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At least 19 recordsLinked to original sources
PubMed1978

Induction of lysosomal storage by suramin.

Isolated livers of rats injected with saline or with suramin (250 mg per kg body weight) 24h previously were perfused with a medium containing radioactively labeled formaldehyde-treated albumin. Suramin-loaded livers released breakdown products at a much lower rate than controls and contained about the double amount of undigested radioactive protein up to about 3 h after the start of the perfusion. These results show that inhibition of proteolysis by suramin as reported previously (Davies et al., 1971; Buys et al., 1973) is not caused by binding of the drug to the substrate in the bloodstream. Electron micrographs of liver sections of suramin-treated rats showed that lysosomes of sinusoidal cells resembled those seen in certain lysosomal storage diseases. The effect of suramin on lysosomal enzymes was studied in vitro. When used at a concentration corresponding to the putative concentration in lysosomes in vivo, the drug inhibited the lysosomal endopeptidases cathepsin Bl and D as well as acid phosphatase. Inhibition of acid phosphatase by suramin in vivo could also be demonstrated by histochemical methods. These results suggest that the observed storage phenomena may be mainly caused by inhibition of lysosomal enzymes.

Albumins↗
PubMed1976

Spectroscopic studies on the complex formation of suramin with bovine and human serum albumin.

The binding of suramin to bovine and human serum albumin was investigated by gel filtration and spectroscopic measurements. Besides some low-affinity binding sites suramin has, on the bovine serum albumin molecule one and on the human serum albumin molecule two, high-affinity binding sites. Spectroscopic measurements reveal that there are large differences between the albumins in the mechanism of binding to the high-affinity binding sites. Further, it is suggested that high concentrations of suramin provoke an unfolding of the albumin moleculse. In order to explain the unusual behaviour of suramin in connection with the displacement of other ligands from the albumin binding the fluorescence probe 1-anilino-8-naphthalenesulfonic acid (ANS) was employed as a reporter group molecule for fluorescence as well as circular dichroism measurements. By these measurements it could be shown that suramin greatly influences the microorganization of both albumin molecules. In the case of these measurements large differences between bovine and human serum albumin were also found.

Anilino Naphthalenesulfonates↗
PubMed1978

Suramin effects on macrophage phagolysosome formation and antimicrobial activity.

The effects of suramin on phagolysosome formation and antimicrobial activity of mouse peritoneal macrophages cultivated in vitro have been studied. Prolonged in vitro pretreatment of macrophages with high concentrations of suramin caused macrophages to form large fragile phagolysosomes in which the concentrations of the various lysosomal enzymes were inferred to be diminished. In addition, suramin-treated macrophages demonstrated enhanced exocytosis of acid phosphatase during phagocytosis of polyvinyl toluene spherules. However, suramin was found not to inhibit formation of phagolysosomes in macrophages that had ingested Listeria monocytogenes when those cells were examined by the electron microscope. Suramin pretreatment did not alter the ingestion or intracellular killing of Staphylococcus aureus or of a strain of L. monocytogenes that was essentially avirulent for mice, but did protect macrophages from destruction by virulent L. monocytogenes ingested in vitro, an effect that appeared to have been mediated through enhancement of the bacteriostatic potential of the macrophages. However, at a single dosage level, the drug did not alter the mortality of mice challenged with virulent L. monocytogenes.

Acid Phosphatase↗
PubMed1976

Effects of suramin on ocular onchocerciasis.

39 patients (Group A) with ocular onchocerciasis in the Sudan-savanna of north Cameroon were given 4-6 g of suramin and followed in detail over 1-2 years. 39 other patients (Group B) received suramin followed 2 weeks later by a 6-7 day course of diethylcarbamazine (DEC). A further 18 patients (Group C) received placebo injections and were followed in the same way by the same observers. Suramin caused serious general reactions among the 100 patients who started the course - 1 case of stomatitis, 1 exfoliative dermatitis, and several cases of severe prostration, among which 2 ended fatally. These reactions underline the urgency for further studies on the toxicity of suramin, which is without doubt an efficient macro- and micro-filaricidal drug. Changes which occurred in the ocular lesions are described in detail. There was an initial aggravation of punctate and sclerosing keratitis, and sometimes a serious aggravation or development of anterior uveitis, corresponding to the peak microfilaricidal effect of the drug. The possibility of a simultaneous adverse effect on the optic disc is discussed. Despite these reactions, which might have been avoided by prior elimination of microfilariae by DEC, the eyes were in general quieter at 3 months and thereafter than before treatment. However, no posterior segment lesion improved after suramin, and the majority remained unchanged. The findings at the end of the trial were as follows: No. of lesions (see article).

