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PubMed1976

[Arsenic metabolism. (17) Studies of placental transfer of arsenic and the effects of antidotes and diet].

Albino rats of Wistar strain (Tamura 1950) breeded in a closed colony were administered arsenic trioxide orally during pregnancy (from the 0 day to the 20th day). Organs of fetuses and mother rats were exenterated on the 21st day of gestation and the contents of arsenic measured using an arsenic analyzer unit with atomic absorption spectrophotometry. Whole organs of the fetus were separated into 3 groupings i.e. liver, brain and remaining organs. The contents of arsenic in the organs in each of these groupings and in the placenta were measured. Even in the non-administered group, arsenic was detected in the every organ. In the arsenic administered group, the content of arsenic in the placenta was the highest among the four preparations tested; and the content in the liver and remaining organs was considerably high, but was low in the brain. The level of accumulation of arsenic differed between each organ. In the placenta, the accumulation reached a plateau, and in the brain this accumulation was below one-tenth that in the liver. In the non-administered group, arsenic was detected in the liver, kidney, spleen and brain of mother rats. In the group on arsenite, the content in the kidney and spleen was large, followed by a large amount in the liver and in the brain respectively. The level of accumulation of arsenic in mother rats differed between each organ. Arsenite was administered with antidotes such as dimercaprol, thioctic acid and L-ascorbic acid during pregnancy (from the 0 day to the 5th day). In this group the content of arsenic in the remaining organs was statistically less than that of the control group. The content in the brain was slightly reduced by a co-administration of the antidotes, however, there was no statistical difference in the placenta and liver between the antidote-treated and control groups. The content of arsenic in the kidney of mother rats treated with antidotes was statistically less than that of the controls. Whether or not the content of arsenic in organs of fetuses and mother rats was affected by a milk diet was also studied. The content of arsenic in the organs of fetuses showed no statistical difference between the animals on an Oriental stock diet group and those on the milk diet. On the other hand, the content of arsenic in the kidney of mother rats on the milk diet was statistically less than seen in those in the Oriental stock diet group.

Animals↗
PubMed1996

[Acute arsenic poisoning].

We report three cases of arsenic poisoning in a chemical factory. Three workers were exposed to vinyzene 10,10'-oxydephenarsine and developed mild symptoms of acute poisoning. All patients were treated with dimercaprol, and recovered after a few days. Urine analysis did not show increased arsenic excretion, but this could be due to the large urine samples taken. It is recommended that a urine sample is taken right after admission to hospital and new samples after eight and 16 hours.

Accidents, Occupational↗
PubMed2002

Interventions for paracetamol (acetaminophen) overdoses.

BACKGROUND: Self-poisoning with paracetamol (acetaminophen) is a common cause of hepatotoxicity in the Western World. Interventions for paracetamol poisoning encompass inhibition of absorption, removal from the vascular system, antidotes, and liver transplantation. OBJECTIVES: The objective was to assess the beneficial and harmful effects of interventions or combination of interventions for paracetamol overdose. SEARCH STRATEGY: The Cochrane Hepato-Biliary Group Controlled Trials Register, The Cochrane Library, MEDLINE, EMBASE, and text searches were combined (until July 2001). SELECTION CRITERIA: Randomised clinical trials (RCTs) and observational studies as well as human volunteer randomised trials were included. The studies could be unpublished or published as an article, an abstract, or a letter and no language limitations were applied. DATA COLLECTION AND ANALYSIS: All the analyses were performed according to the intention to treat. The methodological quality of the included trials was evaluated by components of methodological quality. MAIN RESULTS: Nine RCTs (all small and of low methodological quality), one quasi-randomised trials, 37 observational studies, and nine randomised trials including human volunteers were identified. It was impossible to perform meta-analyses including more than two RCTs. Activated charcoal, gastric lavage, and ipecacuanha are able to reduce the absorption of paracetamol but the clinical benefit is unclear. Of these, activated charcoal seems to have the best risk-benefit ratio. N-acetylcysteine seems preferable to placebo/supportive treatment (relative risk of mortality in patients with fulminant hepatic failure = 0.65; 95% confidence interval 0.43 to 0.99), dimercaprol, and cysteamine, but N-acetylcysteine's superiority to methionine is unproven. It is not clear which N-acetylcysteine treatment protocol offers the best efficacy. No evidence supports haemoperfusion or cimetidine for paracetamol overdose. Liver transplantation has the potential to be life saving in fulminant hepatic failure, but further refinement of selection criteria for liver transplantation and evaluation of the long-term outcome are required. REVIEWER'S CONCLUSIONS: This systematic Review has highlighted a paucity of RCTs on interventions for paracetamol overdose. Activated charcoal seems the best choice to reduce paracetamol absorption. N-acetylcysteine should be given to patients with paracetamol overdose. No N-acetylcysteine regime has been shown to be more effective than any other. It is a delicate balance when to proceed to liver transplantation, which may be life saving in patients with a poor prognosis. Interventions for paracetamol overdose need assessment in high-quality, multi-centre RCTs.

