Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Succimer”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 577 records · Page 32Linked to original sources
PubMed2003

Dimercaptosuccinic acid and Prussian Blue in the treatment of acute thallium poisoning in rats.

INTRODUCTION: Despite being banned as a pesticide, thallium still results in human and animal poisonings. Current recommended treatments include the use of the chemical Prussian Blue. Limitations in its availability may result in Prussian Blue not being obtainable in the thallium-poisoned patient. The chelator 2,3-Dimercaptosuccinic acid (DMSA) is currently FDA-approved for use in childhood lead poisoning and has been reported to be beneficial in treating other heavy metal poisonings. The objective of this study was to determine the efficacy of DMSA as a treatment for thallium poisoning by studying mortality and whole-brain concentrations in thallium poisoned rats. MATERIAL AND METHODS: Rats were gavaged with 30 mg/kg of thallium. After 24 hours they were randomized to DMSA (n = 20) 50 mg/kg twice daily for 5 days, Prussian Blue (n = 20) 50 mg/kg twice daily for 5 days, or control (n = 30). Animals were monitored twice daily for weight loss and mortality. Animals losing greater than 20% of their starting weight were euthanized and counted as a mortality. All surviving rats at 120 hours had their brains harvested and digested and underwent subsequent thallium analysis. RESULTS: The rate of survival in DMSA-treated animals compared to control was 45% vs. 21%, p = 0.07. Mean whole-brain thallium concentrations between DMSA and control rats were 3.4 vs. 3.0 microg/g, p = 0.06. Prussian Blue-treated rats had significantly improved survival (70% vs. 21%, p < 0.01) and lower whole-brain thallium concentrations (1.6 vs. 3.0 microg/g, p < 0.01 tissue) compared to controls. CONCLUSION: DMSA failed to reduce brain thallium concentrations in rats poisoned with thallium and had an indeterminate effect on mortality while Prussian Blue significantly reduces both brain thallium concentrations and mortality.

Acute Disease↗
PubMed2003

A patient with postoperative mercury contamination of the peritoneum.

CASE REPORT: Peritoneal exposure to mercury has been rarely reported and long-term consequences of this type of exposure have not been documented. We report the clinical course of a patient who has survived almost eight years with a massive intraperitoneal load of mercury. She has suffered formication, pruritus, fatigue, irritiability, insomnia, alopecia, dizziness, a gait disturbance, loss of balance and multiple falls, abdominal pain, choking, and headaches. Two courses of chelation with dimercaptosuccinic acid using the standard protocol were undertaken, resulting in increased daily excretion, but without demonstrable objective or subjective benefit or lasting effect. She had multiple medical problems before the mercury intoxication, which complicates the attribution of all her problems to mercury intoxication. It is of particular interest that the patient survived and did not suffer any marked cognitive deterioration. She died in 2002 shortly after being diagnosed with lung cancer and declaring that she would fight it. Phasing out of mercury-weighted tubes is recommended.

Chelating Agents↗
PubMed2003

Vitamin C, glutathione, or lipoic acid did not decrease brain or kidney mercury in rats exposed to mercury vapor.

UNLABELLED: Some medical practitioners prescribe GSH and vitamin C alone or in combination with DMPS or DMSA for patients with mercury exposure that is primarily due to the mercury vapor emitted by dental amalgams. HYPOTHESIS: This study tested the hypothesis that GSH, vitamin C, or lipoic acid alone or in combination with DMPS or DMSA would decrease brain mercury. METHODS: Young rats were exposed to elemental mercury by individual nose cone, at the rate of 4.0 mg mercury per m3 air for 2 h per day for 7 consecutive days. After a 7-day equilibrium period, DMPS, DMSA, GSH, vitamin C, lipoic acid alone, or in combination was administered for 7 days and the brain and kidneys of the animals removed and analyzed for mercury by cold vapor atomic absorption. RESULTS: None of these regimens reduced the mercury content of the brain. Although DMPS or DMSA was effective in reducing kidney mercury concentrations, GSH, vitamin C, lipoic acid alone, or in combination were not. CONCLUSION: One must conclude that the palliative effect, if any, of GSH, vitamin C, or lipoic acid for treatment of mercury toxicity due to mercury vapor exposure does not involve mercury mobilization from the brain and kidney.

Administration, Inhalation↗
PubMed2003

Chronic arsenic toxicity: clinical features, epidemiology, and treatment: experience in West Bengal.

