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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↗
PubMed1988

Survival following massive arsenic ingestion.

A case of a 30-year-old man who ingested a massive quantity of arsenic (approximately 2,150 mg) in an apparent suicide attempt is presented. Aggressive initial therapy, including fluid resuscitation, chelation therapy, and hemodialysis, resulted in the patient's survival. The successful management of arsenic intoxication requires both prompt recognition and the initiation of specific and aggressive therapeutic modalities.

Adult↗
PubMed1992

Whole bowel irrigation in an acute oral lead intoxication.

An 89-year-old man acutely ingested approximately three ounces of a ceramic glaze preparation with a 30% lead oxide content. A blood lead level of 18 micrograms/mL was reported from a sample drawn within 1 hour of ingestion and just prior to gastric lavage. Following lavage, an abdominal radiograph demonstrated lead throughout the small intestine. Whole bowel irrigation was then undertaken and subsequent x-rays demonstrated clearing of all lead in the small bowel. At 16 and 24 hours post-ingestion, blood lead levels rose to 39 micrograms/dL and 42 micrograms/dL, respectively, and the patient then underwent a 5-day course of chelation therapy. This is the first reported case of the use of whole bowel irrigation in an acute lead ingestion. The use of decontamination techniques in acute lead ingestions is reviewed.

Administration, Oral↗
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↗
PubMed1985

Recreational gasoline sniffing: acute gasoline intoxication and latent organolead poisoning. Case reports and literature review.

Gasoline is a readily obtainable intoxicant that unfortunately lends itself to habitual abuse by sniffing, a practice found particularly among children and adolescents. The concerted effects of the multiple hydrocarbon and other constituents of gasoline result in a predictable acute toxic syndrome. Organoleads, primarily tetraethyl lead (TEL), cause a separate toxicologic symptom-sign complex that overlaps with the initial acute toxic syndrome. The different clinical symptomatology, effects on hemoglobin synthesis, and response to chelation therapy are all in keeping with the view that organolead poisoning is a separate and distinct toxicologic entity from that of classical elemental lead poisoning or "plumbism".

Adolescent↗
PubMed1991

Effect of some arsenic antagonists on the toxicity, distribution and excretion of arsenite and arsenate in rats.

1. Arsenite and arsenate poisoned rats were treated with either BAL (2,3-dimercapto-1-propanol), penicillamine (PA) (beta-beta dimethyl cystein) or selenium (Se) (as sodium selenite). 2. The minimal dose of each antagonist that treated arsenic-induced lethality (causing 100% survival) was the same for both arsenite and arsenate. 3. Arsenic mobilization from the tissues (blood, kidney, liver, lungs, spleen, muscles, brain, heart) and its excretion in urine and feces were higher in arsenite-intoxicated animals than in arsenate-intoxicated ones. 4. The effect of each antagonist, when injected alone, on the urinary and fecal excretion of endogenous metals (Cu, Zn, Fe, Ca and Mg) was also examined. 5. The results indicated marked differences in the relative ability of BAL, PA and Se to increase the excretion of the metals.

Animals↗
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↗
PubMed2005

Diphenyl diselenide and 2,3-dimercaptopropanol increase the PTZ-induced chemical seizure and mortality in mice.

The aim of the present study was to evaluate the interaction between a classic GABAergic antagonist -- pentylenetetrazol (PTZ) with an organoselenium compound -- diphenyl diselenide (PhSe)(2) and with the metal chelating agent -- 2,3 dimercaptopropanol (BAL). Mice were pre-treated with 150 micromol/kg (PhSe)(2) or BAL (250, 500 or 1000 micromol/kg) before treatment with PTZ. Pre-treatment with (PhSe)(2) reduced the latency for PTZ-induced seizure at doses of 40 and 60 mg/kg and cause a decrease in the latency for PTZ-induced death at the dose of 60 mg/kg. However, treatment with PTZ at dose of 80 mg/kg was not affected by (PhSe)(2) pre-treatment. Pre-treatment with BAL reduced the latency for PTZ-induced seizure at doses of 40 and 50 mg/kg. In addition, the latency for PTZ-induced death at the dose of 40 mg/kg was decreased significantly by pre-treatment with all doses of BAL. At the dose of 50mg/kg, a significant decrease in the latency for death occurred only in mice pre-treated with 500 and 1000 micromol/kg of BAL. Our results indicate that the PTZ-induced chemical seizures and mortality was enhanced by (PhSe)(2) and BAL. These results indicated that (PhSe)(2) and BAL interact with PTZ possibly by modulating the GABAergic system.

