Summary. Dimethylnitrosarnine (DMN) induced liver
injurq in rats with cell necrosis, inflammation,
hemorrhages, increased collagen type 111 synthesis and
basement membrane component laminin and collagen
IV localization in perisinusoidal sites. Malotilate
ingestion during DMN treatment abolished inflammation
and decreased interstitial collagen deposits and
vascularization. 1 t affected clearly less DMN-caused
hemorrhage. When malotilate treatment was started
subsequently to development of DMN-injury, it also
caused decrease in inflammation, though less, as well as
in collagen 111, BM and fibronectin deposits. We suggest
that the mode of the malotilate effect on reducing the
DMN-induced fibrosis of the liver is via inhibiting the
inflammation. decreased fibronectin deposition possibly
also playing a role.