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PubMed1983

Interaction of methylmercury with microtubules in cultured cells and in vitro.

The effects of methylmercury (MeHg) on cytoplasmic microtubules in cultured fibroblasts and on the in vitro polymerization of microtubules were examined. MeHg caused disruption of cellular microtubules in a concentration- and time-dependent manner. Addition of the metal-chelating agent, dimercaptosuccinic acid (DMSA), both prevented and reversed the effect of MeHg. Comparisons of the cellular levels of mercury and microtubule integrity indicated that microtubules dissociated at levels higher than 0.6 microgram Hg/mg protein. In vitro polymerization was also directly inhibited by MeHg; this effect was prevented by the addition of DMSA.

Cells, Cultured↗
PubMed1984

Differential responses to methylmercury exposure and recovery in neuroblastoma and glioma cells and fibroblasts.

The effects of methylmercury (MeHg) on cytoplasmic microtubules in cultured neuroblastoma cells, glioma cells, and fibroblasts were compared. Neuroblastoma cells appeared to be more sensitive to disruption of microtubules by MeHg than the glioma cells or fibroblasts; cellular concentrations of mercury after MeHg were also higher in neuroblastoma cells. Recovery of microtubule structure was monitored in cells after removal of MeHg; addition of the chelating dimercaptosuccinic acid (DMSA) increased reassembly of microtubules. During MeHg treatment and early recovery, microtubule integrity was dependent on cellular mercury concentrations. However, after prolonged DMSA exposure, mercury appeared to reenter the cell, without causing dissociation of microtubules.

Animals↗
PubMed1982

Preparation of technetium-99-DMS renal complex in solution and its chemical and biological characterization.

99Tc-DMS solution was prepared by double isotope labelling, purified by molecular sieving through Sepharose 2B column, and checked by chromatographic and spectrophotometric methods, as well as by assessment of its biodistribution in rats. The preparations, obtained in a series of nine experiments, showed high renal uptake (30-40% of injected dose per organ) and could be used for further investigations of Tc-DMS biochemical behaviour in kidney tissue at subcellular level. Radioactive concentrations of purified 99Tc-DNS preparations were 37-74 kBq/ml and absorption maxima at 412-425 nm (yellow complex). By application of 99mTc, 99Tc-DMS preparation in rats, good renal scans have been obtained.

Animals↗
PubMed1983

Stability of the radiopharmaceutical [99mTc]DMSA: study of the ligand exchange reaction with [99Tc]EDTA.

A kinetic study was made of the ligand exchange reaction between [99mTc]EDTA and DMSA. The results of this study indicate that this exchange reaction is closely related to temperature and pH. Kinetic and thermodynamic parameters demonstrate that both complexes--[99MTc]EDTA and [99mTc]DMSA--have a similar stability. Furthermore, the existence of an acid-basic catalysis for the global exchange reaction was established, and the catalytic parameters were calculated. These data were obtained by radiochromatography and visible spectrophotometry.

Drug Stability↗
PubMed1985

A convenient method for the preparation of 99mTc(V)dimercaptosuccinic acid (99mTc(V)-DMSA).

Tc(IV)-DMSA for kidney scintigraphy has been prepared in acidic solution. Once the labeling is done in basic solution, upon addition of a small amount of NaHCO3, a mixture of 3-4 other DMSA-complexes is formed, presumably containing Tc(V). Kidney uptake in male adult rats of the 99mTc(V)-DMSA is 1.6% injected dose/g (4.9%/total organ) compared to 16.4% injected dose/g (resp. 50.3%/total organ) for 99mTc(IV)-DMSA.

Animals↗
PubMed1990

Detection of renal scarring by DMSA scanning--an experimental study.

