Semicarbazide-sensitive amine oxidase (SSAO) is a multi-functional enzyme
widely present in nature. It converts primary amines into their
corresponding aldehydes, while generating H(2)O(2) and NH(3). In mammals,
SSAO circulates in plasma, while a membrane-bound form (often referred to
as vascular adhesion protein-1, VAP-1) is found in many tissues and
organs, especially in adipocytes and vascular endothelial and smooth
muscle cells. In recent years, evidence has been accumulating that SSAO
has a role in protein cross-linking, formation of advanced glycation
end-products, atherogenesis, glucose regulation and leukocyte
extravasation at inflammation sites. Plasma SSAO is quite stable in
healthy adults, but is elevated in diabetes mellitus (both type 1 and type
2), congestive heart failure and liver cirrhosis. The origin of
circulating SSAO remains unclear, but recent evidence from clinical
studies and from (transgenic) animal studies suggests that adipocytes and
vascular endothelial cells may be the most important source. Studies with
cell cultures show evidence that the membrane-bound SSAO can be split off
from the cells, thus giving rise to the (truncated) circulating form of
SSAO. In some pathological conditions the diseased organ may be the main
source of the elevated plasma SSAO. Little is known as yet about the
regulation of plasma SSAO. Thyroid hormone appears to play a (modest) role
in this respect. Further evidence from clinical, animal and cell-culture
studies, helped by the new availability of selective SSAO inhibitors, is
needed to shed more light on the question of the regulation of SSAO
