COMPLEX STUDY OF THE PHYSIOLOGICAL-ROLE OF CADMIUM .3. CADMIUM LOADING TRIALS ON BROILER-CHICKENS

Cadmium (Cd) loading trials were conducted on a total of 110 (3 x 10 a nd 4 x 20) broiler chickens prereared for 21 days. The control chicken s received no cadmium, while chickens in the six treatment groups were given different doses of Cd as an aqueous solution of CdSO4 administe red either into the crop or mixed in the feed. The chickens were kept in a climatized animal house and treated usually for 3-5 weeks (maximu m 68 days), with the exception of group Cd-75 chickens which were trea ted up to 239 days of age. The chickens' health status, body mass and feed consumption were monitored throughout the trial. On days 14-20 an d on day 42 of the trial 2 chickens per group, then at the end of tria l a total of 25 chickens were killed in anaesthesia. These birds, toge ther with chickens that died or were killed during the trial, were sub jected to detailed gross pathological examination. From 11 organs (kid ney, liver, spleen, testicle, brain, myocardium, skeletal muscle, lung s, digestive tract, pancreas, tubular bones) of these chickens samples were taken for assay for a total of 16 elements, as well as for light and electron microscopic examination. With the exception of groups Cd -30 and Cd-600, no abnormal clinical signs were observed in the first two weeks of the trial. Chickens of group Cd-30 died before day 8-12 o f the trial among signs of complete anorexia, rapid emaciation, huddli ng and diarrhoea, while chickens of group Cd-600 died before day 28, s howing similar clinical signs. The body mass of chickens fed a Cd-supp lemented diet either remained constant or decreased substantially, in a degree proportional to the Cd load. The only exception was group Cd- 2.5, in which the average body mass of birds at the end of week 8 slig htly exceeded that of the controls. Four out of the 10 cockerel chicks fed a diet containing 75 ppm Cd up to 239 days of age died of intercu rrent diseases; the remaining six grew well and reached a body mass of 3.8-4.3 kg. Feed conversion efficiency was satisfactory in the contro l group and in group Cd-2.5 (2.1 and 2.4 kg, respectively) and could n ot be evaluated in a realistic manner in the other groups. At necropsy , the cockerel chicks of groups Cd-30 and Cd-600 showed severe emaciat ion, liver and kidney degeneration, myocardial hypertrophy and cardiac dilatation. In chickens of groups Cd-75 and Cd-300, a body mass reduc tion, hepatic and renal degeneration, pancreatic, lienal and testicula r atrophy and cardiac hypertrophy were observed. In chickens exposed t o prolonged Cd load, the glandular stomach and the gizzard were dilate d and filled with a mucinous substance; the wall of the gizzard was th inned and its keratinoid layer thickened In chickens exposed to a dail y Cd load of 2.5 mg, which developed well, the substantial hypertrophy and oedematous infiltration of the testicles was a conspicuous findin g. In cocks fed Cd for 239 days the above-mentioned changes of the par enchymal organs were accompanied by the presence of bones which were e asy to cut through. Microscopic findings included more or less severe tubulonephrosis in the kidneys of almost all chickens exposed to Cd lo ad. In individuals treated with higher doses of Cd for a long period f ibrosis was also present. In the livers there was necrosis and biliary duct proliferation; in the spleens an atrophy of the Malpighian corpu scles, in the testicles a damage of the germinal epithelium and, upon higher Cd load, severe atrophy. In the brain there were areas with gli osis and malacia, the skeletal muscles showed oedema and muscle fibre atrophy, and in the myocardium a reactive necrosis could be seen. In t he dilated parabronchi of the lungs a mucinous substance had accumulat ed, the walls of the air and blood capillaries had thinned down and ru ptured. In the glandular stomach the glands of the tunica propria, whi le in the gizzard the mucosal glands were atrophied. The epithelial ce lls of the glandular chambers of the pancreas were also atrophic. In c hickens exposed to a lower Cd load the bones showed a calcification di sturbance of the degenerated epiphyseal cartilage, while in those subj ected to a higher Cd load osteoporosis, osteoclastic osteolysis and bo ne marrow aplasia developed. Electron microscopic examination revealed the welling of mitochondria and endoplasmic reticula in the hepatocyt es. The glandular epithelial cells of the pancreas became depleted in granules, the cisternae of the RER were dilated, and the cytoplasm sho wed partial necrosis and the appearance of autophagous vacuoles. In th e myocardium, dilatation of the sarcoplasmic reticula, oedema, and the formation of giant mitochondria were observed. The tubular epithelial cells of the kidneys contained hyaline droplets and showed mitochondr ial degeneration, the nerve cells of the brain became depleted in glyc ogen and showed a dilatation of the RER cisternae. Depending on the de gree of Cd load, the concentration of Cd increased in all organs. In t he Cd-300 group, the Cd concentration of the liver (667.80 mg/kg) was approx. 4000 times higher than in the control group (0.15 mg/kg). The Cd concentration of the kidney also rose by three orders of magnitude, and reached a maximum of 333.0 mg/kg. Cd accumulation was very substa ntial in the spleen (20.57 mg/kg), testicle (17.50 mg/kg) and pancreas (83.86 mg/kg). The Cd content of the bones showed a less marked incre ase, with a maximum of 4.66 mg/kg. As a result of the Cd load, the Zn content of the bones appreciably decreased. Cd loading exerted a posit ive or negative effect on the metabolism of several microelements (Fe, Zn, Cu, Mn, Mo, B, Sr). Upon Cd loading, the content of P increased i n all organs except the spleen, testicles and the lungs. The same was found for the Ca content of all organs but the bones, the Ca content o f which slightly decreased as a result of higher Cd load.