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 361 records · Page 20Linked to original sources
PubMed1988

Mobilization of aged in vivo cadmium deposits by diethyl dimercaptosuccinate.

Diethyl dimercaptosuccinate (DEDMS) was prepared and found to be capable of mobilizing cadmium from mice one month after they had been given an injection (i.p.) of 0.03 mg CdCl2.2.5H2O containing 1.0 microCi of 109 CdCl2. When pure, DEDMS is a waxy solid with a melting point of 61-62 degrees C which is soluble in warm peanut oil. Its LD50 value (i.p.) in mice is approximately 2.6 mmol/kg, a value which allows it to be given at a higher dosage than other known lipid-soluble dithiols. This compound is especially effective in reducing hepatic and whole body levels of cadmium; it is not as effective as 2,3-dimercaptopropanol (BAL) in reducing renal cadmium levels.

Animals↗
PubMed1991

Mobilization of cadmium by liposome-encapsulated meso-2,3-dimercaptosuccinic acid in pre-exposed mice.

meso-2,3-Dimercaptosuccinic acid (DMSA) treatment in free of liposome-encapsulated form was given to mice pre-exposed to cadmium as CdCl2 (2 intraperitoneal injections; 0.5 mg Cd/kg along with 5 microCi 109CdCl2 in 4 ml volume within 24 h). Both treatments removed cadmium from liver, spleen, testis and blood with liposomal DMSA exhibiting higher efficacy in mobilizing cadmium not only from whole organs but also from liver proteins. It also resulted in higher excretion of cadmium via urine as compared with free DMSA or saline treatment. Whereas this treatment eliminated significantly higher amounts of cadmium via the fecal route throughout the period examined, free DMSA responded only 48 h after treatment and was less effective. The results suggest mobilization of cadmium from intracellular sites of deposition. However, DMSA in the dose administered (24 mumol/kg i.v.) in either form was ineffective in decorporating cadmium from the kidney, the critical organ in cadmium intoxication.

Animals↗
PubMed1992

Toxicity of a family from vacuumed mercury.

A family of four developed toxic blood levels of mercury after the mother vacuumed a spilled jar of liquid mercury from a closet in their apartment. The youngest son developed severe thrombocytopenia which was initially diagnosed as idiopathic thrombocytopenic purpura secondary to viral illness. A possible association between acute mercury toxicity and idiopathic thrombocytopenic purpura has not been previously reported. Chelation therapy with penicillamine for the older child was administered soon after toxic blood mercury levels were known by the physician. Because thrombocytopenia has been reported to occur in up to 5% of patients receiving penicillamine therapy, the younger child was treated with dimercaptosuccinic acid. The mother was also treated with dimercaptosuccinic acid. The father received dimercaprol therapy. The toxic effects and rationale for now outdated therapeutic uses of mercury are discussed.

Adult↗
PubMed1995

Pediatric arsenic ingestion.

Acute arsenic toxicity is rare, and there have been no pediatric cases of acute arsenic poisoning in the recent literature. We report a pediatric case of acute arsenic ingestion treated initially with British antilewisite (BAL) and D-penicillamine (DP), and later with dimercaptosuccinic acid (DMSA). A 22-month-old girl ingested 1 oz 2.27% sodium arsenate and developed immediate vomiting and diarrhea. The patient presented to a community emergency department with the following vital signs: blood pressure 96/72 mm Hg, pulse 160 beats/min, respirations 22 breaths/min. She was pale and lethargic. Gastric lavage was performed, and abdominal X-ray was normal. She continued to have gastrointestinal symptoms and received 3 mg/kg BAL. Sinus tachycardia persisted, with heart rate increasing to 200 beats/min. In 12 hours, she was asymptomatic and was started on oral DP. On day 1, 24-hour urine arsenic was 4,880 micrograms/L. She remained asymptomatic and was discharged on day 6 on oral DP. She did well except for a rash that could have been a side effect of DP. On day 8, when the day 5 24-hour urine arsenic level was returned at 650 micrograms/L, the patient was readmitted and started on DMSA. After 4 days on DMSA, the 24-hour urine arsenic level was 96 micrograms/L. White blood cell count and renal and hepatic function remained normal. The excretion half-life was approximately 2.5 days, which is at least 2 to 3 times faster than the spontaneous excretion half-life expected in adults. Long-term follow-up was unavailable.(ABSTRACT TRUNCATED AT 250 WORDS)

Arsenates↗
PubMed1987

Comparison of two 99mTc(V)-dimercaptosuccinic acid preparations.

