Adult male Wistar rats were enrolled in a study to test the acute hepatic effects of 50 mg/kg fumonisin B 1 in feed for 5 days. Fumonisin B 1 depressed growth and feed intake, and absolute and relative liver weight showed a significant increase. The proportions of C17:0, C18:3 n3, C22:5 n3 and C22:6 n3 fatty acids decreased in the hepatic phospholipid fraction. All proportional decreases modified the hepatocellular membrane lipids into a more rigid state. The fatty acid profile modifications were partly compensated for by endogenous glutathione (preventing the formation of conjugated dienes and trienes as initial phase lipid peroxidation indicators), while the enzymatic antioxidant defence system (glutathione peroxidase) was unaltered. In contrast, hepatic malondialdehyde, the cytotoxic product of end-phase lipid peroxidation showed a concentration increase even after 5 days of feeding. The results indicate a rather strong and rapid hepatic effect of FB 1 , immediately impairing membrane phospholipids, even before the enzymatic antioxidant defence is activated.Key words: Fumonisin B 1 , rat, hepatocellular membrane, fatty acids, oxidative stress, antioxidants Fumonisins are cancer-inducing metabolites of Fusarium proliferatum and Fusarium verticillioides. They have a long-chain hydrocarbon unit (mimicking to a certain extent cellular sphingosine and sphinganine), which plays a determinant role in their cell-membrane-associated toxicity. From the fumonisin group, fumonisin B 1 (FB 1 ) shows strong toxic effects and has been reported to promote hepatic tumour in rats. Fumonisin B 1 , the most abundant of the numerous fumonisin analogues, was classified by the IARC as a Group 2B carcinogen (possibly carcinogenic in humans; IARC, 2002).