Ebselen protects glutamate uptake inhibition caused by methyl mercury but does not by Hg2+.

Alterations of the neurotransmitter release systems in CNS have been reported in a variety of neuropathological processes associated with heavy metal toxicity. Neurotoxic effects of mercurials were investigated in vitro in cerebral cortex slices from young rats. The present study indicates that: (i) the environmental contaminants methylmercury (MeHg) and mercuric chloride (Hg2+) (50 microM) inhibited the glutamate net uptake from the cerebral cortex of 17-day-old rats; (ii) ebselen (10 microM) reverted the MeHg-induced inhibition of glutamate net uptake but did not protect the inhibition caused by Hg2+. At same time, we investigated another diorganochalcogenide, diphenyl diselenide (PhSe)2 and it was observed that this compound did not revert the action of MeHg or Hg2+; (iii) in addition, we observed that exposure of slices to 50 microM MeHg and Hg2+ for 30 min followed by Trypan blue exclusion assay resulted in 58.5 and 67.5% of staining cells, respectively, indicating a decrease in cell viability. Ebselen protected slices from the deleterious effects of MeHg, but not of Hg2+ on cell viability. Conversely, ebselen did not modify the reduction of MTT caused by MeHg and Hg2+; (iv) the protective effect of ebselen on MeHg-induced inhibition of glutamate net uptake seems to be related to its ability in maintaining cell viability.

Candidal infections in neonates of very low birth weight.

Candida infections represent a serious cause of morbidity and mortality in sick low birth weight infants cared for in the neonatal intensive care unit. Often, the infection goes undiagnosed, or the candidal isolate is regarded as a contaminant. There is also fear of potential toxicity from treatment. We have reported a case in which recovery occurred without antifungal therapy, and reviewed the current literature regarding this potentially devastating infection.