Acetaminophen↗
PubMed2006

Interventions for paracetamol (acetaminophen) overdose.

BACKGROUND: Poisoning with paracetamol (acetaminophen) is a common cause of hepatotoxicity in the Western World. Inhibition of absorption, removal from the vascular system, antidotes, and liver transplantation are interventions for paracetamol poisoning. OBJECTIVES: To assess the benefits and harms of interventions for paracetamol overdose. SEARCH STRATEGY: We identified trials through electronic databases, manual searches of bibliographies and journals, authors of trials, and pharmaceutical companies until December 2005. SELECTION CRITERIA: Randomised clinical trials and observational studies were included. DATA COLLECTION AND ANALYSIS: The primary outcome measure was all-cause mortality plus liver transplantation. Secondary outcome measures were clinical symptoms, (eg, hepatic encephalopathy, fulminant hepatic failure), hepatotoxicity, adverse events, and plasma paracetamol concentration. We used Peto odds ratios and odds ratios with 95% confidence intervals (CI) for analysis of outcomes. Random- and fixed-effects meta-analyses were performed. MAIN RESULTS: Ten small and low-methodological quality randomised trials, one quasi-randomised study, and 48 observational studies were identified. It was not possible to perform relevant meta-analyses of randomised trials that have addressed our outcome measures. Activated charcoal, gastric lavage, and ipecacuanha are able to reduce the absorption of paracetamol, but the clinical benefit is unclear. Of these, activated charcoal seems to have the best risk-benefit ratio. N-acetylcysteine seems preferable to placebo/supportive treatment, dimercaprol, and cysteamine, but N-acetylcysteine's superiority to methionine is unproven. It is not clear which N-acetylcysteine treatment protocol offers the best efficacy. No strong evidence supports other interventions for paracetamol overdose. N-acetylcysteine may reduce mortality in patients with fulminant hepatic failure (Peto OR 0.26, 95% CI 0.09 to 0.94, one trial). Liver transplantation has the potential to be life saving in fulminant hepatic failure, but refinement of selection criteria for transplantation and long-term outcome reporting are required. AUTHORS' CONCLUSIONS: Our results highlight a paucity of randomised trials on interventions for paracetamol overdose. Activated charcoal seems the best choice to reduce absorption. N-acetylcysteine should be given to patients with overdose but the selection criteria are not clear. No N-acetylcysteine regime has been shown to be more effective than any other. It is a delicate balance when to proceed to liver transplantation, which may be life-saving for patients with poor prognosis.

Acetaminophen↗
PubMed2003

Are there teratogenic risks associated with antidotes used in the acute management of poisoned pregnant women?

OBJECTIVE: We reviewed evidence suggesting teratogenic risk associated with the use of antidotes in the acute management of poisoned pregnant women. METHODS: Medline, Toxline, and DART/ETIC searches; references of retrieved articles, pertinent databases and textbooks were also searched. RESULTS: There are case reports or case series of women who received antidotes for poisoning during (*) or after (+) the period of organogenesis who showed no fetal adverse effects. Some antidotes, however, have no teratogenic risk: atropine (cohort/surveillance studies)+, calcium (oral supplement: cohort study)+ and pyridoxine (Bendectin studies). Also, ethanol+, methylene blue (intra-amniotic injection but not oral) and penicillamine* can be considered teratogens but their risks in the treatment of poisonings are unknown. There is no epidemiologic study evaluating the risk of the following antidotes during pregnancy: N-acetylcysteine(*+), BAL (dimercaprol)+, black widow spider antivenin+, calcium EDTA+, crotalidae antivenin, crotalidae polyvalent immune FAB, cyanide antidote kit (amyl and sodium nitrate, sodium thiosulfate), deferoxamine(*+), digoxin immune FAB+, DMSA+, flumazenil+, fomepizole, methylene blue (IV), naloxone, physostigmine, pralidoxime+, protamine+; and parenteral pharmacologic doses of calcium+, folinic acid*, glucagon+, hydroxycobalamin, phytonadione (vitamin K), and pyridoxine. CONCLUSIONS: Despite the limited evidence supporting the risk of antidote use during pregnancy, antidotes should be used when there is a clear maternal indication to decrease the morbidity or mortality associated with poisoning. The only exception may be penicillamine, which is a teratogen. Better antidotes exist for most poisonings that penicillamine could potentially treat. At this time, there is no known fetal indication for all antidotes. Reporting the use of an antidote during pregnancy should be encouraged, especially if used during the critical period of organogenesis.

