Biochemical and ultrastructural changes in the liver of Baltic salmon sac fry suffering from high mortality (M74)

A high percentage of fetal Baltic salmon suffers from an abnormal type of s ac fry mortality, designated as the M74 syndrome. Although the cause of the mortality is not known, it has been proposed that a high burden of lipophi lic xenobiotics is a contributing factor The objective of the present study was to investigate hepatocyte ultrastructure and liver biochemical anomali es that could be related to exposure to lipophilic xenobiotics in feral Bal tic salmon sac fry. Electron microscopy of M74 sac fry liver revealed a dil atation of endoplasmic reticulum, numerous myelin figures, some swelling mi tochondria, and an accumulation of lipid droplets. The ratio of reduced glu tathione to oxidized glutathione content in M74 sac fry liver was about 60% of that found in the control sac fry liver. Glutathione reductase, an enzy me responsible for reducing oxidized glutathione to reduced glutathione (GS H), 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 fry Liver compared with th at of the normally developing sac fry liver, whereas glutathione peroxidase activity was at about the same level in the two groups. Hepatic cytochrome P4501A (CYP1A) activity and protein content and NADPH cytochrome c reducta se activity were higher in the liver of M74 sac fry than in the liver of no rmally developing sac fry. Anti-trout LMC2 (CYP2K1) recognized two protein bands, one of which was elevated in the M74 sac fry liver. In conclusion, t he damage and biochemical changes recorded here, in combination with poor v itamin status in the M74 sac fry, may contribute substantially to the morta lity.