99mTc(V)-DMSA labelled either by increasing the pH together with a low concentration of Sn, or by increasing the pH only are compared in vitro and in vivo. The gel chromatographic separation shows that after incubation with blood, all the 99mTc(V)-DMSA preparations are stable and do not bind to the plasma proteins. The behavior in rats as well as in clinical studies does not demonstrate any distinctive characteristics between the different radiomolecules. It seems that the pH of the solution is an important factor which controls the formation of 99mTc(V)-DMSA.

Animals↗
PubMed1989

Physico-chemical study of the radiopharmaceuticals 99mTc-DMSA, 99mTc-EDTA and 99mTc-DTPA interaction with plasmatic proteins.

This report studies the binding rate of the radiopharmaceuticals 99mTc-DTPA, 99mTc-EDTA and 99mTc-DMSA to plasmatic proteins. The proteins bind to the tested radiopharmaceuticals in the following sequence: 99mTc-DTPA less than 99mTc-DMSA(C1) less than 99mTc-EDTA less than 99mTc-DMSA(C2) where C1 and C2 represent two different Tc-DMSA complexes. The thermodynamic study suggests a quantitative relationship of radiopharmaceutical:protein = 1:1 and an almost nonexistent influence of the temperature, which means that the interacting forces in this process are relatively weak.

Blood Proteins↗
PubMed1991

Synthesis and characterization of [186Re]rhenium(V)dimercaptosuccinic acid: a possible tumour radiotherapy agent.

[186Re]Re(V)DMSA, a beta-emitting analogue of the tumour imaging radiopharmaceutical pentavalent [99mTc]Tc(V)DMSA of possible value in tumour therapy, is readily prepared by stannous reduction of [186Re]ReO4 in the presence of dimercaptosuccinic acid at 100 degrees C using a commercial DMSA kit as used for renal imaging with 99mTc, and purified using a disposable sample preparation column. The complex has been identified as [ReO(DMSA)2] by NMR, optical and i.r., spectroscopy and elemental analysis.

Humans↗
PubMed1991

Biolocalization and cell labeling properties of neutral-lipophilic 99mTc-amine-phenol chelates.

99mTc-diamine-diphenol chelates are neutral lipophilic chelates exhibiting good stability in aqueous solutions. The cell labeling and biolocalization properties of four different 99mTc-amine-phenol complexes were determined. All four chelates readily labeled leukocytes and RCBs in high yields. Even though 99mTc was retained by the cells, the elution rate of 99mTc from the labeled cells in plasma at 37 degrees C was unacceptably high for potential utility in scintigraphic imaging. The uptake of 99mTc in brain or heart following i.v. injection of the chelates in rats was low and clearance of activity from the blood was slow.

Animals↗
PubMed1992

Evaluation of a DMSA kit for instant preparation of 99mTc(V)-DMSA for tumour and metastasis scintigraphy.

A kit has been developed to instantly prepare 99mTc(V)-DMSA. The freeze-dried kit consisting of DMSA, stannous chloride and ascorbic acid in appropriate proportions, produces quality 99mTc(V)-DMSA when mixed with 0.2 mL of 3.5% NaHCO3 solution and 2-4 mL of (99mTc)pertechnetate. The radiopharmaceutical characterized by chromatography with ITLC-SG in 0.9% saline and horizontal paper electrophoresis in 50 mM vernol buffer, pH 8.6, at a potential gradient of 15 V/cm showed a different mobility with respect to 99mTc(III)-DMSA, a known agent for kidney imaging. The new agent exhibited less plasma protein binding compared to that of 99mTc(III)-DMSA. Biodistribution of the pentavalent DMSA in mouse demonstrated greater uptake in bone and muscle and lower uptake in liver and kidney with respect to trivalent DMSA. The soft tissue tumour specificity and its suitability for tumour scintigraphy was apparent from the scintigrams of mammary carcinoma in a C3H Jax mouse and medullary carcinoma in a patient. Brain metastatic lesions were also visible in a breast carcinoma patient after administering him with the agent.

Animals↗
PubMed1996

In vivo indices of oxidative stress in lead-exposed C57BL/6 mice are reduced by treatment with meso-2,3-dimercaptosuccinic acid or N-acetylcysteine.

Knowledge of lead's capacity to disrupt the prooxidant/antioxidant balance within mammalian tissues suggests that definitive therapy for chronic lead poisoning should encompass both chelating and antioxidant actions. The dithiol meso-2,3-Dimercaptosuccinic Acid (DMSA) is the first orally administered metal chelating agent to receive U.S. Food and Drug Administration (FDA) approval for the treatment of childhood plumbism and possesses the potential to function as an antioxidant by removing lead from the site of deleterious oxidation reactions. Five weeks of lead exposure was found to deplete glutathione (GSH) levels, increase oxidized glutathione (GSSG), and promote malondialdehyde (MDA) production in both liver and brain samples taken from C57BL/6 mice. GSH levels increased and GSSG and MDA levels decreased in groups of lead-exposed mice that received 1 mmol/kg DMSA or 5.5 mmol/kg N-acetylcysteine (NAC) for 7 d prior to sacrifice. Treatment with DMSA caused a reduction in blood, liver, and brain lead levels consistent with its function as a chelating agent, while treatment with NAC did not reduce these lead levels. However, NAC did cause a reduction in indices of oxidative stress in both brain and liver samples, which implies that this synthetic thiol-containing antioxidant is capable of abrogating lead-induced oxidative stress in vivo. Overall, these results suggest that lead-induced oxidative stress in vivo can be mitigated by pharmacologic interventions, which encompass both chelating as well as thiol-mediated antioxidant functions.