Adolescent↗
PubMed1979

Suramin: a potent inhibitor of the reverse transcriptase of RNA tumor viruses.

Suramin--a well-known antitrypanosomal agent--was found to exert a strong inhibitory effect on the RNA-directed DNA polymerase (reverse transcriptase) activity of several oncornaviruses such as Moloney murine leukemia virus, murine Rauscher leukemia viruses, Moloney murine sarcoma virus and avian myeloblastosis virus. Inhibition of enzyme activity was obtained with both endogenous viral RNA and (A)n . oligo(dT) as the template-primer. Suramin effected a 50% inhibition of the reverse transcriptase activity of oncornaviruses at a concentration range of 0.1--1 microgram/ml. In this aspect it compared favorably to ethidium bromide, another trypanocide drug which is considered as one of the most powerful inhibitors of oncornaviral DNA polymerases. The inhibition of reverse transcriptase activity by suramin was competitive with the template-primer, (A)n . oligo(dT), suggesting that the drug may interact with the template-primer binding site of the enzyme.

Avian Myeloblastosis Virus↗
PubMed1979

Suramin enhancement of the chemotherapeutic actions of cyclophosphamide or adriamycin of intramuscularly-implanted Ehrlich carcinoma.

The chemotherapeutic action of cyclophosphamide or adriamycin monotherapy on hyperdiploid Ehrlich carcinoma was compared with that of sequential combinations of suramin and cyclophosphamide and suramin and adriamycin. The chemotherapeutic action of the suramin-cyclophosphamide combination or of the adriamycin-surmin combination was significantly enhanced when the combination partners were applied at definite intervals.

Animals↗
PubMed1976

The populatin dynamics of Onchocerca volvulus microfilariae during treatment with suramin and diethylcarbamazine.

During treatment with suramin the numbers of O. volvulus microfilariae in the blood, urine, sputum, and anterior chambers of the eye fell before those in the skin. When diethylcarbamazine (DEC) was given after suramin, increased numbers of microfilariae appeared in the blood, urine, cerebrospinal fluid (CSF) and sputum, but the increase in the blood was less marked, and of shorter duration, than in similar patients receiving DEC without previous suramin. Microfilariae are thought to enter the urine, sputum and CSF directly from the blood by penetrating the capillary walls in the glomeruli, pulmonary alveoli, and choroid plexuses. Those in the aqueous humour do not appear to come directly from the bloodstream. The total numbers of microfilariae in the skin of some heavily infected onchocerciasis patients are estimated, as are the total numbers moving into the blood-stream under the influence of DEC and the proportion which escape into the urine, sputum and CSF. It is concluded that the majority of the microfilariae which appear in the blood during DEC therapy must be destroyed in the body, probably in the liver.

Anterior Chamber↗
PubMed1978

Membranous neuronal and neuroglial inclusions produced by intracerebral injection of Suramin.

A single intracerebral injection of 5 micrometer of the trypanocidal drug Suramin, into the left hemisphere of young rats, resulted in the formation of membranous inclusion bodies within the perikarya and processes of neurones and neuroglia. These inclusion bodies were round or oval in shape and 0.5-3.0 micrometer in their longest diameter. They were bounded by a single trilaminar membrane and contained closely packed membranes in concentric, curved or parallel arrays. The inclusions were distributed throughout the cerebral cortex and underlying hippocampus at the injection site, and in reduced numbers up to 1 mm anteriorly and posteriorly from it. They formed within 22 hr of the injection and had increased in numbers and in the complexity of their arrays 3 days after injection. Within 14 days, the inclusions were markedly reduced in number. As Suramin is known to inhibit lysosomal hydrolases required for the degradation of proteins, glycolipids and mucopolysaccharides, the membranous inclusions could form as a result of the accumulation of these substances within lysosomes. These experiments indicate a possible experimental model for storage diseases. It is hoped that the extension of this paradigm to other enzyme inhibitors will provide a new means of identifying some of the unusual inclusions that can be found in neurones and neuroglia (Rees 1975).

