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At least 19 recordsLinked to original sources
PubMed1976

Influence of dimercaprol on the early hepatic uptake of 111In-bleomycin in the BALB/c mouse.

Dimercaprol (BAL) administered 1 hr before 111In-bleomycin in the normal BALB/c mouse produced an early preferential hepatic loading of 111In-bleomycin without a loading of the spleen, skin, bone, or muscle. Liver-to-muscle ratios were increased about threefold under the influence of BAL. Liver (c BAL)/liver (s BAL) ratios also increased threefold at 3 hr whereas relative muscle uptake remained at about unity. Indium-111 chloride (colloid, pH 6.5) used as a control did not show a similar increase. The findings suggest that the kinetics and distribution of 111In-bleomycin in the normal BALB/c mouse can be influenced by pretreatment with BAL.

Animals↗
PubMed1978

Effects of thiol inhibitors on hepatic guanylate cylase activity.

Several thiol blocking agents inhibit basal guanylate cyclase activity of 100 000 X g hepatic supernatant fractions and the stimulation of enzyme activity by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), NaN3, NaNO2 and nitroprusside. The relative potency of the thiol blockers as inhibitors was CdCl2 greater than p-hydroxymercuribenzoate greater than N-ethylmaleimide greater than arsenite greater than iodoacetamide. Inhibition of basal and MNNG-responsive soluble guanylate cyclase activities by arsenite was markedly potentiated by an equimolar concentration of 2,3-dimercaprol, but not by mercaptoethanol. Inhibition of soluble guanylate cyclase by either arsenite or CdCl2 was completely reversed by excess 2,3-dimercaprol. Qualitatively similar effects were observed with DE-52 cellulose purified soluble hepatic guanylate cyclase, and suggested an involvement of closely juxtaposed thiol groups in the regulation of enzyme activity. For several reasons inhibition by thiol blockers appeared to be mediated through multiple mechanisms and/or sites of interaction: (1) Concentrations of the thiol inhibitors which had no effect on basal activity strikingly inhibited the responsiveness of the enzyme to a submaximal concentration of MNNG. (2) CdCl2 abolished the action of excess MnCl2 to stimulate purified guanylate cyclase, but was a relatively ineffective inhibitor when MnCl2 and GTP were present in equimolar concentrations. By contrast, arsenite-2,3-dimercaprol was uniformly effective in inhibiting guanylate cyclase activity in the presence or absence of excess MnCl2. (3) Arsenite-2,3-dimercaprol increased the Km for MnGTP (control, 0.13 +/- 0.02 mM; 0.2 mM arsenite-2,3-dimercaprol, 0.31 +/- 0.03 mM), whereas CdCl2 had no effect on this parameter. (4) Hepatic particulate guanylate cyclase activity was significantly inhibited by arsenite 2,3-dimercaprol but not by CdCl2. Thus, the data not only indicate that vicinal dithiol groups are required for expression of basal guanylate cyclase activity and enzyme responses to agonists, but strongly suggest the involvement of more than one interacting site containing free thiol residues.

Animals↗
PubMed1977

D-penicillamine therapy of acute arsenic poisoning.

Severe poisoning resulting from single ingestions of rodenticides, herbicides, or insecticides containing arsenic have been frequently recognized. We record three cases of solubilized arsenic trioxide poisoning in Navajo Indian children and one case of sodium arsenate ingestion in an infant. One fatality occurred during dimercaprol therapy prior to initiation of therapy with D-penicillamine. Three survivors were treated with 2.3-dimercaprol intramuscularly and with oral D-penicillamine. The use of D-penicillamine in arsenic poisoning has not been generally appreciated. Excretion data from the three children are presented which document the effectiveness of D-penicillamine, administered orally in four daily doses of 25 mg/kg/dose, in the therapy of arsenic intoxication. Excretion data for the trace metals, zinc and copper, during D-penicillamine chelation therapy are also reported.

Acute Disease↗
PubMed1978

Changes in the hepatic copper conent after treatment with foreign compounds.

The effects of dimercaprol, CaNa2EDTA, D-penicillamine, diethyldithiocarbamate, disulfiram, pyrazole and phenobarbital on the hepatic copper content were studied. Adult male albino rats were given these compounds subcutaneously or intragastrically for 4 or 7 days, and the copper content in the hepatic crude homogenate was measured with an atomic absorption spectrophotometer. The metal chelating compounds dimercaprol, D-penicillamine and diethyldithiocarbamate only slightly decreased the level of copper in the liver. CaNa2 EDTA caused no change in the copper content. A slight decrease was found also after phenobarbital treatment. On the contrary, disulfiram and pyrazole increased the copper content 3- and 2-fold, respectively. It is suggested that the accumulation of copper in the liver is due to the cholestatic action of disulfiram and pyrazole.

Animals↗
PubMed1977

Acute copper intoxication. Pathophysiology and therapy with a case report.

