Se-enriched Lactobacillus bulgaricus (L. bulgaricus) was generated by administration of sodium selenite (0, 1, 4, 8, 16, 32, and 64 mg/L, respectively) in MRS medium and enriched selenium manifestation in L. bulgaricus was investigated using transmission electron microscopy and energy-dispersive X-ray spectrometry and alterations of essential elements and amino acids in the organism were evaluated. We demonstrate that administration of sodium selenite in the dosage of 1-16 mg/L is suitable for selenium enrichment in L. bulgaricus and can enhance nutritive value in the organism by elevating the contents of essential elements including P, Mg, Mn, Zn, Ca, and total amino acids as well as reducing selenite to insoluble elemental selenium, an electron-dense and amorphous Se (0) granule, thereby depositing it both in the cytoplasm and in the extracellular space of L. bulgaricus. Thus, Se-enriched Lactobacillus can provide a potential dietary source of nontoxic selenium and functional regulator used for food and medical industry.

We studied cadmium toxicity in murine hepatocytes in vitro. Cadmium effects on intracellular free Ca(2+) concentration ([Ca(2+)](i)) were assayed, using a laser scanning confocal microscope with a fluorescent probe, Fluo-3/AM. The results showed that administration of cadmium chloride (CdCl(2), 5, 10, 25 microM) resulted in a dose-dependent decrease of hepatocyte viability and an elevated aspartate aminotransferase (AST) activity in the culture medium (p<0.05 for 25 microM CdCl(2) vs. control). Significant increases of lactate dehydrogenase (LDH) activities in 10 and 25 microM CdC1(2)-exposed groups were observed (p<0.05 and p<0.01, respectively). A greatly decreased albumin content and a more malondialdehyde (MDA) formation also occurred after CdC1(2) treatment. The Ca(2+) concentrations in the culture medium of CdCl(2)-exposed hepatocytes were significantly decreased, while [Ca(2+)](i) appeared to be significantly elevated (p<0.05 or p<0.01 vs. control). We found that in Ca(2+)-containing hydroxyethyl piperazine ethanesulfonic acid-buffered salt solution (HBSS) only, CdCl(2) elicited [Ca(2+)](i) increases, which comprised an initially slow ascent and a strong elevated phase. However, in Ca(2+)-containing HBSS with addition of 2-aminoethoxydiphenyl borane (2-APB), CdCl(2) caused a mild [Ca(2+)](i) elevation in the absence of an initial rise phase. Removal of extracellular Ca(2+) showed that CdCl(2) induced an initially slow [Ca(2+)](i) rise alone without being followed by a markedly elevated phase, but in a Ca(2+)-free HBSS with addition of 2-APB, CdCl(2) failed to elicit the [Ca(2+)](i) elevation. These results suggest that abnormal Ca(2+) homeostasis due to cadmium may be an important mechanism of the development of the toxic effect in murine hepatocytes. [Ca(2+)](i) elevation in acutely cadmium-exposed hepatocytes is closely related to the extracellular Ca(2+) entry and an excessive release of Ca(2+) from intracellular stores.