Chronic arsenic toxicity due to drinking arsenic-contaminated water has been one of the worst environmental health hazards affecting eight districts of West Bengal since the early eighties. Detailed clinical examination and investigation of 248 such patients revealed protean clinical manifestations of such toxicity. Over and above hyperpigmentation and keratosis, weakness, anaemia, burning sensation of eyes, solid swelling of legs, liver fibrosis, chronic lung disease, gangrene of toes, neuropathy, and skin cancer are some of the other manifestations. A cross-sectional survey involving 7683 participants of all ages was conducted in an arsenic-affected region between April 1995 and March 1996. Out of a population of 7683 surveyed, 3467 and 4216 people consumed water containing As below and above 0.05 mg/L, respectively. Except pain abdomen the prevalence of all other clinical manifestations tested (e.g., pigmentation, keratosis, hepatomegaly, weakness, nausea, lung disease and neuropathy) were found to be significantly higher in As exposed people (water As > 0.05 mg/L) compared to control population (water As level < 0.05 mg/L). The prevalence of pigmentation and keratosis, hepatomegaly, chronic respiratory disease and weakness rose significantly with increasing arsenic concentrations in drinking water. The respiratory effects were most pronounced in individuals with high arsenic water concentrations who also had skin lesion. Therapy with chelating agent DMSA was not found to be superior to placebo effect. However, therapy with DMPS caused significant improvement of clinical condition of chronic arsenicosis patients as evidenced by significant reduction of total clinical scores from 8.90 +/- 2.84 to 3.27 +/- 1.73; p < 0.0001. Efficacy of specific chelation therapy for patients suffering from chronic As toxicity has further need to be fully substantiated. However, supportive treatment could help in reducing many symptoms of the patients. Treatment in hospital with good nutritious diet has been found to reduce symptom score in a subset of placebo treated patients in West Bengal during the course of DMSA and DMPS trial. People should be advised to stop drinking As contaminated water or exposure to As from any other source. The various clinical manifestations should be treated symptomatically.

Abdominal Pain↗
PubMed2003

The efficacy of monoisoamyl ester of dimercaptosuccinic acid in chronic experimental arsenic poisoning in mice.

The therapeutic efficacy of monoisoamyl meso-2,3-dimercaptosuccinic acid (MiADMSA), a new monoester of 2,3-dimercaptosuccinic acid on arsenic induced oxidative stress in liver and kidneys, alterations in hematopoietic system and depletion of arsenic burden was assessed, in mice. Three different doses of MiADMSA (25, 50 or 100 mg/kg) for five consecutive days were administered in chronically arsenic exposed mice (10 ppm in drinking water for six months). Oral administration of MiADMSA particularly at a dose of 50 mg/kg, produced relatively more pronounced beneficial effects on the inhibited blood delta-aminolevulinic acid dehydratase (ALAD), biochemical variables indicative of hepatic and renal oxidative stress and depletion of arsenic concentration in blood, liver and kidneys, compared with intraperitoneal administration of the drug. The treatment with MiADMSA although, produced essential metals imbalance which could be a restrictive factor for the possible therapeutic use of this compound in chronic arsenic poisoning and thus require further exploration.

Administration, Oral↗
PubMed2003

Arsenic uptake by native fern species in Thailand: effect of chelating agents on hyperaccumulation of arsenic by Pityrogramma calomelanos.

Nineteen native fern species collected from an area in Thailand with high arsenic concentration in soil and in ground water as a result of tin mining was screened for elevated arsenic concentration in fronds. Two species of fern were found to contain elevated arsenic in their fronds in nature: Pityrogramma calomelanos (108-1156 microg g(-1) dried weight) and Pteris vittata (79 microg g(-1) dried weight). Under hydroponic culture Pityrogramma calomelanos (a silver back fern) accumulated arsenic in its shoot at rate of 4616 microg(-1) (dried weight). The accumulation of arsenic in Pityrogramma calomelanos shoot doubled with the addition of an EDTA (Ethelenediamine tetraacetic acid) chelating agent. The highest accumulation occurred 6 weeks after exposure to 10 mg L(-1) arsenic as disodium hydrogen arsenate. The addition of another chelating agent, DMS (Dimercaptosuccinic acid), resulted in a 5-fold decrease in arsenic concentration in the Pityrogramma calomelanos shoot compared to control after 6 weeks of exposure to arsenic. The contrasting effect of the EDTA and DMSA chelating agent was attributed to the strong binding of the thiol group to arsenic ion. This study indicated that Pityrogramma calomelanos uptake and translocate arsenic in the form of arsenate and arsenite rather than the As-DMSA complex. Using phytoextraction efficiency calculations, it was determined that Pityrogramma calomelanos gave the highest arsenic phytoextraction efficiency at 6 weeks after exposure to arsenic in the EDTA treatment, with an efficiency of 77.8 mg As based on whole plant biomass.

Arsenic↗
PubMed2001

Associations of blood lead, dimercaptosuccinic acid-chelatable lead, and tibia lead with neurobehavioral test scores in South Korean lead workers.