Abnormalities, Drug-Induced↗
PubMed1978

Synthesis and evaluation of sulfur-containing steroids against methylmercuric chloride toxicity.

Sulfur-containing steroids, analogs, and derivatives were synthesized for evaluation in mice suffering acute toxicity from methylmercuric chloride. Steroids were administered by intraperitoneal injection, by stomach tube feeding, or by absorption through the tail skin. Thiocholesterol and the thiocholanoic acids were effective if given prior to poisoning. The thiosteroids were significantly more effective than penicillamine or dimercaprol under these conditions.

Administration, Oral↗
PubMed1980

New evaluation of potential methylmercury scavengers.

A biological assay was developed to evaluate rapidly the relative efficacy of marketed and experimental mercurial scavengers. Rat liver mitochondrial protein (1.0 mg) was titrated against methyl-mercuric chloride to the inhibitory level of mitochondrial respiration. Respiration induced by adenosine 5'-diphosphate with succinate (plus rotenone) as the substrate was inhibited consistently by 20.7 +/- 3.9 nmoles of methylmercury/mg of protein. Adenosine 5'-diphosphate-stimulated respiration (State 3) was restored with dimercaprol, penicillamine, and cysteine but not with serine. The antagonists glutathione, 3-mercapto-propionic acid, 2-mercaptoethanol, dithiothreitol, thioglucose, mercaptosuccinic acid, and thiosalicylic acid and mercaptosuccinic acid. Sodium sulfide, thioacetamide, and ethylenediaminetetraacetic acid were completely inactive. Substitution of glutamate (plus malate) for succinate (plus rotenone) as the substrate did not alter the responses significantly. The rat liver mitochondrial assay provides preliminary information about the efficacy and toxicity of water-soluble thiols. Investigations utilizing encapsulated water- and lipid-soluble mercaptans are in progress.

Animals↗
PubMed1992

The effects of cadmium in vitro on adenosine triphosphatase system and protection by thiol reagents in rat brain microsomes.

Cadmium (Cd) inhibited the activities of Na(+)-K+ ATPase (IC50 = 5.0 x 10(-5) M), K(+)-p-nitrophenyl phosphatase (PNPPase) (IC50 = 4.0 x 10(-5) M) and 3H-ouabain binding (IC50 = 7.5 x 10(-5) M) in rat brain microsomes. Monothiols (cysteine but not glutathione and D-penicillamine) and dithiols (dimercaprol, dimercaptosuccinic acid and dithiothreitol) offered varied levels of protection against Cd-inhibition of Na(+)-K+ ATPase. Protection of Na(+)-K+ ATPase by these sulfhydryl (SH) agents was higher at 7.5 as compared to 8.5 pH. The present data suggest that Cd-inhibited Na(+)-K+ ATPase, by interfering with phosphorylation of enzyme molecule and dephosphorylation of the enzyme-phosphoryl complex and exerts a similar effect to that of SH-blocking agents.

Animals↗
PubMed1981

Hemoperfusion for organic mercury detoxication?

A case is reported with suicidal ingestion of 125 g Ceresan, a fungicide containing 3.5% Hg2=s methoxyethylmercury-chloride. Final absorption of mercury was approximately 706 to 977 mg, as extrapolated from mercury eliminated in urine. Activated charcoal hemoperfusion removed only 1% to 2% of the amount absorbed. During treatment with D-penicillamine and dimercaprol, which were alternated fortnightly, the mercury elimination half life was 25 days, as calculated from blood concentrations and 23 days as calculated from urine data. Except for local cauterization of the mouth and throat, no signs of liver, kidney or central nervous system intoxication were seen within a 3-month follow-up period.

