Action of Some Organomercury Compounds on Photosynthesis in Spinach Chloroplasts

The effects of five organomercury compounds (methylmercuric chloride, phenylmercuric acetate, phenylmercuric borate, phenylmercuric citrate and diphenylmercury) on photosynthetic electron transport (PET) in spinach chloroplasts were investigated. The IC50 values of organomercury compounds related to PET inhibition in spinach chloroplasts varied in the range from 468 mmol dm-3 to 942 mmol dm-3 and were approximately by one order higher than the corresponding value determined for HgCl2 applied also in DMSO solution (IC50 = 58 mmol dm-3). Due to extremely low aqueous solubility of diphenylmercury, the corresponding IC50 value could not be determined. Using EPR spectroscopy as probable sites of action of organomercury compounds in photosynthetic apparatus ferredoxin on the acceptor side of PS 1 and the quinone electron acceptors QA or QB on the reducing side of PS 2 were suggested.

Coordination Deficits Induced in Young Adult Mice Treated with Methylmercury

Male and female C57BL/6J mice starting at postnatal (P) day 34 were exposed orally to five divided doses totaling 1.0 or 5.0 mg/kg of methylmercury (MeHg; given as methylmercuric chloride) or sterile deionized water in moistened rodent chow. After a 5-day waiting period, control and MeHg-treated mice were subjected to a standard battery of behavior tests for balance and motor coordination. Latency to falling on the accelerating rota-rod was significantly decreased in 5.0 mg/kg MeHg-exposed mice when compared to control mice. In the open field, horizontal exploration with respect to total distance traveled during the first 5 min on the first test day was significantly reduced in 1.0 mg/kg MeHg-exposed mice when compared to control mice. Rearing activity was not affected by MeHg treatment. In the footprint analysis, angle of foot placement measured in 1.0 mg/kg MeHg-treated mice was significantly greater compared to control mice. Base stance and stride length were unaffected by MeHg treatment. On the vertical pole test, 10 mice from each treatment group fell off the pole during the time the pole was shifted from a horizontal position to a vertical position, whereas none of the control mice fell. These results indicate that short-term, low to moderate doses of MeHg in young adult mice can be detrimental to motor coordination and balance.

Mechanisms involved in methylmercuric chloride (MeHgCl)-induced suppression of human neutrophil apoptosis

We have previously demonstrated that concentrations of 1-10 μM of methylmercuric chloride (MeHgCl) that are cytotoxic to monocytes-macrophages can curiously inhibit neutrophil apoptosis by a yet unknown mechanism. In the present study, we demonstrate that, as with the cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), a classical inhibitor of neutrophil apoptosis, treatment of cells with 5 M MeHgCl inducesde novo protein synthesis and prevents the loss of expression of the antiapoptotic Mcl-1 protein. The expression of the cytoskeletal proteins gelsolin, paxillin and vinculin was similar in MeHgCl or GM-CSF-induced suppression of apoptosis. However, MeHgCl prevents the degradation of vimentin differently than GM-CSF. Apoptosis was further confirmed by flow cytometry (FITC annexin-V), and by monitoring CD16 cell surface expression. Curiously, unlike GM-CSF, MeHgCl did not prevent CD16 shedding. We conclude that, like GM-CSF, MeHgCl can delay neutrophil apoptosis by inducing de novoprotein synthesis and by preventing the loss of the antiapoptotic Mcl-1 protein. However, unlike GM-CSF, MeHgCl induces an atypical degradation of vimentin without preventing CD16 shedding.