The authors performed a cross-sectional study to evaluate associations between blood lead, tibia lead, and dimercaptosuccinic acid (DMSA)-chelatable lead and measures of neurobehavioral and peripheral nervous system function among 803 lead-exposed workers and 135 unexposed controls in South Korea. The workers and controls were enrolled in the study between October 1997 and August 1999. Central nervous system function was assessed with a modified version of the World Health Organization Neurobehavioral Core Test Battery. Peripheral nervous system function was assessed by measuring pinch and grip strength and peripheral vibration thresholds. After adjustment for covariates, the signs of the beta coefficients for blood lead were negative for 16 of the 19 tests and blood lead was a significant predictor of worse performance on eight tests. On average, for the eight tests that were significantly associated with blood lead levels, an increase in blood lead of 5 microg/dl was equivalent to an increase of 1.05 years in age. In contrast, after adjustment for covariates, tibia lead level was not associated with neurobehavioral test scores. Associations with DMSA-chelatable lead were similar to those for blood lead. In these currently exposed workers, blood lead was a better predictor of neurobehavioral performance than was tibia or DMSA-chelatable lead, mainly in the domains of executive abilities, manual dexterity, and peripheral motor strength.

Adult↗
PubMed2003

The role of oxidative stress in the in vitro induction of micronuclei by pesticides in mouse lung fibroblasts.

The involvement of the antioxidant enzymes catalase and glutathione peroxidase (both at 0.1 mg/ml) in defence against the genotoxicity of phosphamidon (80 microg/ml) and dieldrin (25 microM) was investigated in order to demonstrate that the two pesticides damage DNA through the generation of reactive oxygen species and therefore of oxidative stress. The pesticide genotoxicity was determined by the cytokinesis-block micronucleus test performed on primary mouse lung fibroblast cultures. Also, 3-aminotriazole (40 mM) and mercaptosuccinate (0.5 mM), inhibitors of catalase and glutathione peroxidase, respectively, were added to the cultures. Data indicate that catalase causes a decrease only in the damage induced by phosphamidon, while glutathione peroxidase protects against damage induced by both phosphamidon and dieldrin. Simultaneous treatment with antioxidant inhibitors and pesticides results in a decrease in micronucleus frequency and cell number, due to apoptotic death. Our results indicate that clastogenic DNA damage produced by the two pesticides is modulated by antioxidant enzymes and their inhibitors and thus could be due to oxidative stress induction.

Amitrole↗
PubMed1994

99mTc-DMSA imaging with tomography in renal transplant recipients with abnormal lower urinary tracts.

This study examined whether renal parenchymal imaging using 99mTc DMSA scintigraphy with tomography is a sensitive measure of renal scarring in renal transplant recipients with an abnormal lower urinary tract and whether such scars correlate with impairment of renal function. Three groups of patients were compared: group 1, patients with an abnormal lower urinary tract and deteriorating renal function (n = 9); group 2, abnormal lower urinary tract and stable renal function (n = 5); and group 3, normal lower urinary tract and deteriorating renal function (n = 8). Eight of the nine patients in group 1 had multiple scars visible on 99mTc DMSA scans and this correlated with histology when a renal biopsy was performed; the only patient without scars had a transplant glomerulopathy. The presence of scars was associated with either raised intravesical pressures or recurrent urinary tract infections (UTIs). Only one patient in each of groups 2 and 3 had visible scars and both these patients had a history of recurrent UTIs. Patients in group 3 with deteriorating renal function due to chronic rejection documented by biopsy did not have cortical scars visible with 99mTc DMSA tomography. 99mTc DMSA scanning with tomography is a useful investigation in the management of renal transplant patients with declining renal function; multiple scars may indicate abnormal lower urinary tract function and are not seen in chronic rejection.

Cicatrix↗
PubMed2000

The effects of sulfur, thiol, and thiol inhibitor compounds on arsine-induced toxicity in the human erythrocyte membrane.