We report a case of cupric sulfate intoxication in a child who had a serum copper level of 1,650 mug/100 ml. His course was accompanied by hemolytic anemia and renal tubular damage. We review the pathophysiology of copper metabolism and intoxication. We also review modes of therapy, with specific reference to the initial approach, using dimercaprol (BAL) and edetic acid rather than penicillamine.

Acute Disease↗
PubMed1976

Methodologic problems in plasma renin activity measurements.

The influence of pH and angiotensinase inhibitors on the in vitro generation of angiotensin I during PRA measurements has been investigated. PRA values obtained at pH 5.7 are higher than those obtained at pH 7.4. At pH 5.7, values obtained using diisopropylfluorophosphate (DRP 9 mM) as an angiotensinase inhibitor are higher than values obtained with a mixture of dimercaprol (BAL, 1.6 mM) and hydroxyquinoline (8-OHQ, 3 to 4 mM). Since the two methods for inhibiting angiotensinase are completely and equally efficient, it is suggested that these inhibitors might interfere with the renin angiotensinogen reaction. Significant correlations are observed between the PRA values obtained by the different methods which have been studied. Using an incubation pH of 5.7, and BAL and 8-OH quinoline as angiotensinase inhibitors, the distribution of PRA values in a population of 124 hospitalized hypertensive patients ingesting a normal sodium diet had been studied, and it has been demonstrated that the sensitivity of this method of measurement can detect small changes in PRA in patients with low renin activity.

Adenoma↗
PubMed1976

Non-invasive quantitation of corneal copper in hepatolenticular degeneration (Wilson's disease).

The corneal copper content was measured by X-ray excitation spectrometry in two controls and in seven patients with Wilson's disease. Patients who were treated irregularly or not treated at all showed a high corneal copper content. Those who were adequately treated had low levels, comparable to the controls. In one case the corneal copper content declined 45%, after a course of dimercaprol. The corneal copper measured showed no correlation with the slit-lamp appearance of the Kayser-Fleischer ring. It is suggested that non-invasive X-ray excitation spectrometry can provide a fast and reliable method for the early diagnosis of Wilson's disease and for the objective evaluation of the efficacy of the treatment of this disease.

Adolescent↗
PubMed1975

Problems connected with plasma renin activity measurements by angiotensin I radioimmunoassay.

The main application of the radioimmunoassay for angiotensin I is the measurement of plasma renin activity (PRA). Methods published for the measurement of PRA differ in many details and make the comparison of results difficult. This paper deals with some of the problems. 1. The radioactive labelling of angiotensin I using chloramine-T requires the purification of the labelled peptide. A method applying both anion exchange chromatography and gel filtration is described. It resulted in tracer angiotensins of very reproducible characteristics. 2. For the measurement of PRA, the pH of the plasma has to be adjusted prior to the incubation. The adjustment to the physiologic pH of 7.4 is recommended. 0.1 volume of a concentrated buffer controlled the pH during a three hours incubation without diluting the plasma too much. 3. At pH 7.4, EDTA, dimercaprol, and 8-hydroxyquinoline were found to inhibit converting enzyme and angiotensinases better than EDTA and DFP and should therefore be used as inhibiting agents. 4. Nonspecific cross reaction of antisera are the cause of the blank values when angiotensin I is measured in unextracted plasma. The problem of subtraction of a blank may be minimized by the selection of an antiserum of high specificity which shows no or only little nonspecific cross reaction. Lor or unmeasurable blank values will result.

Angiotensin II↗
PubMed1979

Acute respiratory failure following severe arsenic poisoning.

A 47-year-old man had an episode of severe respiratory failure after acute intoxication with arsenic. Features of the initial clinical presentation included nausea, vomiting, and diarrhea, acute psychosis, diffuse skin rash, and marked pancytopenia. A peripheral neuropathy then developed which resulted in severe weakness of all muscles of the limbs, the shoulder and pelvis girdles, and the trunk. The neuropathy continued to progress despite treatment with dimercaprol (BAL in oil). Five weeks after the initial exposure, the patient was no longer able to maintain adquate ventilation and required mechanical ventilatory support. Improvement in the patient's neuromuscular status permitted successful weaning from the ventilator after one month of mechanical ventilation. Long-term follow-up revealed no further respiratory difficulty and slow improvement in the strength of the peripheral muscles.

Arsenic Poisoning↗
PubMed1979

Atempted homicide with arsenic.

An unusual method of introducing arsenic to water with homicidal intentions, where five members of the same family were poisoned, is reported. The obvious initial diagnosis of food poisoning or food allergy was reviewed when the story of noticing an unusual substance in the well was revealed. The patients recovered fully after conventional intramuscular dimercaprol.

Adult↗
PubMed1976

Cardiac action of thiamine derivatives in guinea pig atria.

