Arginine deiminase in Staphylococcus epidermidis functions to augment biofilm maturation through pH homeostasis.

Allelic replacement mutants were constructed within arginine deiminase (arcA1 and arcA2) to assess the function of the arginine deiminase (ADI) pathway in organic acid resistance and biofilm formation of Staphylococcus epidermidis 1457. A growth-dependent acidification assay (pH ∼5.0 to ∼5.2) determined that strain 1457 devoid of arginine deiminase activity (1457 ΔADI) was significantly less viable than the wild type following depletion of glucose and in the presence of arginine. However, no difference in viability was noted for individual 1457 ΔarcA1 (native) or ΔarcA2 (arginine catabolic mobile element [ACME]-derived) mutants, suggesting that the native and ACME-derived ADIs are compensatory in S. epidermidis. Furthermore, flow cytometry and electron paramagnetic resonance spectroscopy results suggested that organic acid stress resulted in oxidative stress that could be partially rescued by the iron chelator dipyridyl. Collectively, these results suggest that formation of hydroxyl radicals is partially responsible for cell death via organic acid stress and that ADI-derived ammonia functions to counteract this acid stress. Finally, static biofilm assays determined that viability, ammonia synthesis, and pH were reduced in strain 1457 ΔADI following 120 h of growth in comparison to strain 1457 and the arcA1 and arcA2 single mutants. It is hypothesized that ammonia synthesis via the ADI pathway is important to reduce pH stress in specific microniches that contain high concentrations of organic acids.

Glutathione and associated enzymes in toxic cataractogenesis-selenite model.

Glutathione, gamma-glutamyl cysteine synthetase (gamma -GCS) and glutathione reductase (GSH-R) activity were determined biochemically in the lens during various stages after subcutaneous administration of sodium selenite in multiple low dosages and single high dosages. The GSH concentration and gamma-GCS and GSH-R activity declined progressively after the selenite administration. The changes observed were discussed in relation to the possible role of selenite interaction with GSH and the enzymes.

Selenite cataract and its attenuation by vitamin E in Wistar rats.

PURPOSE: To study the role of vitamin E in preventing cataract formation in experimental animals. METHODS: An experimental model (selenite cataract) was selected for this study. Selenite cataract was produced in rats by subcutaneous administration of sodium selenite. Biochemical and histological changes following induction of selenite cataract in weanling Wistar rats were studied vis-a-vis the role of vitamin E in attenuating or preventing cataractogenesis. RESULTS: Vitamin E was capable of preventing selenite cataractogenesis. Selenite cataract did not develop in 91.6% (11 of 12) and 76.7% (8 of 12) vitamin E treated rats, when administered on the 12th and 10th post partum day respectively. CONCLUSION: The study confirmed that selenite induced cataract in Wistar rats is attenuated by vitamin E.