The feeding of housed lambs on conserved forages and pelletedrattons is accompanied by a high risk of chronic capper tCu) poisoning (CeF) which might be reduced by sekcting sires for low liver Cu status. Livers were therefore retrieved from Suffolk, Texel and Charollais lambs, slaughtered during the course ofa performance trial, to ascertain sire and possibly breed effects on the rate of Cu accretion in the liver. In total, 160 livers were obtained, 100from Suffolk, 40 from Texel and 20from Charoiiaie lambs, the progeny of 14, eightand eightsires, respectively. Lambs came from three separately managed flocks but were brought together at B weeks of age, weaned onto a common complete diet containing 6·1mg Cu per kg dry matter (DM) and offered ad libitum. One-fifth of each breed grouptvas slaughtered at 14, 18 or22 weeks and the remaining 40% at 26 weeks afage. Mean (s.e. ) liverCu concentrations at those ages were 3220 (450), 4639(464)/ 6426 (468), anti 6513 (370) gmol/kg OMfor Suffolk, and 5843(811), 6579 (857), 8017 (811) and 10406 (589) gmollkg OM for Texel, respectively. The pattern olliver Cu accretion differed, the Suffolk starting at a low value yetreaching a plateau at about 22 weeks of age (significant quadratic regression coefficient), the Texel, continually increasing from a high initial value at an average rate of 53·7 (s.e.10·6)gmol/kg OM per day. There was a significant effect of sire onliver Cuin theSuffolk(P <0·05) with a heritability of 0·85 (s.e. 0·44); in the Suffolk and Texei combined/ the heritability was 0·60 (s.e. 0·33). The data available on theCharollais were too limited to test for sire effects but at 26 weeks of age, where mast information was available, the mean liver Cu concentration was 7285 is.e. 826) }1mollkg DM. At a given age, food intake/ liver weight and live weight were each lowest in the Texel but When expressed as a proportion ofliveweight (LW), bath food intake (43g/kg LW)and liver weight (5·15g OM per kg LW) were similar among breeds (P> 0·05). Thus, differences in lioerCu accretion are unlikely to reflect differences in Cu intake per unit liver weight. There was a tendencyfor liversize perkg LW to decrease as.liver Cu rose in the Texel but not in theSuffolt Continued hepatic Cuaccreiion in the Texel may reflect a breed-specific inability to c()pe with Cu overload. Increases in liver Cu to marginally toxic levels in some Suffolk, some Charollaisand most Texellamoe. and toa level commonly associated with toxicityin one Texellamb, on a ration ofmoderate Cu concentration highlights thedifficulty of controlling risk ofCCPby.manipulating dietary composition. The current EC limit for Cuin ooine diets, 17 mg Cu perkg DM, is clearly too high for the breeds and dietary conditions used in this study. However a safe limit would be hard to achieve andhence the need to exploit sire variation in propensity to accumulate liver Cu to reduce disease risk. gradually introduced to this same ration, with ad libitum access to hay, over several weeks. All lambs were housed together in a single sh...