Trimethylamine taint in eggs: The occurrence of the causative metabolic defect in commercial hybrids and pure breeds in relation to shell colour

Abstract

Six commercial foundation flocks (Rhode Island Red, New Hampshire Red and White Leghorn hybrids) and four pure breeds (Rhode Island Red, Light Sussex, White and Brown Leghorns) were included in a survey which was carried out to facilitate the elimination of the tainting defect from commercial stock by selective breeding. The defect results from an inherited inability to synthesise adequate amounts of trimethylamine (TMA) oxidase, and was detected by estimating the activity of the enzyme in the livers of young chickens, or by measuring the amount of [14C]-TMA oxide in the plasma after the injection of [14C]-TMA. It was present in two of the brown-egg breeds (Rhode Island Red and Light Sussex) and in one of the white-egg breeds (Brown Leghorn), and therefore was not associated with shell colour. There was no significant correlation between depth of shell colour and TMA oxidase activity in a commercial Rhode Island Red flock.

Nutritional and physiological effects of rapeseed meal sinapine in broiler chickens and its metabolism in the digestive tract

“…11 -13 SNP may be hydrolysed to SA and choline by intestinal bacteria, and the choline is further modified to trimethylamine (TMA) prior to absorption. 14 Usually the TMA is oxidised and excreted via the kidney, but some hens lack or have low levels of TMA oxidase and, as a consequence, TMA is deposited in developing eggs, causing the fishy taint.…”