The cytotoxicity of HgCl2, as assessed by inhibition of lactate dehydrogenase activity, exhibited a steep concentration dependence.
2
One hundred micromolar HgCl2 caused all cells to become necrotic within 3 hr.
3
The enzymatic activity was inhibited by p-chloromercuribenzoate and HgCl2, suggesting an important role of SH group(s) in enzyme function.
4
Three of these underwent in vivo fixation with glutaraldehyde prior to the HgCl2 SPAR to prevent toxic effects of mercury on peritoneal tissues.
5
At concentrations of HgCl2 greater than or equal to 0.25 mM, cellular necrosis occurred rapidly in all PT cells.
6
Preincubation of PT cells from both NPX and SHAM rats with glutathione provided the cells with concentration-dependent protection from the cytotoxic effects of HgCl2.
7
First, we prepared an immunoprecipitate of caspase-3 and measured the concentration of NO released from the precipitated complex by HgCl2.
8
Pre-treatment with HgCl2 decreased insulin-mediated glucose transport 1.3-fold suggesting that exposure to mercury may contribute to pathologies associated with glucose homeostasis.
9
Fifteen rabbits were investigated during a one-hour dwell with 0.1 mM HgCl2 containing 3.86% glucose-based dialysis solution, while they were anesthetized.
10
The cell line LLC-PK1 was used as a model for renal proximal tubule cells, and the effects of different concentrations of HgCl2 were studied.