Using the established piglet model, renal scars were produced by a combination of vesicoureteric reflux and urinary infection. The presence and extent of scarring, as determined by postmortem examination, was compared with that detected by technetium 99m dimercaptosuccinic acid (DMSA) scans performed before sacrifice. Sixty female piglets (62 refluxing units) were studied. Overall the sensitivity (true-positive/(true-positive + false-negative)) of DMSA scanning in detecting macroscopic scarring was 85% and the specificity (true-negative/(true-negative + false-positive)) was 97%. There were five false-negatives, four of which were in kidneys with minor scarring and one in which there was major scarring. There were three false-positives. We conclude that DMSA scanning has a high specificity and sensitivity in detecting renal scars in female piglets, and suggest it is the preferred method for detecting renal scars in clinical practice.

Animals↗
PubMed1996

Survival in patients with amyotrophic lateral sclerosis, treated with an array of antioxidants.

Between 1983 and 1988 we treated 36 patients with sporadic amyotrophic lateral sclerosis (ALS) by an array of antioxidants and added other drugs to the regimen whenever a patient reported deterioration. Our customary prescription sequence was N-acetylcysteine (NAC); vitamins C and E; N-acetylmethionine (NAM); and dithiothreitol (DTT) or its isomer dithioerythritol (DTE). Patients with a history of heavy exposure to metal were also given meso 2,3-dimercaptosuccinic acid (DMSA). NAC, NAM, DTT, and DTE were administered by subcutaneous injection or by mouth or by both routes, the other vitamins and DMSA by mouth alone. The hospital pharmacy supplied NAC and NAM injections fluid as 100 ml bottles of 5.0 and 5.85% solutions, respectively. DTT was delivered in special double-walled capsules of 200 mg. DTT/DTE injection fluid was added to the NAC and NAM bottles, the final DTT/DTE concentrations never exceeding 0.5%. DMSA was provided in 250 mg capsules. All of the 36 patients used NAC and DTT/DTE; 29 also used vitamins C and E; 21 also used NAM; and 7 also used DMSA, DMSA, NAM, vitamins C and E were tolerated well. In many patients, DTT, DTE, NAC and NAM induced pain, redness and swelling at the injection sites in that order of decreasing frequency. DTT and DTE did often and NAC did sometimes cause gastric pain, nausea and other abdominal discomfort. Comparison of survival in the treated group and in a cohort of untreated historical controls, disclosed a median survival of 3.4 years (95% confidence interval: 3.0-4.2) in the treated and of 2.8 (95% confidence interval 2.2-3.1) years in the control patients. This difference may be explained by self-selection of our highly motivated treated group and by its initial survival of diagnosis for an average of 8.5 months before onset of treatment. We conclude that antioxidants neither seem to harm ALS patients, nor do they seem to prolong survival.

Acetylcysteine↗
PubMed1982

Anti-lewisite activity and stability of meso-dimercaptosuccinic acid and 2,3-dimercapto-1-propanesulfonic acid.

Meso-dimercaptosuccinic acid (DMSA) and the sodium salt of 2,3-dimercapto-1-propanesulfonic acid (DMPS) are analogous in chemical structure to dimercaprol (BAL, British Anti-Lewisite). Dimercaprol was among the first therapeutically useful metal chelating agents and was developed originally as an anti-lewisite agent. Either DMSA or DMPS protects rabbits from the lethal systemic action of dichloro(2-chlorovinyl)arsine (29.7 mumols/kg, also known as lewisite. The analogs are active in this respect when given either sc or po. The stability of each of the three dimercapto compounds in distilled H2O, pH 7.0 at 24 degrees, has been examined for seven days. DMSA retained 82% of its mercapto groups, but no titratable mercapto groups remained in the DMPS or BAL solutions. At pH 5.0, however, there was no striking difference in the stability of the three dimercapto compounds (78-87%) over a seven day period. DMSA and DMPS warrant further investigation as water soluble metal binding agents in both in vivo and in vitro experiments.

Administration, Oral↗
PubMed1990

Effects of oral meso-2,3-dimercaptosuccinic acid (DMSA) administration on late gestation and postnatal development in the mouse.

