singlet oxygen modifies HCN channels— "pacemaker channels" that contribute to memory, heart rate, pain sensation, and other functions. By applying millisecond laser light pulses to HCN channels tagged with a fluorescent photosensitizer, Zhou and colleagues were able to elicit the production of small amounts of singlet oxygen in a precise location and monitor its effects on the channels in open and closed states. Their results indicate that some of its effects on HCN channels are state specific and involve specific modifications near the activation gate.

The findings not only help explain how singlet oxygen functions, they introduce a method that can be used for further exploration of this important signaling factor.

INFORMATION: Gao, W., et al. 2014. J. Gen. Physiol. doi:10.1085/jgp.201311112

About The Journal of General Physiology Founded in 1918, The Journal of General Physiology (JGP) is published by The Rockefeller University Press. All editorial decisions on manuscripts submitted are made by active scientists in conjunction with our in-house scientific editor. JGP content is posted to PubMed Central, where it is available to the public for free six months after publication. Authors retain copyright of their published works and third parties may reuse the content for non-commercial purposes under a creative commons license. For more information, please visit http://www.jgp.org.

Research reported in the press release was supported by Virginia Commonwealth University and the American Heart Association.

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