Animals↗
PubMed1975

Radioimmunoassay of plasma renin activity.

Plasma renin activity is quantitated by measuring the rate of angiotensin generation during incubation of plasma renin with endogenous renin substrate. The angiotensin is quantitated by radioimmunoassay. Our studies indicate that the incubation step is best carried out in undiluted plasma at the pH optimum for renin (pH 5.7) in the presence of EDTA, neomycin, and DFP or PMSF. By using these conditions, incubation of low-renin samples can be prolonged for up to 18 hr, because angiotensinases and converting enzyme are completely inhibited. Accuracy is enhanced by prolongation of the incubation time, which results in more angiotensin and eliminates the need for blank subtraction. Incubation at pH 7.4 is disadvantageous because of lower rates of generation of angiotensin 1, because of the inability to maintain pH constant without addition of strong buffer, and because the incubation step cannot be prolonged beyond 3 hr. Dilution of plasma is undesirable because it results in a slower reaction rate due to dilution of both enzyme and substrate, and it is not possible to correct for the effect of substrate dilution. The radioimmunoassay of angiotensin I presents few unusual problems. The volume of plasma assayed should be 20 muI or less. If blank subtraction is used, antibodies should be screened to determine the extent to which they bind nonspecific substances in plasma, and then to ascertain whether the blank is entirely additive when angiotensin is added to it. Assay sensitivity is an important issue, since approximately 30 percent of patients with essential hypertension have subnormal plasma renin activity. In a study of three different commercial kits we found that many low-renin samples were undetectable and major fractions could not be discriminated with precision or consistency from normal renin samples. However, the incubation conditions can be easily modified, so that an 18-hr incubation can be utilized and then low-renin samples can be detected with the same degree of accuracy as those with normal plasma renin activity.

Angiotensin II↗
PubMed1996

The importance of 2,3-dimercaptopropinol (British anti-lewisite, BAL) in the trypanocidal activity of topical melarsoprol.

Both melarsomine dichlorhydrate (mel Cy, Cymelarsan) and melarsen oxide can be dissolved in dimethylsulfoxide and converted into a gel by the addition of hydroxypropylcellulose. When Trypanosoma brucei brucei-infected mice are treated topically with these gels the circulating trypanosomes are rapidly cleared from the circulation but the infections relapse soon after the last application. However, when these two compounds are allowed to react with 2,3-dimercaptopropinol (British anti-lewisite, BAL) and form "melarsoprol" their efficacy, especially in the case of mel Cy, is restored to that of commercial melarsoprol (Arsobal) and trypanosomes in the central nervous system (CNS) can be eliminated. This would indicate that the dimercaptopropinol portion of the molecule does not act solely as an "antidote" to arsenic toxicity, but also plays an important role in the absorption of melarsoprol through the skin and/or blood-brain barrier into the CNS and/or into the trypanosome.

Administration, Topical↗
PubMed1998

Nitric oxide downregulates lung macrophage inflammatory cytokine production.

BACKGROUND: Inflammatory cytokine production contributes to lung injury after lung ischemia reperfusion and during lung transplant rejection. Although nitric oxide has been demonstrated to reduce lung injury associated with the adult respiratory distress syndrome, it remains unknown whether the mechanism of nitric oxide's beneficial effects involves reducing lung macrophage inflammatory cytokine production. The purpose of this study was to determine whether nitric oxide downregulates lung macrophage inflammatory cytokine production. METHODS: Lung macrophages were harvested by bronchoalveolar lavage (10(6) macrophage per milliliter from normal Sprague-Dawley rats, 6 animals per group) and treated under ex vivo tissue culture conditions with the nitric oxide releasing compound S-nitoso-N-acetyl-D, L-penicillamine (0, 10(-5) 10(-4), 10(-3), 10(-2) mol/L) before induction of inflammatory cytokines with endotoxin, (50 ng/mL for 24 hours). Supernatants were assayed for inflammatory cytokine production (tumor necrosis factor alpha, interleukin-1beta) by enzyme-linked immunosorbent assay. RESULTS: Continuous nitric oxide release by S-nitoso-N-acetyl-D, L-penicillamine decreased lung macrophage tumor necrosis factor-alpha and interleukin-1beta production in a dose-dependent fashion (6 rats per group; data were analyzed for significance [p < 0.05] using two-way analysis of variance with Tukey's post-hoc correction). CONCLUSIONS: Nitric oxide decreases inflammatory cytokine production by lung macrophage. The mechanism of nitric oxide's beneficial effects may be partially attributable to decreased production of inflammatory cytokines. Nitric oxide may serve an expanded role for reducing inflammatory cytokine production during acute lung injury, ischemia-reperfusion-induced inflammation, or lung transplant rejection.

