The Effect of NO and CO on Cellular Iron Metabolism
A comparison of two diatomic cell signalling molecules
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Nitric oxide (NO) and carbon monoxide (CO) are toxic gases in the atmosphere that are usually associated with pollution. Surprisingly, both have been found to be synthesised within the body and have functions as signalling molecules. It has been shown that they actuate their signal by interacting with iron (Fe) in Fe-containing proteins. Fe is an obligate requirement for cells as many important enzymatic proteins utilise this element for redox activity. Activated macrophages produce large quantities of NO and it has been hypothesised that one of the cytotoxic mechanisms of activated macrophage...
Nitric oxide (NO) and carbon monoxide (CO) are toxic
gases in the atmosphere that are usually associated
with pollution. Surprisingly, both have been found
to be synthesised within the body and have functions
as signalling molecules. It has been shown that
they actuate their signal by interacting with iron
(Fe) in Fe-containing proteins. Fe is an obligate
requirement for cells as many important enzymatic
proteins utilise this element for redox activity.
Activated macrophages produce large quantities of NO
and it has been hypothesised that one of the
cytotoxic mechanisms of activated macrophages is the
NO crossing into the target cell and removing the Fe
from the proteins and effluxing it from the cell. CO
also interacts with Fe, but its effects on
cellular Fe metabolism have not been examined in as
great detail as NO has. This work has examined the
effects of NO donors and CO gas and donors on
cellular Fe metabolism. It describes the pathway NO
utilises in its removal of Fe from cells and
compares these results with CO. It indicates that
although both molecules interact with Fe they have
different effects on cellular Fe metabolism.
gases in the atmosphere that are usually associated
with pollution. Surprisingly, both have been found
to be synthesised within the body and have functions
as signalling molecules. It has been shown that
they actuate their signal by interacting with iron
(Fe) in Fe-containing proteins. Fe is an obligate
requirement for cells as many important enzymatic
proteins utilise this element for redox activity.
Activated macrophages produce large quantities of NO
and it has been hypothesised that one of the
cytotoxic mechanisms of activated macrophages is the
NO crossing into the target cell and removing the Fe
from the proteins and effluxing it from the cell. CO
also interacts with Fe, but its effects on
cellular Fe metabolism have not been examined in as
great detail as NO has. This work has examined the
effects of NO donors and CO gas and donors on
cellular Fe metabolism. It describes the pathway NO
utilises in its removal of Fe from cells and
compares these results with CO. It indicates that
although both molecules interact with Fe they have
different effects on cellular Fe metabolism.
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