Dimethylnitrosamine (DMN) induced liver injury in rats with cell necrosis, inflammation, hemorrhages, increased collagen type III 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. It 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 III, 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.