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At least 19 recordsLinked to original sources
PubMed2005

Treatment of paediatric visceral leishmaniasis: amphotericin B or pentavalent antimony compounds?

Pentavalent antimony compounds and amphotericin B lipid formulations have been found highly active for the treatment of visceral leishmaniasis. This study focuses on which treatment is preferable in the best interests of the child. Records were reviewed of children in our hospital aged 0-14 years, diagnosed with visceral leishmaniasis, during the last 4 years. Twenty-nine children were identified. Ten were treated with meglumine antimonate (20 mg/kg/day for 21 days) and remained in hospital for 11-28 days (median 19 days), while 19 patients received liposomal amphotericin B at four different dosage schemes and were in hospital for 6-11 days (median 7 days). All of the patients were cured regardless of the treatment regime they followed. No relapses were noted. Liposomal amphotericin B would be preferable to meglumine antimonate if the reduction in hospital stay and hence the convenience of the patient balance the cost of medication. The optimal duration of treatment with liposomal amphotericin B remains to be determined.

Adolescent↗
PubMed2005

Occupational exposure to antimony compounds.

The toxicology of antimony and its compounds is known from three sources: its medicinal use over centuries, studies of process workers in more recent times, and more recent still, studies of its presence in modern city environments and in domestic environments. Gross exposure to antimony compounds over long periods, usually the sulfide (SbS3) or the oxide (Sb2O3) has occurred in antimony miners and in antimony process workers. There have been relatively few of these, and few studies of possible symptoms have been made. Antimony sulfide imported from, at different times, China, South Africa, and South America was processed in the North-East of England from about 1870 to 2003. The process workers in North-East England have been studied at different times, notably by Sir Thomas Oliver in 1933, and by the Newcastle upon Tyne University Department of Occupational Medicine on later occasions. Studies which have been made of the working environment, and in particular of the risk of lung cancer in process workers, have underlined the high levels of exposure to antimony compounds and to other toxic materials. However, the working conditions in antimony processing have improved markedly over the last 30 years, and the workforce had been much reduced in numbers following automation of the process. Prior to the cessation of the industry in the UK it had become a 'white coat' operation with relatively few people exposed to high concentrations of antimony. Antimony, which is normally present in domestic environments, has also been studied as a possible cause of cot death syndrome (SIDS) but extensive investigations have not confirmed this. The full importance of environmental antimony has still to be determined, and evidence of specific effects has not yet been presented.

Air Pollutants, Occupational↗
PubMed1996

Mutagenicity, carcinogenicity and teratogenicity of antimony compounds.

The paper reviews the information available concerning the mutagenic, teratogenic and carcinogenic effects of antimony. A claim that antimony compounds could have mutagenic properties is based on insufficient and not particularly relevant data. Additional experiments, particularly with organic antimony compounds, would be desirable, but from what we know already, one may be confident that antimony is less a mutagenic risk than many other metals such as As, Cr, Ni, among others. Evidence for a carcinogenic risk of antimony in experimental animals was judged by the IARC sufficient for antimony trioxide and limited for antimony trisulfide. In man, IARC considered antimony trioxide as possibly carcinogenic. However, exposure in all studies on which these conclusions are based also involved other proven or likely carcinogenic compounds. Studies with pure antimony compounds, especially those used in therapy, need to be performed to clarify the situation. Although some indications exist that antimony trioxide could interfere with embryonic and fetal development, the studies seem not entirely conclusive. It is regrettable that, at least to our knowledge, the outcome of pregnancy in women treated with antimony compounds for leishmaniasis has not been studied. In conclusion, it appears that mutagenic, carcinogenic and teratogenic risks of antimony compounds, if they exists at all, are not very important.

Animals↗
PubMed2002

Inhibition of DNA-double strand break repair by antimony compounds.

DNA double strand breaks (DSBs), induced by gamma-irradiation in Chinese hamster ovary cells, were used to examine whether antimony compounds affect the repair of DNA damage. The cells were first incubated with antimony trichloride or antimony potassium tartrate (both Sb(III)) for 2 h, and then irradiated with gamma-rays at a dose of 40 Gy. The DNA DSB was quantified with pulsed field gel electrophoresis immediately after irradiation (non-repair group) as well as at 30 min post-irradiation (repair group). The degree of repair inhibition was determined by the differences in the amount of DNA DSB between non-repair and repair groups. Both antimony compounds inhibited repair of DNA DSB in a dose dependent manner. In trichloride, 0.2 mM antimony significantly inhibited the rejoining of DSB, while 0.4 mM was necessary in potassium antimony tartrate. The mean lethal doses, D(0), for the treatment with antimony trichloride and antimony potassium tartrate, were approximately 0.21 and 0.12 mM, respectively. This indicates that the repair inhibition by antimony trichloride occurred in the dose range near D(0), but the antimony potassium tartrate inhibited the repair at doses where most cells lost their proliferating ability. This is the first report to indicate that antimony compounds may inhibit the repair of radiation-induced DNA DSB.

