phenylmercuric-acetate and methylmercuric-chloride

In the present study, the frequency of sister chromatid exchanges (SCEs) was assayed to evaluate the genotoxic effects of mercury nitrate (Hg2+), methylmercury chloride (CH3HgCl and phenylmercury acetate (PMA) on human lymphocytes. The free radical scavengers, catalase (CA) and superoxide dismutase (SOD) were tested for their antigenotoxic effects toward PMA. PMA (1-30 microM) increased SCE frequency in a concentration-dependent manner. However, CH3HgCl significantly increased SCE frequency only at a concentration of 20 microM, and all concentrations treated with Hg2+ did not induce a positive effect. On the other hand, we first reported that 30 microM Hg2+, 20 microM CH3HgCl and (3-30 microM) PMA significantly increased the frequency of endoreduplicated mitosis. PMA was about 3- or 5-fold more effective in inducing endoreduplication than CH3HgCl or Hg2+ at equivalent toxic concentrations, respectively. However, neither CA nor SOD in concentrations of 75 and 150 microg/ml showed antagonistic action on the genotoxic effects of PMA. The results suggest that the mechanism of PMA-induced genotoxicity is not mediated by superoxide anion nor H2O2. It is concluded that PMA, which was more effective in inducing the elevation of both SCEs and endoreduplication, may be especially hazardous of the three mercury compounds tested.

Topics: Adult; Catalase; DNA Replication; Free Radical Scavengers; Humans; Karyotyping; Lymphocytes; Male; Mercury Compounds; Methylmercury Compounds; Mitomycin; Mutagenicity Tests; Mutagens; Nitrates; Phenylmercuric Acetate; Sister Chromatid Exchange; Superoxide Dismutase

Comparative effects of inorganic mercury (Hg2+), methylmercury (MeHg) and phenylmercuric acetate (PMA) on central synaptic transmission were examined by recording field potentials from CA1 neurons of rat hippocampal slices before and after acute bath application of mercurials at 20 and 100 microM. At 100 microM, Hg2+ decreased the amplitude of population spikes (PSs) to complete block; average time to block was 25 +/- 4 min. Application of 20 microM Hg2+ for 120 min gradually decreased PS amplitude to 33% of control. Effects of Hg2+ on excitatory postsynaptic potentials (EPSPs) were comparatively slow. Application of 100 microM Hg2+ for 120 min only reduced EPSP amplitude to 60% of control; no complete block occurred, suggesting an effect primarily on the postsynaptic CA1 cell membrane. In contrast to Hg2+, MeHg at 20 and 100 microM first increased amplitudes of PSs and EPSPs significantly and then decreased both to complete block. Average times to block of PSs and EPSPs by 100 microM MeHg were 41 +/- 4 and 42 +/- 4 min, respectively. PMA caused similar effects on PSs and EPSPs as did MeHg. However, unlike MeHg, the increased amplitudes of PSs and EPSPs by PMA were not statistically significant. At 20 microM, PMA appeared to be more effective at blocking PSs and EPSPs than were Hg2+ and MeHg. Washing slices with artificial cerebrospinal fluid containing 1 mM D-penicillamine completely reversed the effects of Hg2+ on PSs and EPSPs and effects of MeHg on EPSPs in 90 min, but only partially reversed the effects of MeHg on PSs. D-penicillamine could reverse neither the effects of PMA on PSs nor EPSPs. It is concluded that these perturbations produced damage to the associated physiological functions leading to CNS dysfunctions.

Topics: Animals; Cell Membrane; Evoked Potentials; Hippocampus; In Vitro Techniques; Lipids; Male; Mercuric Chloride; Methylmercury Compounds; Neurons; Phenylmercuric Acetate; Rats; Rats, Sprague-Dawley; Solubility; Synaptic Transmission

Topics: Adenosine Diphosphate; Drug Synergism; Humans; Mercuric Chloride; Methylmercury Compounds; Phenylmercuric Acetate; Phenylmercury Compounds; Platelet Aggregation

Susceptibility to inorganic mercuric ions and to organomercurials of 237 Pseudomonas aeruginosa clinical strains isolated in Mexico was determined by agar dilution tests. Resistant strains fell into two classes: i) narrow-spectrum resistant strains (27% of total isolates) resistant only to mercuric ions and to merbromin, and most grouped in pyocin type 1; and ii) broad-spectrum resistant strains (5%) with additional resistances to thimerosal, phenylmercury, methylmercury and p-hydroxymercuribenzoate, that belonged mostly to pyocin type 10. Mercurial resistant isolates showed a higher proportion of resistance to antibiotics and metals than did mercurial sensitive isolates, and broad-spectrum resistant strains had the highest frequency of resistance to antibiotics and to tellurite and arsenate.

Topics: Humans; Hydroxymercuribenzoates; Merbromin; Mercuric Chloride; Mercury; Methylmercury Compounds; Phenylmercuric Acetate; Pseudomonas aeruginosa; Thimerosal

The effects of methylmercuric chloride, mercuric chloride, and phenylmercuric acetate (10(-6) - 10(-3) mole/liter) on thrombin-induced release of adenine nucleotides from washed pig platelets were investigated. The inhibitory effects of mercurials were always reached when the higher thrombin concentration (0.74 units NIH/ml) was used. Incubation of washed pig platelets with methylmercuric chloride caused a decrease of intracellular level of platelet ATP and statistically significant changes in ATP/ADP ratio.

Topics: Adenine Nucleotides; Animals; Blood Platelets; Mercuric Chloride; Mercury; Methylmercury Compounds; Phenylmercuric Acetate; Phenylmercury Compounds; Swine; Thrombin

Studies have been made on the toxicities of three inorganic (HgCl2, HgSO4, and NH2HgCl) and two organic (CH3HgCl and phenyl mercuric acetate (PMA)) mercury derivatives on planktonic algae (Nitzschia acicularis W. Sm. and Tetraselmis suecica Butch.) Growth kinetics and flourescence changes were used as criteria for assessing algal-metal responses. Methylmercury chloride was found to be the more toxic form, inhibiting growth of both species at levels of 0.025 ppm Hg. PMA inhibited Nitzschia at the same concentration. Inorganic forms prevent growth of the diatom at 0.15-0.20 ppm Hg. Addition of inorganic mercury at concentrations of 0.05 ppm Hg resulted in reduction of the lag phase, increase in exponential growth rate, or both. Increasing mercury concentrations caused a gradual increase in the lag phase in T. suecica and in N. acicularis only with mercuric sulphate. Populations recovered from this initial effect and started to grow. The effect of inoculum size on mercurial toxicity was tested. The higher concentrations of mercury that still permit growth restricted the chlorophyll fluorescence to the central cellular area and the cells appear slimmed. This effect is highest in concentrations that inhibit growth.

Topics: Ammonia; Dose-Response Relationship, Drug; Kinetics; Mercuric Chloride; Mercury; Mercury Compounds; Methylmercury Compounds; Phenylmercuric Acetate; Plankton; Sulfates