Animals↗
PubMed1976

The natural history of ocular onchocerciasis over a period of 14--15 years and the effect on this of a single course of suramin therapy.

In 1959 a population of 638 persons over the age of seven years, suffering from heavy endemic onchocerciasis in the Sudan-Savannah of West Africa was examined, and approximately half were allotted to a group for treatment with suramin (up to a total of 4-2 g for healthy adults). In 1973 and 1974 it was possible to re-examine 145 persons allotted to the treatment group and 118 persons allotted to the control group. Measurements were made of the incidence of new "eye lesions", the progress of pre-existing "eye-lesions" and the deterioration in visual acuity. These were greater in men than in women, and increased with age. They were also greater in persons who in 1959 had microfilariae in the anterior chamber, and particularly in those who had already developed "eye lesions". Severe reactions occurred in a significant proportion of patients who received suramin, and one died. However, these was less deterioration in the eyes of persons in the treated than in the control group.

Adolescent↗
PubMed1975

Induction of chain formation in Clostridium sporogenes by suramin.

Cl. sporogenes NCTC 532 was grown in serial doubling dilutions of Suramin from 1% to 0.125% w/v in BHI broth containing 1% glucose. After overnight incubation the culture grew into extremely long chains on transfer into suramin free medium reverted to normal morphology.

Cell Division↗
PubMed1975

[Trial prevention of the embryolethal properties of suramin in the mouse by adjuvant progesterone].

Suramine, a trypanocidal drug, has an embryo-lethal and teratogenic action in Rodents. Like Triton W.R. 1339 suramine modifies the lysosomes of the visceral yolk sac. In the mouse the attempts to correct the embryolethal action by a simultaneous progesterone treatment failed while the hormonal treatment is capable to suppress the embryolethality in Triton W.R. 1339 treated mice.

Abnormalities, Drug-Induced↗
PubMed1975

Phenotypic chain formation in Clostridium welchii by suramin.

Cl. welchii NCTC 6785 was grown in 1% glucose containing medium having 1% Suramin w/v. The cells grew into long chains of thirty units. This effect was not found beyond 0.5% concentration. On transfer into Suramin free medium the chains reverted to normal morphology indicating the change in morphology to be phenotypic.

Clostridium perfringens↗
PubMed1979

Inhibition of lactate dehydrogenase activity from Dirofilaria immitis by suramin.

Lactate dehydrogenase from adult D. immitis was partially purified and characterized. The molecular weight of the enzyme was determined to be 130 000. The specific activity of the lactate dehydrogenase was 4.1 U/mg in the direction of NADH-oxidation and 0.38 U/mg protein in the direction of NAD-reduction. The Michaelis constants were determined to be 0.028 mM and 0.9 mM for NADH and NAD, respectively. Suramin was found to be a potent inhibitor of the lactate dehydrogenase activity. The inhibition constant was calculated to be 0.006 mM. The type of inhibition by suramin was competitive with respect to the cofactors. The Km-values for pyruvate and lactate were determined to be 0.3 mM and 11mM, respectively.

Animals↗
PubMed1976

Suramin stimulates B-lymphocyte proliferation in the mouse.

Suramin, a drug against trypanosomiasis and onchocerciasis, stimulates in vitro mouse B-lymphocytes to transform into blastcells, to incorporate 3H-thymidine and to go into mitosis. Thymus cells (hydro-cortisone-sensitive or resistant) do not respond whereas cells from homozygous nude mice are stimulated. The large majority of the blast-cells have surface immunoglobulins, and the proportion of cells with intracellular immunoglobulin increases during the course of the cultures.

Animals↗