The present study was conducted to evaluate the effects of meso-2,3-dimercaptosuccinic acid (DMSA) on late gestation and postnatal viability and growth in the mouse. DMSA was given po to four groups of pregnant Swiss mice at 0, 200, 400, and 800 mg/kg/day from day 14 of pregnancy until postnatal day 21. At birth, the following data were recorded: length of gestation, number of live, dead, and abnormal pups, sex, and individual pup weights. Each pup was weighed again on day 4, 14, and 21 of lactation. Pinna detachment, incisor eruption and eye opening were also monitored. No treatment-related signs of toxicity were noted in any of the dams during the study. No adverse effects on offspring survival or development were evident in the 200 or 400 mg DMSA/kg/day groups. However, on days 14 and 21 of lactation a significant decrease in pup body weight was observed in the 800 mg/kg/day group. Also, a significant increase in the relative weight of the brain was seen in this group. The "no observable effect level" (NOEL) for health hazards to the developing pup was greater than 400 mg/kg/day. This dose is higher than the amounts of DMSA usually given in the treatment of human heavy metal intoxications.

Administration, Oral↗
PubMed1995

DMSA chelation during co-exposure to lead: increased locomotor activity in lead-exposed mice but not controls.

We investigated the effect of chelating agent meso-2,3 dimercaptosuccinic acid (DMSA) on indices of "hyperactive" behavior in lead-exposed and control Binghamton Heterogeneous Stock (Het) mice. As expected, 6 weeks of ingestion of 0.5% lead acetate in drinking water reduced immobility in a forced water swim relative to controls. DMSA did not attenuate this behavioral change. In fact, DMSA interacted with lead exposure to increase locomotor activity in the forced water swim. DMSA also apparently excacerbated lead's tendency to reduce immobility. While any generalizations to human populations should be cautioned, these results and others suggest the need for further research.

Animals↗
PubMedDate not supplied

Acute and longer term effects of meso-2,3 dimercaptosuccinic acid (DMSA) on the behavior of lead-exposed and control mice.

We investigated the effect of chelating agent meso-2,3 dimercaptosuccinic acid (DMSA) on spatial learning and forced-swim immobility in Binghamton Heterogeneous Stock (HET) mice. Forced-swim immobility (characterized by increasingly frequent bouts of complete motionlessness in a forced-swim test, i.e., behavioral despair) is reduced by exposure to lead. In Experiment 1, male and female HETs (n = 81) were assigned to lead-exposed (0.5% lead acetate ad lib in drinking fluid), pair-fed (PF), or water control groups. Six weeks after the termination of lead exposure, half of each group was injected intraperitoneally (IP) with 50 mg/kg DMSA or vehicle once per day for 5 days. Following treatment, all animals were tested for acquisition and extinction in the Morris Water maze, followed by immobility testing in an inescapable forced-swim task. Neither Pb nor DMSA affected Morris maze performance. However, consistent with previously published work, Pb reduced immobility in the forced-water swim relative to both PF and water controls. Additionally, lead-exposed males, but not females, showed sustained improvement following DMSA treatment on immobility measures. Experiment 2 was designed to demonstrate the effect of the above DMSA protocol on blood-Pb, and also examined the immediate effects of DMSA on immobility during treatment. Thus, in Experiment 2, animals were exposed to an identical Pb and DMSA treatment protocol, but the effects of DMSA on immobility during the course of DMSA treatment were measured, and animals were sacrificed immediately after treatment so that blood-Pb measures could be taken. Under these circumstances, DMSA markedly reversed the lead-induced reduction in immobility immediately during the treatment phase. Although DMSA clearly reduced blood-lead in males, its influence on female blood levels was far less. Taken together, the data from these experiments suggest that DMSA ameliorates lead-induced immobility changes in mice, but that gender may modulate DMSA's effect on blood-lead and longer-term behavioral effects. However, further work is needed to clarify the role of gender in response to DMSA.

Animals↗