The mechanism of arsine (AsH(3)) toxicity is not completely understood. The first cytotoxic effect of AsH(3) is disruption of ion homeostasis, with a subsequent hemolytic action. The only accepted treatment for AsH(3) toxicity is exchange transfusion of the blood. In this study the effect of sulfur, sulfur compounds, thiol-containing compounds, and thiol inhibitors on AsH(3)-induced disruption of membrane transport and hemolysis in human erythrocytes was investigated in vitro. Elemental sulfur, sodium thiosulfate, 5, 5'-dithio-bis(2-nitrobenzoic acid), and meso-2,3-dimercaptosuccinic acid were successful in delaying hemolysis, but the most successful agent was the sulfhydryl inhibitor, N-ethylmaleimide (NEM). This indicated that sulfhydryl groups, possibly membrane sulfhydryls, are major factors in the hemolytic mechanism of AsH(3). Measuring intracellular ion concentrations tested the effect of NEM on AsH(3)-induced disruption of membrane transport. AsH(3) alone caused all ions tested to flow with their concentration gradients: Intracellular K+ and Mg++ decreased, whereas Na+, Cl-, and Ca++ increased. NEM was unable to prevent ion loss except for Ca++, whose increase was prevented for 1 h after AsH(3) treatment. The influx of Ca++ in AsH(3)-treated erythrocytes is an irreversible event leading to hemolysis. Reduction of oxygenated hemoglobin to carboxyhemoglobin completely inhibited AsH(3)-induced hemolysis. In addition, AsH(3) and NEM had no direct chemical interactions. We concluded that membrane sulfhydryl groups are likely targets of AsH(3) toxicity, with NEM being able to prevent AsH(3)-induced hemolysis.

Adult↗
PubMed2006

Dithiol compounds at low concentrations increase arsenite toxicity.

Inorganic trivalent arsenicals are vicinal thiol-reacting agents, and dithiothreitol (DTT) is a well-known dithiol agent. Interestingly, both decreasing and increasing effects of DTT on arsenic trioxide-induced apoptosis have been reported. We now provide data to show that, at high concentrations, DTT, dimercaptosuccinic acid (DMSA), and dimercaptopropanesulfonic acid (DMPS) decreased arsenic trioxide-induced apoptosis in NB4 cells, a human promyelocytic leukemia cell line. In contrast, at low concentrations DTT, DMSA, and DMPS increased the arsenic trioxide-induced apoptosis. DTT at a high concentration (3 mM) decreased, whereas at a low concentration (0.1 mM), it increased the cell growth inhibition of arsenic trioxide, methylarsonous acid (MMA(III)), and dimethylarsinous acid (DMA(III)) in NB4 cells. DMSA and DMPS are currently used as antidotes for acute arsenic poisoning. These two dithiol compounds also show an inverse-hormetic effect on arsenic toxicity in terms of DNA damage, micronucleus induction, apoptosis, and colony formation in experiments using human epithelial cell lines derived from arsenic target tissues such as the kidney and bladder. With the oral administration of dithiols, the concentrations of these dithiol compounds in the human body are likely to be low. Therefore, the present results suggest the necessity of reevaluating the therapeutic effect of these dithiol compounds for arsenic poisoning.

Apoptosis↗
PubMed2001

BAL modulates glutamate transport in synaptosomes and synaptic vesicles from rat brain.

The therapeutic use of BAL (2,3-dimercaptopropanol) as treatment for poisoning has been halted by data suggesting serious neurotoxicity. This article is a report on the effects of BAL and other dithiols, DMSA (meso-2,3-dimercaptosuccinic acid) and DMPS (2,3-dimercaptopropane-1-sulfonic acid), on [3H]glutamate release and uptake by rat brain synaptosomes and [3H]glutamate uptake by synaptic vesicles. BAL (100 microM) inhibited glutamate uptake (30%) and stimulated its basal release (30%) in synaptosomes, without affecting K+-stimulated release. BAL also inhibited glutamate uptake by synaptic vesicles (up to 60%). DMPS and DMSA (100 microM) had no significant effects on these parameters. The data reported here provide some evidence of glutamate involvement in BAL-induced neurotoxicity by demonstrating direct effects of BAL on glutamatergic system modulation.

Animals↗
PubMed1979

Renal function studies using 99mTc-dimercaptosuccinic acid.

99mTc-dimercaptosuccinic acid (DMSA), provides both a well defined renal image via preferential cortical accumulation, and a quantitative assessment of separate kidney function, correlating well with renal plasma flow obtained from the 131I-Hippuran renogram of each kidney. 99mTc-DMSA is capable of labeling the functioning nephrons in the cortex without interference by the activity of urine flow, suggesting that DMSA should be termed a cortical tubular marker. 99mTc-DMSA scintigraphy has advantages over conventional methods in that it can be performed repeatedly with little discomfort to the patients, as a routine clinical examination.

Child↗
PubMed1980

Increased renal accumulation of Tc-99m-MDP in renal artery stenosis.

Abnormal increased renal accumulation of Tc-99m-MDP was observed in a patient found subsequently to have stenosis of the ipsilateral renal artery. The case is both interesting in itself and for its possible implications regarding the use of radiolabeled phosphates in renal ischemia.

Aged↗
PubMed1980

Position-related false-positive renal imaging.

A case report of false-positive renal imaging due to anterior displacement of the upper pole of the left kidney with the patient in the prone position is presented. False imaging can be avoided by imaging the kidneys with the patient in the supine position and with the detector behind the patient.

False Positive Reactions↗