Mj. Groot et al., COMBINATIONS OF GROWTH PROMOTERS IN VEAL CALVES - CONSEQUENCES FOR SCREENING AND CONFIRMATION METHODS, Journal of veterinary medicine. Series A, 45(6-7), 1998, pp. 425-440
This study investigates the influence of low dosages of beta-agonists
combined with other growth promoters on screening and confirmation met
hods in male veal calves. Five groups of four calves were treated for
6 weeks with combinations of low dosages of beta-agonists (beta AG, cl
enbuterol, mabuterol and mapenterol, 0.4 mu g/kg each twice daily) in
combination with 17 beta-estradiol (E2, 5 mg per animal per 14 days),
methylthiouracil (MTU, 2.857 mg/kg bw twice daily) and dexamethasone (
DEX, 4 mg per animal per 10 days during the last 20 days of treatment)
. Another group of four untreated animals served as controls. The weig
ht and size of the thymus was reduced in the DEX group, the MTU group
showed enlarged thyroids. Histologically the prostates showed vacuolar
degeneration in the beta AG animals and metaplasia in the E2 group. S
ome vacuolization was also observed in the controls. The testis.showed
impaired development in all treatment groups, E2 leading to the most
severe changes. DEX led to cortical atrophy of the thymus. MTU induced
hyperplastic changes in the thyroid. These results indicate that come
dication does not markedly affect the histological changes induced in
the hormonal target tissues. For screening purposes histology of the p
rostate can be used as a marker for oestrogens, whereas the weight of
the thymus and thyroid can be used as an indication for the use of cor
ticosteroids and thyreostatics, respectively. Vacuolization in the pro
state appeared no reliable indication for beta-agonists. Samples of ur
ine, faeces, liver and eye (retina/choroid) were analysed for beta-ago
nists. E2 significantly increased the levels of all beta-agonists in t
he liver and faeces, whereas DEX significantly reduced these levels. T
hese observations show that additional medication with different group
s of growth promoters can markedly alter the excretion of beta-agonist
s and thus influence (regulatory) control.