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.

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