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A high percentage of feral Baltic salmon suffers from an abnormal type of sac fry mortality, designated as the M74 syndrome. Although thecause of the mortality is not known, it has been proposed that a high burden of lipophilic xenobiotics is a contributing factor. The objective of the present study was to investigate hepatocyte ultrastructure and liver biochemical anomalies that could be related to exposure to lipophilic xenobiotics in feral Baltic salmon sac fry. Electron microscopy of M74 sac fry liver revealed a dilatation of endoplasmic reticulum, numerous myelin figures, some swelling mitochondria, and an accumulation of lipid droplets. The ratio of reduced glutathione to oxidized glutathione content in M74 sac fry liver was about 60% of that found in the control sac fry liver. Glutathione reductase, an enzyme responsible for reducing oxidized glutathione to reduced glutathione (GSH), was elevated in the M74 sac fry liver, indicating an adaptive response to an increased demand for GSH. Hepatic glutathione S-transferase activity was significantly higher in the M74-affected sac fryliver compared with that of the normally developing sac fry liver, whereas glutathione peroxidase activity was at about the same level inthe two groups. Hepatic cytochrome P4501 A (CYP I A) activity and protein content and NADPH cytochrome c reductase activity were higher in the liver of M74 sac fry than in the liver of normally developing sac fry. Anti-trout LMC2 (CYP2K1) recognized two protein bands, one ofwhich was elevated in the M74 sac fry liver In conclusion, the damage and biochemical changes recorded here, in combination with poor vitamin status in the M74 sac fry, may contribute substantially to the mortality. [ABSTRACT FROM AUTHOR]