Female↗
PubMed1982

Gold toxicity presenting as peripheral neuropathy.

A patient with rheumatoid arthritis developed gold induced peripheral neuropathy after 255 mgs of aurothioglucose. This neuropathy is characterized by weakness and numbness of the hands and feet in association with hyperalgesia of the palmar surface of the hands. The absence of vasculitis permits differentiation of gold neuropathy from the neuritis associated with rheumatoid arthritis or systemic lupus erythematosus. Treatment consists in cessation of gold and possibly the use of dimercaprol; recovery is slow but generally complete.

Adult↗
PubMedDate not supplied

Lead intoxication.

Lead intoxication was recognised as early as 2000 BC and the widespread use of lead has been a cause of endemic chronic plumbism in several societies throughout history. In the twentieth century, lead intoxication is still a common problem. In children it is largely due to ingestion of pica and environmental exposure, whereas adult groups at greatest risk are the industrially exposed: thus, screening of these workers should be undertaken at regular intervals. The clinical features of lead intoxication are nonspecific and often go unrecognised. The early manifestations are largely neuropsychiatric, followed by more significant disturbances of the central and peripheral nervous systems, symptomatic gastrointestinal, musculoskeletal, haematological and endocrine abnormalities. The association of lead poisoning with renal disease is well documented and must be considered, particularly if there is associated hypertension and/or gout. Blood lead concentrations are an unreliable predictor of body lead stores as they are indicative only of recent exposure. Haematological parameters have been used to assess those at risk of toxicity, but although more reliable than blood concentrations, they also fail to predict those patients at risk of toxicity. The recommended assessment for patients with suspected lead intoxication is a calcium disodium edetate chelation test, which is a sensitive marker for assessing body stores and subsequent intoxication. In children the dosage should be 50 mg/kg up to 1000 mg, and in adults 1000 mg administered intravenously or 2000 mg intramuscularly in divided doses 12 hours apart with subsequent 72 hour urinary lead estimations. Lead excretion levels greater than 350 micrograms/72 hours should be considered as suggestive of intoxication, particularly if supported by historical, clinical or biochemical evidence of lead exposure. Treatment of patients with positive chelation tests involves symptomatic treatment and a course of chelation therapy utilising calcium disodium edetate in doses similar to those used for testing, and in the more severely intoxicated patient, the addition of dimercaprol in doses of 75 mg/m2 every 4 hours to a total of 300 mg/m2/day. The safety of these treatment regimens is well documented.

Chelating Agents↗
PubMedDate not supplied

Pharmacokinetics and toxicity of bismuth compounds.

Inorganic bismuth salts are poorly soluble in water: solubility is influenced by the acidity of the medium and the presence of certain compounds with (hydr)oxy or sulfhydryl groups. The analysis of bismuth in biological material is not standardised and is subject to large variation; it is difficult to compare data from different studies, and older data should be approached with caution. The normal concentration of bismuth in blood is between 1 and 15 micrograms/L, but absorption from oral preparations produces a significant rise. Distribution of bismuth in the organs is largely independent of the compound administered or the route of administration: the concentration in kidney is always highest and the substance is also retained there for a long time. It is bound to a bismuth-metal binding protein in the kidney, the synthesis of which can be induced by the metal itself. Elimination from the body takes place by the urinary and faecal routes, but the exact proportion contributed by each route is still unknown. Elimination from blood displays multicompartment pharmacokinetics, the shortest half-life described in humans being 3.5 minutes, and the longest 17 to 22 years. A number of toxic effects have been attributed to bismuth compounds in humans: nephropathy, encephalopathy, osteoarthropathy, gingivitis, stomatitis and colitis. Whether hepatitis is a side effect, however, is open to dispute. Each of these adverse effects is associated with certain bismuth compounds. Bismuth encephalopathy occurred in France as an epidemic of toxicity and was associated with the intake of inorganic salts including bismuth subnitrate, subcarbonate and subgallate. In the prodromal phase patients developed problems in walking, standing or writing, deterioration of memory, changes in behaviour, insomnia and muscle cramps, together with several psychiatric symptoms. The manifest phase started abruptly and was characterised by changes in awareness, myoclonia, astasia and/or abasia and dysarthria. Patients recovered spontaneously after discontinuation of bismuth. Intestinal lavage, forced diuresis and haemodialysis have been tried without positive effects on the clinical condition of the patient or on blood bismuth concentration, and the use of dimercaprol as an antidote has produced reports of both positive and negative findings. To confirm the diagnosis of bismuth encephalopathy, it is essential to find elevated bismuth concentrations in blood, plasma, serum or CSF. A safety level of 50 micrograms/L and an alarm level of 100 micrograms/L have been suggested in the past, but no proof is available to support the choice of these levels.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1982