Acetylcysteine↗
PubMedDate not supplied

MRI and scintigraphic features of extraabdominal desmoid tumors.

To determine whether extraabdominal desmoid can be correctly diagnosed using both magnetic resonance imaging (MRI) and scintigraphy with pentavalent technetium-99m dimercaptosuccinic acid and gallium-67 citrate, MRI (T1- and T2-weighted images) and scintigraphy were performed in 18 patients with 27 histologically proved extraabdominal desmoid tumors. The extraabdominal desmoid tumors were characterized by positive uptake of pentavalent technetium-99m dimercaptosuccinic acid and lack of uptake of gallium-67 citrate on scintigraphy. These tumors were isointense to skeletal muscle on T1-weighted MRIs and hyperintense on T2-weighted images. They also displayed septum-like internal inhomogeneity and surrounding hypointense capsular band. The combination of scintigraphy and MRI is of value in correctly diagnosing extraabdominal desmoid tumors except in the rare case of fibrotic verylow-grade sarcoma.

Desmoid Tumors↗
PubMed1995

[Arterial hypertension due to mercury poisoning: diagnostic value of captopril].

BACKGROUND: Mercury poisoning is a rare cause of hypertension in children. Urinary excretion sometimes remains low despite severe clinical intoxication. CASE REPORT: A 32 month-old girl was admitted with hypertension, tachycardia, apathy, irritability and excessive sweating. Erythromelalgia and neurologic symptoms permitted the diagnosis of acrodynia. Urine mercury remained normal until chelation. Captopril significantly increased urine mercury concentration but failed to improve clinical manifestations. Clinical improvement required infusions of BAL for 5 days then oral dimercaptosuccinic acid for 3 months. Metal vapors originated from the mercury which spilled from a broken thermometer onto the carpet. COMMENTS: Low basal urine mercury could be associated with real mercury poisoning. Small amounts of metal mercury held in a thermometer could produce a high level of mercury vapor leading to intoxication in young children. The binding capacity of metal ions by captopril could be used to increase urine mercury output. Nevertheless, captopril therapy fails to improve acrodynia. Total elimination of mercury requires long-term therapy with BAL or dimercaptosuccinic acid. CONCLUSIONS: An unexpected mode of intoxication and low basal urine mercury are not decisive arguments against mercury poisoning, which is the only cause of acrodynia.

Administration, Oral↗
PubMed1993

Compensatory renal response after unilateral partial and whole volume high-dose irradiation of the human kidney.

Renal function was prospectively analysed in 26 patients treated with radiotherapy for various types of malignancies. In patients with gastric non-Hodgkin's lymphoma stage I-II (gNHL, n = 5), the 99mTc-diethylene-triamine-penta-acetic acid (99mTc-DTPA) renal uptake and the relative 99mTc-dimercapto-succinyl acid (99mTc-DMSA) accumulation decreased gradually and concomitantly in the high-dose, whole-volume irradiated left kidney (40 Gy/5, 5 weeks), down to 25 +/- 10% (mean +/- 1 S.E.M.) and 31 +/- 11%, respectively, after 6-9 years. The absolute 99mTc-DMSA uptake in the left kidney declined down to 33 +/- 12% whereas in the low-dose, whole-volume irradiated right kidney (12-13 Gy/3 weeks) it increased up to 187 +/- 11%. When considering renal volume changes with single photon emission computed tomography, the left kidney in the gNHL patients was reduced to 30 +/- 13%, with, surprisingly, a contralateral enlargement up to only 119 +/- 7% (P < 0.05). The overall renal function in this group of patients, as assessed by creatinine clearance and by [125I]iothalamate/[131I]hippuran clearance was reduced to 48-68%. In the Hodgkin's disease patients (HD, n = 7) given 40 Gy in 4 weeks to 30-50% of the left kidney, the 99mTc-DTPA filtration and the relative 99mTc-DMSA uptake in the left kidney was reduced to 75 +/- 4% and 81 +/- 3%, respectively. The absolute 99mTc-DMSA changes were 78 +/- 10% and 135 +/- 13%, respectively. No significant renal functional alterations were observed in patients with either ovarian carcinoma (n = 7) or seminoma (n = 7). These data suggest a significant, compensatory response of the non-irradiated or low-dose irradiated kidney which, however, appears to be incomplete after contralateral, whole-volume, high-dose irradiation. Such compensatory response might be overestimated when considering only relative or absolute changes in radioactivity uptake.

