Cold injury is a tissue trauma produced by exposure to freezing temper
atures and even brief exposure to a severely cold and windy environmen
t. Rewarming of frozen tissue is associated with blood reperfusion and
the simultaneous generation of free oxygen radicals. In this review i
s discussed the current understanding of the mechanism of action of fr
ee oxygen radicals as related to cold injury during rewarming. Decreas
ed energy stores during ischaemia lead to the accumulation of adenine
nucleotides and liberation of free fatty acids due to the breakdown of
lipid membranes. On rewarming, free fatty acids are metabolized via c
yclo-oxygenase and adenine nucleotides are metabolized via the xanthin
e oxidase pathway. These may be the source of free oxygen radicals. Le
ukocytes may also play a major role in the pathogenesis of cold injury
. Oxygen radical scavengers, such as superoxide dismutase and catalase
, may help to reduce the cold induced injury but their action is limit
ed due to the inability readily to cross the plasma membrane. Lipid so
luble antioxidants are likely to be more effective scavengers because
of their presence in membranes where peroxidative reactions can be arr
ested.