Inhibition of rat brain microsomal (Na+ + K+)-ATPase and K+-p-nitrophenylphosphatase by periodic acid.

The effects of mild periodate exposure on the kinetics of (Na+ + K+)-ATPase and K+-p-nitrophenylphosphatase were studied using rat cerebral microsome preparations. Fifty percent inhibition of both enzyme activities was attained near 3 microM periodate concentrations. This inhibition was biphasic with time. Mg2+-ATPase and Mg2+-p-nitrophenylphosphatase activities were much less inhibited by periodate. Periodate inhibition was partially reversed by dimercaprol and dithiothreitol but not by diffusion. The possible reaction products formic acid, formaldehyde, glyceraldehyde, and acetaldehyde had no inhibitory effects in similar concentrations. Periodate exposure produced no detectable changes in the activation of (Na+ + K+)-ATPase by Na+, K+, Mg2+, or ATP. Residues shared by both (Na+ + K+)-ATPase and K+-p-nitrophenylphosphatase are both critical to hydrolytic function and sensitive to mild oxidation by periodate.

4-Nitrophenylphosphatase↗
PubMed1990

Chelation of mercury by ouabain-sensitive and ouabain-resistant renal Na,K-ATPase.

The SH-reactive HgCl2 inhibits the Na,K-ATPase activity potently in a manner antagonized only partially by EDTA or cysteine; solely dimercaprol, a dithiol antidote for mercury, blocks the HgCl2 effects entirely as confirmed also by 203Hg-binding experiments. The results reveal the presence of a chelating component in pure Na,K-ATPase with an affinity for mercury superior to EDTA. The mercury-sensitivity of the Na,K-ATPase is not related to the ouabain-sensitivity. This criterion will be useful for the distinction between ouabain-like and mercury-like inhibitors from body fluids and tissues.

Animals↗
PubMed1975

The reliability of the measurement of plasma renin activity by radioimmunoassay.

A radioimmunoassay of angiotensin I has been applied to the measurement of plasma renin activity. Angiotensin I was generated in plasma samples by 3 h incubation at 37 degrees C and pH 5.6 after addition of EDTA and Dowex. The generated amount of angiotensin I was measured by radioimmunoassay in the eluate of the Dowex column. With this method a negligible amount of angiotensin I was measured after incubation at 4 degrees C (0.8 ng/ml per 3 h). Eluate of blank plasma had no measurable effect on the standard curve. The mean recovery of angiotensin I was 87%. The limit of detection of the assay was 0.5 ng/ml per 3 h. The results obtained using different antisera were equal. A marked variation was found in immunological properties of different standard preparations of angiotensin I tested. The mean value of angiotensin I generation per Goldblatt Unit (G.U.) renin was 3.9 with 10-4 ng/h. In normotensive control subjects, the plasma renin concentration, whileon unrestricted diet and after 3 h of ambulation, was on average 0.39 with 10-minus 4 G.U./ml, range 0.12 with 10-minus 4-0.91 with 10-minus 4. With the use of the same plasma extracts for radioimmunoassay and bioassay, a perfect correlation was found between the plasma renin activities measured with both assays. The differences found between the results of both assays could be fully explained by the different biological activities of the standards used (Angiotensin I, Schwarz Mann, and Angiotensin II, Ciba-Geigy). With a direct radioimmunoassay, angiotensin I was generated in plasma by 3 h incubation at 37 degrees C and pH 5.6 after addition of phenylmethanesulfonyl fluoride, 8-hydroxyquinoline and 2,3-dimercaptopropanol (dimercaprol). The generated amount of angiotensin I was measured by the above mentioned radioimmunoassay. A fairish correlation was found between the generated amounts of angiotensin I measured in the Dowex eluate and those found in the incubated plasma. Especially in the lowest range, lower values were obtained by the latter assay. However, the generated amounts of angiotensin I measured in non-incubated plasma samples (3 h at 4 degrees C) was on average 6.4 ng/ml per 3 h and accounted for 748% of the amounts found after incubation at 37 degrees C.

