Lesions of thymus and decreased percentages of the peripheral blood T-cell subsets in chickens fed on diets excess in selenium.

Selenium is an essential trace element possessing immune-stimulatory properties. The purpose of this 42-day study was to investigate the effects of excess dietary selenium on cellular immune function by determining morphological changes of thymus and peripheral blood T-cell subset. Three hundred 1-day-old avian broilers were fed on a basic diet (0.2 mg/kg selenium) or the same diet amended to contain 1, 5, 10, 15 mg/kg selenium supplied as sodium selenite (n = 60/group). Pathological lesions were progressed with the dietary Se level increased. Grossly, the volume of thymus was decreased. Histopathologically, lymphopenia and congestion were observed. Ultrastructurally, mitochondria injury was observed. In comparison with that of control group, 5, 10 and 15 mg/kg dietary Se decreased the percentage of CD3(+), CD3(+)CD4(+) and CD3(+)CD8(+) T cells of the peripheral blood, as measured by flow cytometry. The results showed that excess selenium (more than 5 mg/kg) intake could cause lesions of thymus and decrease of T-cell subsets. The cellular immune function was finally impaired in broilers.

Selenium intoxication with selenite broth resulting in acute renal failure and severe gastritis.

Selenium (Se) is an essential trace element in human and animal nutrition. It is also widely utilized in industrial processes. Reports of acute selenium toxicity in humans are rare. We report a case of a 23-year-old female who consumed about 100 mL of liquid selenite broth and presented with severe nausea, vomiting, abdominal pain, hematemesis and acute renal failure (ARF). The serum selenium level was significantly increased. Gastro-duodenoscopy revealed severe corrosive gastritis. Renal biopsy showed features of acute tubular necrosis (ATN), affecting primarily the proximal tubules. The patient was managed with gastric lavage, blood transfusions, infusion of fresh frozen plasma (FFP) and platelet concentrates and hemo-dialysis. The patient was discharged five weeks after admission and her renal functions recovered completely by eight weeks after admission. She continues to be on regular follow-up for any possible sequelae of mucosal corrosive damage. This case highlights a case of selenium intoxication from selenite broth resulting in ARF and corrosive gastritis. The recovery was complete.

Acute selenium poisoning.

Reports of acute human selenium toxicity are rare. We report 2 new cases. One patient ingested a mouthful of selenic acid (30 g/L); he only suffered mild gastrointestinal disturbances. Serial measurements of plasma selenium concentrations were performed. The first plasma level was obtained 3 h after ingestion and was the highest (931 micrograms/L); plasma concentrations subsequently decreased with a half-life of 17.5 h. The second patient ingested 1.7 g of sodium selenite. He suffered severe gastroenteritis, had transient electrocardiographic changes and developed a slight elevation of serum bilirubin. The first serum concentration measurement was performed 3 h after ingestion; the selenium level was 2.716 micrograms/L. These data are compared to those from other published cases. The prognostic significance of the blood selenium concentration is discussed.