Abstract:The biochemical and histological sequelae resulting from a diet containing 50.20 mg cadmium/kg were studied in Lohmann brown cockerels from hatching until 30 days of age. The additional cadmium chloride (CdCl 2 ) to the diet induced the formation of lipid peroxides, which via a chain reaction led to accumulation of malondialdehyde in intestinal mucosa. At the end of the study (after 30 days of cadmium exposure) total protein and metallothionein levels in the intestinal mucosa and the relative ileal and duodenal weight increased. Histological data show that CdCl 2 causes an increase in number of goblet cells and granular lymphocytes in the intestinal mucosa. Down-regulation of the serotonin-positive cells in the cadmium-treated animals was observed. Growth retardation (by 27%) occurred in chicken fed the cadmium-enriched diet for 30 days. Cadmium accumulation in the intestine was markedly higher (154 times) in the cadmium-treated animals compared to the control group. Cadmium induced a decrease in zinc (but not copper) content in intestinal mucosa. We suggest that cadmium uptake triggers an inflammatory and secretory response in chicken small intestine.

The effects of high dose ascorbic acid (10 000 mg·kg(-1) in the diet) and the transition metal on the presence of oxidative stress in the internal organs of growing chicks, as well as on the innate immune system status, were investigated. Supplementation with a high dose of ascorbic acid had pro-inflammatory effects on the intestinal mucosa, and lysozyme levels were decreased significantly in all organs studied. High-dose ascorbic acid caused an imbalance between prooxidative and antioxidative activities and was associated with the generation of semiquinone radicals. We observed that ascorbic acid increased iron and cadmium absorption. When a high dose of ascorbic acid was applied, elevated kidney and intestinal mucosa iron concentrations were observed. The amount of free malondialdehyde in the above organs has increased as well. These data have important implications for the mechanism of the oxidative stress development under the influence of high dose of ascorbic acid, indicating the importance of the side reactions of the mitochondrial electron transport chain with the formation of semiquinone radicals and the role of transition metals in this process.

Lohman Brown chickens with age from the 1stto 35thday received the food with high doses ofselenium (Se1 mg/kg), copper (Cu100 mg/kg), or both elements (Se1 + Cu100). Live weight increaseof all three experimental chicken groups was by 9.3, 12.9 and 8.1%, respectively, in comparisonwith the control. The concentration of selenium in the blood of the Se1 group chickenswas by 45.5, in liver by 63.4 and in kidney by 19.7% higher that in organs of control group chickens.Selenium accumulation in organs of Se1 group chickens was highly correlated with increaseof glutathionperoxidase activity in blood (r = 0.90) and in liver (r = 0.85) and with decrease of glutathioneconcentration in liver. In Cu100 group chickens, copper concentration increased by 11.7in blood, in liver by 23.7, and in kidney by 19.9%. Together with more intensive excretion of glutathionefrom hepatocytes, copper concentration in bile increased by 17.7% compared to that incontrol group chickens. Also wing feathers participated in the regulation of copper homeostaticbalance, as copper concentration in feathers increased by 66.7%. The concentration of malondialdehidein liver of chickens from all groups was similar (43.5-45.2 μmol·g-1wet wt.), indicatingthat overload of selenium and copper did not cause profuse production of oxyradicals in the organism.Increased accumulation of selenium and copper in chickens influenced biochemical regulationof iron, zinc and cadmium deposition in liver, kidney, tibia and feather, changing therelations between Se and Fe, Se and Cd, Cu and Fe, Cu and Zn, and Cu and Cd concentrations.The analysis indicates increased tolerance of chicken to loads of selenium (1 mg/kg) and copper(100 mg/kg) doses

Communicated by Henriks Zenkeviès