Animals↗
PubMed1998

Lack of inhibition of human plasma cholinesterase and red cell acetylcholinesterase by antimony compounds including stibine.

1. The toxic gas hypothesis proposes exposure to stibine (antimony trihydride) generated from microbial contamination of cot mattress materials as a possible cause of unexplained death in infancy (SIDS) as a consequence of cholinesterase inhibition. We have measured the direct effects of antimony compounds including stibine on the activity of plasma cholinesterase, red blood cell acetylcholinesterase (AChE) and mouse neuronal AChE in vitro. 2. Colorimetric assays for the different esterases with potassium antimonyl tartrate or antimony trichloride at concentrations up to 10(-3) M in the presence of substrate concentrations sufficient to produce 80% of the maximum reaction rate produced no inhibition of enzyme activity. Exposure of enzyme preparations to stibine gas at concentrations sufficient to cause denaturation of red cell haemogloblin caused no measurable inhibition of esterase activity. 3. We conclude that stibine gas or soluble antimony compounds are not capable of inhibiting cholinesterase activity at toxicologically relevant concentrations.

Acetylcholinesterase↗
PubMed1991

Chemotherapy of trypanosomiasis: the potentiation of antimonial compounds by difluoromethylornithine (DFMO).

The currently available anti-leishmanial antimonial drugs, together with other antimony compounds were individually tested, in combination with difluoromethylornithine (DFMO), against experimental murine trypanosomiasis with central nervous system involvement. Satisfactory cure rates could be achieved using a combination treatment of DFMO with most of these anti-leishmanial drugs, but in general, only when they were administered at least twice daily. Of the compounds tested, the most effective was antimony dimercaptosuccinate (Astiban).

Animals↗
PubMed1992

Subacute toxicity of pentavalent antimony compounds in rats.

A subacute toxicity study of pentavalent antimony (Sb) compounds, sodium stibogluconate (SSG) and meglumine antimoniate (MA) was carried out in rats. Three groups of 10 rats each were treated with saline (control group), 300 mg Sb kg-1 d-1 or 900 mg Sb kg-1 d-1 of SSG for 30 d. A parallel study of similar type was conducted for MA. Compared with controls, drug-treated rats showed an impairment of feeding habits and retardation of weight gain (P less than 0.01) during the treatment period. In both SSG- and MA-treated rats there was a dose-related reduction in haemoglobin concentration (P less than 0.001), and hematocrit (P less than 0.001). Red cell count was reduced in SSG-treated rats only. Both drugs, however, significantly raised the white cell count (P less than 0.05). These changes were more pronounced with SSG them with MA. There was no change in MCV, MCH and MCHC. SSG, 900 mg Sb kg-1 d-1, significantly raised AST (P less than 0.005), ALT (P less than 0.01) and alkaline phosphatase activity (P less than 0.01). SSG-treated rats also had raised BUN (P less than 0.01) and creatinine (P less than 0.001), but no significant change in bilirubin levels. MA significantly raised AST (P less than 0.01), ALT (P less than 0.01), BUN (P less than 0.001) and serum creatinine levels (P less than 0.001), but had no appreciable effect on bilirubin and alkaline phosphatase levels. Both SSG and MA decreased blood glucose levels (P less than 0.01) and induced proteinuria.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗
PubMed2005

Differential toxicity of antimonial compounds and their effects on glutathione homeostasis in a human leukaemia monocyte cell line.

Trivalent antimonial compounds (Sb(III)), originally used in the treatment of leishmaniasis, are now being proposed as a novel therapy for acute promyelocytic leukaemia (APL). Here, we examine the effects of Sb(III) and pentavalent antimonial drugs (Sb(V)) on glutathione homeostasis, oxidative stress and apoptosis in the human leukaemia monocyte cell line, THP-1. Although growth of THP-1 macrophages is unaffected by Sb(V), macrophages are extremely sensitive to Sb(III). On exposure to Sb(III), intracellular free glutathione (GSH) levels in macrophages decrease linearly by 50% over 4h, associated with efflux of both GSH and accumulation of intracellular glutathione disulphide (GSSG). Together these effects increase the redox potential of the GSSG/GSH couple from -282 to -225mV. Sb(III)-induced GSH efflux from THP-1 macrophages is accompanied by the concomitant efflux of Sb(III) at a constant molar ratio of 3 (GSH) to 1 (Sb(III)), respectively. Sb(III) directly inhibits glutathione reductase activity in macrophages, significantly retarding the regeneration of GSH from GSSG, following diamide oxidation. Sb(III)-treated THP-1 macrophages go on to exhibit elevated levels of reactive oxygen species and show the early signs of apoptosis. The absence of these effects in Sb(V)-treated THP-1 cells suggests that macrophages do not efficiently reduce Sb(V) to Sb(III). Collectively, these findings suggest that Sb(III) seriously compromises thiol homeostasis in THP-1 macrophages and that this may be an early defining event in the mode of action of antimonials against leukaemia cells.