Angiotensin II↗
PubMed1988

Measurement of plasma renin activity in the freshwater turtle.

Components of the renin angiotensin system have been identified in many nonmammalian vertebrates. However, in many of these animals, including reptiles, the physiological functions and importance of the system remain unclear. To aid in the study of the system in a reptile we modified a commercially available radioimmunoassay (RIA) kit containing antibody against human angiotensin I (ANG I) for use in the freshwater turtle, Pseudemys scripta. Cross-reactivity between anti-human ANG I antibodies (Rainen Angiotensin I RIA Kit, New England Nuclear) and turtle ANG I was demonstrated. Cross-reactivity with the antibody in two other human ANG I assay kits (Travenol-Genentech and Biotecx) was very limited. Blood for assay was collected from conscious turtles in EDTA, centrifuged, and the plasma frozen at -20 degrees. Turtle ANG I was generated by incubation at 0.5 ml plasma at pH 5.5 for 2 hr at 30 degrees with addition of dimercaprol and 8-hydroxyquinoline. Angiotensin generation increased with temperature and with generation time. The recovery of turtle ANG I added to turtle plasma prior to incubation was 92-97%. The assay procedure was used to measure plasma renin activity (ng/ml/hr incubation) from unstimulated turtles.

Angiotensin I↗
PubMed1980

A simple microassay for the estimation of renin concentration in plasma.

A simple assay for the measurement of renin concentration and renin substrate concentration in microliter quantities of rat plasma is described. In the plasma renin concentration assay 5 microliter of rat plasma was incubated for 2 hr at 37 degrees C in the presence of 20 microliter renin substrate (plasma from nephrectomized rats) and 5 microliter inhibitor-buffer solution pH 7.4. At the end of the enzymic incubation the generated angiotensin I was estimated by radioimmunoassay. Angiotensin I antisera and iodinated angiotensin I were added to the same tube and left to equilibrate at 45 degrees C for 15 hr. EDTA, dimercaprol, and 8-hydroxyquinoline were used to inhibit converting enzymes and angiotensinases. Reproducibility of the assay was good, and recovery of added angiotensin I complete. The normal range of plasma renin in rats was between 7 and 15 pmol angiotensin l/ml/hr.

Angiotensin I↗
PubMed1992

Mobilization of lead in mice by administration of monoalkyl esters of meso-2,3-dimercaptosuccinic acid.

The following six monoalkyl esters of meso-2,3-dimercaptosuccinic acid (DMSA) were synthesized and evaluated for relative activities in mobilizing lead from kidneys and brains of lead-bearing mice: n-propyl (Mn-PDMS), i-propyl (Mi-PDMS), n-butyl (Mn-BDMS), i-butyl (Mi-BDMS), n-amyl (Mn-ADMS) and i-amyl meso-2,3-dimercaptosuccinate (Mi-ADMS). DMSA was used as a positive control. When each was administered intraperitoneally (i.p.) as a single dose of 2.0 mmol/kg, DMSA lowered the kidney lead concentration 52%, while the monoesters effected reductions of 54-75%. Mn-ADMS was toxic at this dose. DMSA lowered the brain lead level 20% when given as a single dose, while the monoesters conferred reductions of 64-87%. When given as 5 daily i.p. injections at 0.5 mmol/kg, DMSA reduced the kidney lead concentration 45%, while the monoesters caused reductions of 56-73%. DMSA lowered the brain lead concentration 35% on the 5-day treatment regimen, while the monoesters evoked reductions of 59-75%. Mi-ADMS was equally effective when given orally or i.p. The i.p. LD50 value of this analog in mice is 3.0 mmol/kg, a value which lies between the reported LD50 doses of DMSA (16.0 mmol/kg) and dimercaprol (1.1 mmol/kg). It is suggested that the ability of these monoesters to cross cell membranes may account for their superiority to DMSA in mobilizing brain lead in this animal model.

Animals↗