Animals↗
PubMed2004

2,3-Dimercaptopropanol, 2,3-dimercaptopropane-1-sulfonic acid, and meso-2,3-dimercaptosuccinic acid inhibit delta-aminolevulinate dehydratase from human erythrocytes in vitro.

The effects of dithiol chelating agents meso-2,3-dimercaptosuccinic acid (DMSA), 2,3-dimercaptopropane-1-sulfonic acid (DMPS), and 2,3-dimercaptopropanol (BAL) on delta-aminolevulinate dehydratase (delta-ALA-D) from human erythrocytes were evaluated. Furthermore, possible protective effects of zinc chloride (ZnCl(2)), dithiothreitol (DTT), and cysteine were studied. delta-ALA-D activity from human erythrocytes was inhibited by dithiol chelating agents in a concentration-dependent manner. Cysteine, at all concentrations tested, did not protect the inhibitory effect of 1 and 4 mM DMPS and DMSA, but protected 1 mM BAL inhibition. Dithiotreitol was able to protect the inhibition caused by 1 mM BAL (28%), DMPS (56%), and DMSA (40%) in a concentration-dependent manner. Zinc chloride protected and restored 1 mM BAL inhibitory effect on delta-ALA-D. Zinc chloride at 500 microM and 1 mM, respectively, protected inhibitory effects of DMPS and DMSA (1 and 4 mM), but did not reverse its effects. The preincubation of dithiol chelating agents with enzyme demonstrated that DMSA was the most potent delta-ALA-D inhibitor of human erythrocytes. These data are in agreement with delta-ALA-D activity from purified enzyme. ZnCl(2) (1 microM) added, in the reaction mixture, increased enzyme activity and DTT (100 microM) totally restored the enzyme activity for all chelating agents tested.

Chelating Agents↗
PubMed1999

An unusual case of lead poisoning in an infant: nursing-associated plumbism.

Lead poisoning remains a common environmental threat for children today. The majority of cases of lead poisoning are caused by oral intake of lead dust or lead-containing paint flakes and thus occur during the second and third years of life. An unusual case of severe lead poisoning in a breast-feeding infant girl is here presented; the source proved to be a nipple shield made of a lead-containing metal. Despite the severity of the intoxication, by the end of treatment and for a year afterwards the infant has been well and her psychokinetic development has been normal.

Alkaline Phosphatase↗
PubMed1992

Controlled study of meso-2,3-dimercaptosuccinic acid for the management of childhood lead intoxication.

We examined the efficacy and safety of meso-2,3-dimercaptosuccinic acid (DMSA) in children with markedly elevated blood lead (BPb) concentrations. Among 19 children with BPb concentrations of 50 to 69 micrograms/dl (2.41 to 3.33 mumol/L) who received a 5-day inpatient oral course of DMSA (1050 mg/m2 per day), the mean BPb concentration decreased by 61%; in four who received calcium disodium ethylenediaminetetraacetic acid (CaNa2EDTA) (1000 mg/m2 per day intravenously), it decreased by 45% (p less than 0.0007). Urinary lead excretion was comparable in both groups. Treatment with DMSA was more effective than treatment with CaNa2EDTA in restoring metabolic activity to the heme pathway and was well tolerated even among nine patients who received concomitant iron supplementation and two who had homozygous deficiency of glucose-6-phosphate dehydrogenase. On discharge, these 19 children received either no chelation therapy or DMSA, 350 or 700 mg/m2 per day for 14 days on an outpatient basis. After 14 days the mean BPb values for the no-chelation, low-DMSA, and high-DMSA groups were 73%, 66%, and 50% of the pretreatment values, respectively. We conclude that a 5-day oral course of DMSA is effective in the treatment of children with severe lead poisoning. In addition, on an outpatient basis the administration of DMSA, 700 mg/m2 per day, is capable of delaying the typical rebound in BPb values and should ultimately reduce the need for repeated hospitalizations.

Administration, Oral↗