Antimony Potassium Tartrate↗
PubMed2001

[Direct determination of selenium and bismuth in antimony and antimony compound by hydride generation-atomic fluorescence spectrometry].

The interference of Sb in determination of Se and Bi in antimony powder and antimony compound has been studied in different acidity, it is found that the interference of antimony has been reduced apparently in high acidity. Simultaneously, according to the difference of hydride generation reaction between Sb5+ and Sb3+, a sensitive and rapid method has been developed and used to determine Se and Bi in real samples. The recovery of the method is 95%-105% for practical samples. Detection limits are 0.00004 x 10(-2) (content) for Se and 0.0001 x 10(-2) mg.L-1 (content) for Bi respectively. The relative standard deviations of Se are 2.4% (content = 0.00169 x 10(-2) mg.L-1) and 5.4% (content = 0.00056 x 10(-2) mg.L-1). The relative standard deviations of Bi are 5.0% (content = 0.00024 x 10(-2) mg.L-1) and 1.3% (content = 0.00229 x 10(-2) mg.L-1). The method has been applied to determination of Se and Bi in practical samples with satisfactory results.

Antimony↗
PubMed1997

A comparative controlled trial of intralesionally-administered zinc sulphate, hypertonic sodium chloride and pentavalent antimony compound against acute cutaneous leishmaniasis.

A comparative clinical trial between two newly introduced intralesional treatments for acute leishmaniasis and the established treatment of intralesionally-administered pentavalent antimony compounds was performed. Treatments were allocated randomly to a total of 63 patients who received 2% zinc sulphate, 7% sodium chloride solutions or sodium stibogluconate intralesionally. A number of patients were left without treatment as controls. Patients were followed-up for 45 days, the results showing that the three treatments gave comparable cure rates by the end of the follow-up period. However, zinc sulphate gave a high cure rate (94.8%) usually with a single injection.

Acute Disease↗
PubMedDate not supplied

Clinical healing of antimony-resistant cutaneous or mucocutaneous leishmaniasis following the combined administration of interferon-gamma and pentavalent antimonial compounds.

In an open trial, longer courses of pentavalent antimonials (Sbv) at sub-optimal doses (10 mg/kg body weight), in association with recombinant human interferon-gamma (IFN-gamma) (100 micrograms/m2 of body surface area) were administered, by daily intramuscular injections, to 13 patients with diagnoses of cutaneous or mucocutaneous leishmaniasis unresponsive to Sbv. Four patients presented with large skin ulcers, and 9 had mucosal involvement as the main manifestation, the latter affecting the nose (3 cases), nose and septum (2 cases), nose and oral cavity (1 case), and nose, pharynx and larynx (3 cases). Except for one case with severe involvement of the upper respiratory tract, the lesions were fully resolved by the end of therapy (mean duration 40 +/- 12 [SD] d, range 30-60 d) in the 11 patients who completed therapy. The main side effects were headache and fever (7 cases), together with leucopenia and eosinophilia (4 cases). It is concluded that combined administration of low doses of Sbv plus IFN-gamma may provide a novel therapeutic approach for the treatment of antimony-resistant cutaneous or mucocutaneous leishmaniasis. The possible mechanisms by which IFN-gamma contributes to resolution of the disease are discussed.

Adolescent↗
PubMed2002

Simultaneous determination of selenium and antimony compounds by capillary electrophoresis with indirect fluorescence detection.

Capillary electrophoresis (CE) with indirect fluorescence detection was used to analyze selenium (selenite, selenate, selenomethionine, and selenocystine) and antimony (antimonite and antimonate) compounds. The separation was achieved by CE in 6 min with a 1.2 mM fluorescein solution at pH 9.5. Fluorescein also functioned as a background fluorophore for the indirect detection of these nonfluorescent species. Linearity of more than two orders of magnitude was generally obtained. Precision of migration times and peak areas was less than 1.0% and 7.2%, respectively. The concentration limits of detection (CLODs) was in the microM range. The detection sensitivity was generally dependent upon the transfer ratio (TR, defined as the number of moles of fluorescein ions displaced by one mole of analyte ions) of each species.

Antimony↗