Pharmacological studies were performed on allithiamine (TAD), thiamine propyl disulfide (TPD), and thiamine tetrahydrofurfuryl disulfide (TTFD) to investigate positive inotropic and negative chronotropic effects seen when they are applied to spontaneous beats in isolated guinea pig atria at concentrations higher than 10-5 g/ml. 1. The effects of thiamine 8-(methyl-6-acetyldihydrothioacetate) disulfide (TATD) and thiamine hydroxyethyl disulfide (TOED) at 5 x 10-4 were slight, and those of dibenzoyl thiamine (DBT) and thiamine were limited at any concentration. 2. Dimethyl propyl disulfide (DMPD) which has anti-thiamine activity, showed these effects at concentrations higher than 10-5. 3. The negative chronotropic effect of TAD, TPD, and TTFD was not influenced by the prior application of atropine, and the positive inotropic effect was not influenced by propranolol. 4. The effects of TTFD on the electrically driven left atrial muscle were remarkable when the muscle was driven at low frequency, while they were less remarkable at high frequency. 5. The decrease in tension of the electrically driven left atria induced by mersalyl at 5 x 10-4 g/ml was recovered by the subsequent addition of TTFD or TPD at 5 x 10-4 as well as dimercaprol at 5 x 10-5. From the results, it was assumed that (a) the effects of TAD, TPD and TTFD might relate to their common chemical structure of the disulfide, especially to the alkyldisulfide chain, (b) the effects are irrevelant to their common activity as an vitamin B1 and to either cholinergic or adrenergic effect, and (c) a mutual dependence is seen between the positive inotropic effect and the negative chronotropic effect.

Animals↗
PubMed1977

[Encephalopathy due to organomercuric compounds].

A 27 year old agricultural worker presented about one month after treating cereal seeds with an alcoxyalkyl mercurial derivative, an encephalopathy with a confusional state, a cerebellar stato-kinetic syndrome, an intention tremor and grand mal epileptic fits. Treatment with dimercaprol produced a clinical improvement on the fourth day with a fall in blood mercury from 3.5 mug to 2.2 mug whilst urinary excretion of mercury remained low. A fortnight later the patient was completely cured. Although less common than collective poisoning by ingestion, organo-mercurial encephalopathies due to occupational exposure are a real danger although it is not known whether the relative rareness of published cases is due only to lack of observance of security rules or to individual sensitivity which might be due to increased absorption of mercury through the lungs or skin. This case shows that although alkyl mercurial derivatives are reputed to be the most dangerous, alcoxyalkyl derivatives may also cause encephalopathies. Also, as long as non-toxic substances remain unavailable for use in agriculture, one should emphasise the necessity of careful observance of the security rules during manipulation of these products.

Adult↗
PubMed1978

Acute selenium poisoning: case report.

A case of self-poisoning with sodium selenate sheep drench, along with blood and urine levels of selenium, is reported. Treatment included gastric lavage, diuresis, vitamin C, and dimercaprol, and the patient recovered without sequelae.

Acute Disease↗
PubMed1975

[Phalloidin antagonists 4th communication: Thioctic acid, SH-compounds, rifampicin, choleretics, dexamethasone, estradiol, unspecific inhibitors, and ineffective compounds (author's transl)].

1. Thioctic acid used clinically in poisoning by A. phalloides, protected perfused livers and also isolated hepatocytes against phalloidin, when given in high concentrations. 2. Some SH-compounds like coenzyme A, dimercaprol, cysteine and cysteamine were found to be protective in different concentrations. 3. Rifampicin protects mice against lethal doses of phalloidin, and inhibits poisoning of isolated hepatocytes at low concentrations. 4. Some choleretic drugs like dehydrocholate, temoebilin (extr. cucumae xanth.), ethacrynic acid influenced phalloidin poisoning by inhibition of binding. 5. Doses of 0.2 to 4.0 mg dexamethasone added to 100 ml of perfusion medium did not protect perfused rat livers against 0.5 mg phalloidin. 6. Pretreatment of female rats with estrogens effected protection against phalloidin in vivo. The same procedure resulted in moderate decrease of phalloidin effects when the livers of pretreated animals were poisoned in vitro. In male rats estrogen pretreatment was less effective. Castration did not augment the protective effect. 7. Secophalloidin, a biologically inactive derivative, did not influence phalloidin poisoning in perfused livers, even when applied in excessive concentrations. 8. Concanavalin A, probably bound in the neighborhood of binding sites for phalloidin, did not protect perfused livers against phalloidin. 9 Diethyldithiocarbamate, a compound protecting livers against carbon tetrachloride and halothane, was ineffective in phalloidin poisoning. 10. Further protective actions of Evans blue, of some phenanthrolines and of EDTA are discussed. 11. Pretreatment of animals with hepatotoxic compounds (CCl4, CHCl3, cinchophen) decreased the toxicity of phalloidin in vivo. Possible mechanisms are discussed.

Animals↗
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↗