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Gut 1998;42:313-314; doi:10.1136/gut.42.3.313
Copyright © 1998 BMJ Publishing Group Ltd & British Society of Gastroenterology.
GUT 1998;42:313-314 ( March )

COMMENTARY

See article on page 334

Nitric oxide as an antimicrobial agent: does NO always mean NO?

The first 150 words of the full text of this article appear below.

Nitric oxide (NO) synthesised from L-arginine subserves multiple physiological functions in the cardiovascular, respiratory, gastrointestinal, genitourinary, and central and peripheral nervous systems.1 But synthesis of NO also contributes to host defence and seems to have cytostatic and cytotoxic effects against certain pathogens, and even against host cells themselves.1 How is this double act achieved? What determines the switch from physiological mediator to lethal gas and how is bacterial killing achieved?

The simple and standard answer to the dual action of NO is that its effects depend on the amounts generated and the local concentrations achieved. In the nanomolar concentrations generated by constitutive NO synthase (NOS) isoforms, NO acts as a cell signalling molecule and interacts preferentially with its physiological target enzymes---the most significant of which seem to be soluble guanylyl cyclase and possibly cytochrome C oxidase. At the higher concentrations generated when the other enzymes become targets for . . . [Full text of this article]


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