Abstract
A βfishyβ or βcrabbyβ taint in brown eggs from commercial flocks was associated with the use of capelin meal as a protein supplement and was reproduced under controlled conditions. Analysis of eggs and samples of the meal established that trimethylamine (TMA) was responsible for the taint and that the meal may contain rich sources of TMA in the form of TMA oxide and choline. Only certain hens were affected and their ability to metabolise TMA was very low as indicated by the oxidation of an intravenous dose of ^14^CβTMA and the activity of hepatic TMA oxidase. Oxidation of the ^14^CβTMA was further depressed by feeding the meal or injecting nonβradioactive TMA. Experiments with hens and chickens which had been bred for sensitivity to the inhibition of TMA oxidation by thionamides (and rapeseed meal) gave no indication that the meal supplied a potent inhibitor of this kind. It was concluded that the tainting is caused by overloading hens with TMA and that these hens have a genetic defect which impairs their synthesis of TMA oxidase and consequently their ability to metabolise TMA. The removal of this defect from commercial flocks by selective breeding would probably prevent tainting by both fish and rapeseed meals.