The occurrence of a 'fishy' or 'crabby' taint in eggs and liver damage culminating in massive haemorrhage has greatly restricted the commercial utilisation of rapeseed meal as a relatively cheap protein supplement for laying hens in the UK. Recent work on these problems is reviewed. It has elucidated the cause of the taint and identified the rapeseed constituents that are involved. A genetic defect impedes the synthesis of trimethylamine oxidase in susceptible hens and goitrin and tannins inhibit the enzyme. This biochemical lesion severely impairs the metabolism of trimethylamine which is released from sinapine and other dietary sources of choline by enteric bacteria. Consequently, excessive amounts pass into the yolk and produce the taint. Liver haemorrhage is associated with hepatocyte degeneration, abnormalities in the biliary system and the leakage of cellular enzymes into the plasma. The toxic substance(s) responsible has (have) not yet been identified.

The relationships between plasma insulin, glucose, non-esterified fatty acid (NEFA) and \g=a\-amino nitrogen concentrations in the domestic fowl have been studied. During a 72-hr. fast the plasma glucose concentration fell while the NEFA concentration rose but there was no change in plasma insulin concentration. Both oral and intracardiac glucose increased the plasma insulin concentration and lowered the plasma NEFA and \g=a\-amino nitrogen concentrations. Oral amino acids increased plasma insulin and glucose concentrations but had no effect on plasma NEFA. Intracardiac ox insulin depressed plasma glucose and \g=a\-amino nitrogen and increased the plasma NEFA concentration. Intracardiac glucagon increased both plasma glucose and NEFA and depressed the plasma \g=a\-amino nitrogen concentrations but had no significant effect on plasma insulin. Intracardiac adrenaline had no effect on plasma NEFA but increased plasma glucose concentration and caused a small depression in plasma insulin concentration.

Whole meals prepared from four cultivars (Tower, ‘French’ (unknown cultivar from France), Duo and Tandem) contained sufficient progoitrin and soluble tannins to impair trimethylamine (TMA) oxidation, and thereby allow the TMA content of eggs to rise above the tainting threshold, when they were fed as protein supplements (100 g kg−1) to hens which had been bred for low TMA oxidase activity. Hulls from Tower and ‘French’ seed produced small, but detectable, effects and since the potencies of dehulled and whole meals were similar, it was established that the hulls make only a very minor contribution to the tainting potential. Although the addition of neomycin to the drinking water when the Tandem whole meal was fed appeared to diminish its effects to a certain extent, it had little value as a prophylactic measure. It was concluded that these meals could produce widespread tainting if used commercially in the UK, and that the removal from the laying hens of the genetic defect which restricts the synthesis of TMA oxidase and thereby confers susceptibility is the only effective way of eliminating the problem.

Treatment of high glucosinolate Brassica nupus meals with lime, ammonia or by micronisation lowered their tainting potential by reducing their progoitrin, soluble tannin and sinapine contents. These effects were not sufficient to prevent inhibition of trimethylamine oxidation and the consequent rise in egg trimethylamine levels above the tainting threshold when the meals were fed to susceptible hens as sources of protein (100 g kg-' diets).

Agricultural Research Council Food Research Institute, Colney Lane, Norwich, Norfolk NR4 7UANeither the administration of sinapine bisulphate in the diet, nor the repeated intramuscular or intravenous injection of large doses of this substance, reduced the ability ofchicks or laying hens to oxidise trimethylamine (TMA), as measured by the activity of TMA oxidase in hepatic microsomes or the amounts of 14C-TMA oxide that appeared in the plasma after the infusion of a standard dose of 14C-TMA. Thus, in contrast to its behaviour in vitro, sinapine did not produce significant inhibition of TMA oxidase under these conditions. Since the amount included in the diet was similar to that which would be provided by a diet containing 10% rapeseed meal, it was concluded that sinapine is not involved in the depression of TMA oxidation that occurs when the meal is fed and acts solely as a source of TMA in the consequent production of egg taint.