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Twelve male lambs (30.5±2.1 kg) with cannulas in the rumen were divided into three groups to evaluate the accidental toxicity of selenium (Se) via digestive tract. The first group received intraruminal bolus without a Se source; the second group received intraruminal bolus with sodium selenite (SS: Na2SeO3); the third group received intraruminal bolus with barium selenate (BS: BaSeO4). The ruminal boluses were immediately degraded by a manufacturing defect, releasing an amount of 366 mg Se via rumen. All lambs had tachypnea (80 cycles per minute), a metallic smell in the oral cavity and laminitis foot. Analyses of necropsy and histopathology showed frequencies of lesions in the myocardium and skeletal muscle, lesions in the myocardium were more common in lambs intoxicated with SS or BS than the control group (P<0.05); the tissues were swollen and there were hyaline fibres (Zenker degeneration), as well as fragments and proliferation of the nuclei with necrosis. Se concentration in lambs intoxicated with SS and BS were: myocardium: 0.389 and 0.332; skeletal muscle: 0.583 and 0.492; and kidney: 2.871 and 2.841 μg/g fresh tissue, respectively. The Se concentration in blood increased over 2.5 times in the intoxicated lambs with both sources of Se (0.14 vs. 0.36 μg/mL) from baseline to the 22 days of sampling. There was a lower correlation (r=0.46) in SS intoxication group than the control and BS group (r≥0.93). As a conclusion, high dosages of 366 mg Se or 12 mg Se/kg BW in an accidental dosage did not cause a severe mortality but all lambs immediately showed reduced feed intake, metallic smell exhalation and depression.

Pathophysiological response to experimental oral overdose of different forms of selenium in lambs