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Lake trout are used as bioindicators for toxics exposure in the Great Lakes ecosystem. Here the first lake trout (Salvelinus namaycush) liver proteomics study is performed and searched against specific databases: (NCBI and UniProtKB) Salvelinus, Salmonidae, Actinopterygii, and Oncorhynchus mykiss, and the more distant relative, Danio rerio. In the biological replicate 1 (BR1), technical replicate 1 (TR1), (BR1TR1), a large number of lake trout liver proteins are not in the Salvelinus protein database, suggesting that lake trout liver proteins have homology to some proteins from the Salmonidae family and Actinopterygii class, and to Oncorhynchus mykiss and Danio rerio, two more highly studied fish. In the NCBI search, 4194 proteins are identified: 3069 proteins in Actinopterygii, 1617 in Salmonidae, 68 in Salvelinus, 568 in Oncorhynchus mykiss, and 946 in Danio rerio protein databases. Similar results are observed in the UniProtKB searches of BR1RT1, as well as in a technical replicate (BR1TR2), and then in a second biological replicate experiment, with two technical replicates (BR2TR1 and BR2TR2). This study opens the possibility of identifying evolutionary relationships (i.e., adaptive mutations) between various groups (i.e., zebrafish, rainbow trout, Salmonidae, Salvelinus and lake trout) through evolutionary proteomics. Data are available via the PRIDE Q2 (PXD011924)., (© 2019 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Decabromodiphenyl ether (BDE 209) is the main congener in the commonly used commercial flame retardant mixture, "deca-BDE". There is evidence showing that fish can debrominate BDE 209 into potentially more toxic congeners. The objective of this study was to evaluate BDE 209 uptake and its potential effects on juvenile lake whitefish (Coregonus clupeaformis). Lake whitefish were fed BDE 209 at four nominal concentrations (control, 0.1, 1, and 2 microg/g-diet) for 30 days. Livers and carcasses were analyzed for 11 polybrominated diphenyl ether (PBDE) congeners (BDE 47, 99, 100, 153, 154, 196, 197, 206, 207, 208, and 209) and daily otolith increment width was measured as an estimate of growth before and after exposure. Four congeners (BDE 206, 207, 208, and 209) were detected in livers and carcasses. Hepatic BDE 209 concentrations in the 1 and 2 microg/g treatments were significantly higher than in the control group (1.25 and 5.80 nmol/g-lipid compared to 0.183 nmol/g-lipid). The concentration of BDE 209 detected in the tissues of the control group resulted from BDE 209 in the base diets. Concentrations of all congeners from the 1 and 2 microg/g groups were higher in livers than carcasses, indicating the liver was the primary organ of BDE 209 accumulation. Compared to the fraction in diets, the molar fraction of BDE 209 was lower in livers and carcasses, whereas the fractions of BDE 206, 207, and 208 were higher. These different distributions of PBDE congeners resulted from differential adsorption and metabolism. One congener, BDE 206, could be a major metabolite from BDE 209 debromination. Otolith increment widths were narrower in fish from the highest diet concentration administered, suggesting BDE 209 may have affected growth rates. In conclusion, this in vivo study with lake whitefish showed that BDE 209 was debrominated into lower PBDE congeners and that exposure to 2 microg/g may have affected fish growth.

Brook charr (Salvelinus fontinalis) were maintained at one of two stocking densities (SD) (30 or 120 kg/m3) and fed either a control or a T3-supplemented (20 mg/kg) diet for 30 days in order to investigate possible interactive effects of SD and T3-administration on growth, feeding rate, food conversion efficiency, and hepatic and dark muscle enzyme activity. In addition, liver slices were incubated in vitro for 6 h with epinephrine, norepinephrine, isoproterenol, propranolol, insulin, glucagon, or somatostatin to evaluate possible SD-T3 interactive effects on hepatic responses to hormonal stimulation. Maintaining the fish at high SD appeared to increase the clearance rate of T3 from the T3-supplemented group. There was no clear evidence of SD-T3 interactive effects on growth rate, feeding rate, or food conversion efficiency, although T3-administration decreased food conversion efficiency, and high SD decreased growth and feeding rates. Of the hepatic enzymes studied, HOAD, malic enzyme, G6PDH, CS, PFK, HK, and GDH activities all showed changes suggestive of interactive SD-T3 effects. Although hepatic FBPase was stimulated by both high SD and T3-administration, there was no evidence of interactive SD-T3 effects. Dark muscle HOAD, CS, and PFK also showed SD-T3-related responses; dark muscle malic enzyme, G6PDH, HK, and GDH were unaffected by either altered SD or T3-administration. Prior treatment of the fish with T3 and high SD had significant effects on free fatty acid (ffa) release to the medium and on hepatic lipid content, but had no effect on the responses to the various endocrine agents used. Glucose release from liver slices of fish stocked at high density (both T3-supplemented and controls) was higher than that of the fish stocked at low density; with the exception of insulin and glucagon, glucose release was similar in all pre-treatment groups. The insulin- and glucagon-stimulated changes in glucose release seen in the fish fed non-supplemented diets were not found in the two groups of fish fed the T3-supplemented diets. High SD and/or T3-administration induced significant lowering of hepatic glycogen content, but there was no effect of pre-treatment on the response to any of the endocrine agents used. The data show a marked effect of SD on energy partitioning processes in brook charr and the animal's ability to respond to T3-stimulation, but provided no evidence of such effects on the liver response to the various agents used.

Cyanide markedly affected growth and resting metabolic rate while causing degenerative hepatic necrosis in juvenile rainbow trout (Salmo gairdneri, Richardson). This was revealed during two experiments performed in continuously renewed water at 12.5 degree C with fish fed a restricted artificial diet and exposed to assayed cyanide concentrations of 0.00, 0.01, 0.02, or 0.03 mg/L hydrogen cyanide (HCN) for 18 days. At 0.02 and 0.03 mg/L, HCN growth was reduced by 40 to 95% after 18 days. At all concentrations, cyanide caused a severe initial repression of specific growth rate, followed by a highly significant increase which was insufficient to compensate for the original repression. Previous exposure to cyanide promoted a higher resting metabolic rate during the six days following exposure, the effect increasing with cyanide concentration. At all concentrations tested, widespread cyanide-induced degenerative necrosis of hepatocytes was observed; it was more intense at higher cyanide concentrations and well established even at 0.01 mg/L HCN.

The objective of the present work was to determine the dietary biotin requirements of young, rapidly growing rainbow trout according to independently measured parameters. Two experiments were conducted with a purified diet which had a basal biotin level of 0.01-0.02 mg/kg. A third study was done with a nonpurified diet with or without a supplement of 1.0 mg biotin/kg. Each study was initiated with fry weighing less than 2 g/fish, and was continued for 16-20 wk at 15 degrees C. The first experiment, a cross-over design with pair-feeding, showed that the unsupplemented purified diet produced a biotin-specific deficiency condition in the trout. Dietary requirements could therefore be estimated (expt 2): maximal weight gain and maximal liver biotin concentration, 0.08 mg/kg; maximal activity of hepatic pyruvate carboxylase and acetyl CoA carboxylase, 0.05 mg/kg; and maximal white muscle pyruvate carboxylase activity, 0.14 mg/kg. No differences were found between fish fed the supplemented nonpurified diet and fish fed its unsupplemented counterpart (expt 3). The biotin requirement of the trout for growth does not exceed that of other vertebrates. These results also raise a question as to the level of supplementation which may be necessary for trout diets under field conditions.