Blood Pressure↗
PubMed1995

Synthesis and preclinical evaluation of technetium-99m-labeled hippurate analogues.

We have synthesized seven 99mTc-labeled hippurate analogues: 99mTc-hippurate. 99mTc-alpha-hydroxyhippurate, 99mTc-m-hydroxyhippurate. 99mTc-o-hydroxyhippurate [99m-salicylglycine (99mTc-SG)], 99mTc-p-hydroxyhippurate, 99mTc-salicylglycylglycine and 99mTc-salicylglycylglycylglycine. All of the 99mTc-hippurates were cleared rapidly from the rat blood and accumulated in the kidney. Of them 99mTc-SG has the desirable biological properties of two diagnostic agents. 99mTc-mercaptoacetyltriglycine (99mTc-MAG3) and 99mTc-dimercaptosuccinate (99mTc-DMSA). A fraction of 99mTc-SG showed a transit time in the kidney and was excreted rapidly into the urine, being similar to 99mTc-MAG3. The binding ratio to the plasma proteins was 96.0% (91.1% in the albumin), being higher than that of 99mTc-DMSA, at 30 min. The lipophilicity revealed far less pH-dependent changes in a range of pH 4.0 to 7.4. 99mTc-SG distributed about 91% in the renal cortex, being similar to that of 99mTc-DMSA. From the present studies, the biological properties of 99mTc-SG suggest that it is a promising agent for measuring renal plasma flow and renal morphology.

Animals↗
PubMed1995

Reliable preparation of 99mTc (V) DMSA by a simple modified method using a commercial kit for 99mTc (III) DMSA.

99mTc pentavalent dimercaptosuccinic acid [99mTc (V) DMSA], a useful agent for imaging thyroid medullary carcinoma and other tumors, can be reliably prepared by addition of NaHCO3 and then Na99mTcO4 to a commercial kit for 99mTc trivalent DMSA [99mTc (III) DMSA], followed by bubbling oxygen through the solution for 10 min. 99mTc (V) DMSA made by this method is radiochemically pure and stable for 24 h, and it gives a rat biodistribution similar to that of the agent made by previous methods. Clinical biodistribution and radiation dosimetry studies are planned.

Animals↗
PubMed1996

Evaluation of dithiol chelating agents as potential adjuvants for anti-IL-2 receptor lead or bismuth alpha radioimmunotherapy.

The dithiol chelating agents 2,3-dimercapto-1-propanesulfonic acid (DMPS) and meso-2,3-dimercaptosuccinic acid (DMSA) were evaluated for use as potential adjuvants to reduce or prevent radiotoxicity in anti-interleukin-2 receptor (IL-2R) Lead-212 or Bismuth-212 alpha-radioimmunotherapy. DMPS was less toxic than DMSA to tumor cell lines in culture. No adverse effects on the ability of an anti-IL-2R monoclonal antibody (MAb) to bind to its specific antigen were detected using DMPS or DMSA at concentrations up to 600 ug/mL in 10% or 100% mouse serum. After a 5-day oral administration of chelating agent, neither acute nor chronic toxicities on blood hematology, blood chemistry or organ weights were observed for treated mice. DMPS and DMSA were effective in accelerating whole body clearance of the gamma-emitting tracer Bismuth-206. Both chelates significantly reduced femur uptake of tracer when compared to nontreated control mice. However, only DMPS prevented early (2 h postinjection) renal accumulation. These studies support the use of DMPS as a potential adjuvant chelation therapy in Lead-212 or Bismuth-212 radioimmunotherapy protocols.

Adjuvants, Immunologic↗
PubMed2006

Autonomic dysfunction due to lead poisoning.

We present a case history of a 24 years old male who developed autonomic dysfunction, intestinal pseudo-obstruction and anemia due to lead poisoning. Concomitant recording of blood levels of lead and autonomic function showed a gradual decline in blood lead level (98.8 microg/dL at week 0, 56 microg/dL at week 6, and 40 microg/dL at week 52) and gradual improvement in autonomic functions. Decrease in blood lead levels with DMSA (Meso-2, 3-dimercaptosuccinic acid) therapy showed improvement in autonomic functions. At week 0, the patient had severe loss of autonomic tone and autonomic reactivity which improved at week 6. At the 52nd week, most of the autonomic parameters had normalized except for the persistence of mild loss of parasympathetic reactivity.

Adult↗