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At least 19 recordsLinked to original sources
PubMed1989

Phototoxicity of tin protoporphyrin, tin mesoporphyrin, and tin diiododeuteroporphyrin under neonatal phototherapy conditions.

Tin metalloporphyrins are being considered as therapeutic agents for neonatal hyperbilirubinemia, and it is possible that concurrent exposure to phototherapy will occur during their use. Euthymic hairless guinea pigs, Crl:IAF(HA)BR, were given daily intraperitoneal injections of tin protoporphyrin (SnPP), tin mesoporphyrin (SnMP), or tin diiododeuteroporphyrin (SnI2DP) for 3 successive days. They were concurrently exposed to ambient light or two different kinds of phototherapy light under conditions similar to that found in neonatal intensive care units. Phototherapy light exposure was for a continuous period of approximately 72 hours following the first injection of metalloporphyrin. The presence or absence of phototoxicity under these conditions was determined by observations for an erythematous response on the back and ears of the guinea pigs. The dosages used were 0.75, 3.75, and 7.5 mg/kg per day of SnPP, 0.075, 0.375, and 0.75 mg/kg per day of SnMP, and 0.9, 4.5, and 9.0 mg/kg per day of SnI2DP. These dosages for each drug were approximately 1 times, 5 times, and 10 times, respectively, the maximum anticipated clinical dosage. At equal multiples of the clinical dosages, SnI2DP was less phototoxic than SnPP, and SnMP was the least phototoxic of the three compounds. SnPP was marginally phototoxic at the lowest dosage. SnMP was phototoxic only at the highest dosage under phototherapy light emitting ultraviolet A irradiation, but when phototherapy light not emitting ultraviolet A irradiation was used, SnMP was not phototoxic. In all cases, the phototoxic response was reversible when the drug and phototherapy treatment were discontinued.

Animals↗
PubMed1991

Tin compounds inhibit the plasma cell response to metallic tin. Transfer of inhibition by parabiosis.

Injection of metallic tin powder causes intense proliferation of plasma cells in draining lymph nodes of Lewis rats. Pretreatment orally with soluble tin salts prevents this response to subsequently injected metallic tin. In the present work, pretreatment with tin salts by parenteral injection was just as effective as addition to the drinking water. This new approach made the following experiments possible. Poorly soluble tin compounds were found to be inhibitory when injected parenterally. Tin salts injected parenterally into one of two rats joined in parabiotic union prevented the plasma cell response to metallic tin in both parabionts. The transfer of the inhibitory effect via the cross-circulating blood represents significant progress toward understanding the mechanisms involved. The evidence suggests the possibility that tin salts elicit an intermediary substance or process that is responsible for inhibition of the plasma cell response to metallic tin.

Animals↗
PubMed1978

[Modified biological behaviour of 99mTc-pertechnetate in man as a result of a preceeding administration of tin (tin effect) (author's transl)].

An increased image of blood-filled spaces (Plexus choriodeus, Sinus transversus) was observed in 99mTc-pertechnetate scintigraphy when it had been preceded by the administration of tin (e.g. of 99mTc-Sn-diphosphonate). We have called this behaviour the "tin effect". In vitro studies demonstrated binding of about 80% of the administered activity in the blood with a biological half-life of about 44 hr and an effective half-life of about 5.3 hr. 95% of the blood activity was bound to red cells and 5% to plasma. This resulted in an increased radiation dose to the bone marrow of about 530 mrad/mCi 99mTc-pertechnetate (following tin). The extent of the tin effect decreased with the length of the interval between tin and 99mTc-pertechnetate administration. Because of the tin effect 99mTc-DTPA or 99mTc-citrate should be used for brain scintigraphy if this has to be performed within the first 5 or 7 days following a bone scintigraphy with a tin-containing radiopharmaceutical. The "tin effect" might be taken advantages of when labelling red cells and imaging vascular spaces.

Brain↗
PubMed1991

[A study on urinary tin in healthy adults: relationship between the concentration of urinary tin and life style].

The concentrations of urinary tin in healthy adults in Aichi prefecture were determined by anodic stripping voltammetry over a period of three years (1986-1988), to obtain the normal tin level in urine and to elucidate the influence of environmental alterations on health conditions in the future. In addition to the above-mentioned method, the relationship to life style, dietary habits, smoking habits and living environment were studied, and the following results were obtained. 1) The mean +/- standard deviation of urinary tin levels for males was 3.7 +/- 2.2 (micrograms/g creatinine), and 5.9 +/- 3.0 (micrograms/g creatinine) for females. The data showed logarithmic normal distributions in both sexes, and the mean concentration for females was significantly higher than that for males (P less than 0.001). The levels of urinary tin concentrations significantly increased according with age. 2) Significant correlations of urinary tin concentrations between two observations were noticed in repeated by observed subjects. 3) As to the dietary habits, fish intake increased the urinary tin concentration, but no definite association with canned-food intake was observed. 4) Smoking habits and living environment also showed a tendency to increase the urinary tin concentration, but the difference was not statistically significant.

Adult↗
PubMed1989

Pharmacokinetics of tin-mesoporphyrin in man and the effects of tin-chelated porphyrins on hyperexcretion of heme pathway precursors in patients with acute inducible porphyria.

Tin-mesoporphyrin shares many of the properties of its parent compound, tin-protoporphyrin. These include competitive inhibition of heme oxygenase, amelioration of jaundice and suppression of chemically induced hepatic porphyria. Tin-mesoporphyrin is cleared from the plasma of normal subjects with dose-dependent pharmacokinetics (T1/2 = 3.8 hr following i.v. administration of 1 mumole per kg body weight), and small amounts (less than 1% of administered dose) are excreted into the urine and feces. Intramuscular administration of tin-mesoporphyrin resulted, within 2 hr, in plasma concentrations identical to those obtained following i.v. administration, but the compound was not absorbed orally. The only dose-limiting side effect was transient cutaneous photosensitivity. High doses (1 mumole per kg body weight) of tin-mesoporphyrin resulted in significant decreases in plasma bilirubin concentrations at 24 and 48 h after treatment of normal subjects. Administration of both tin-protoporphyrin and tin-mesoporphyrin resulted in decreases in the urinary excretion of heme pathway intermediates in stable hyperexcreters with acute hepatic porphyria.

Acute Disease↗
PubMed1979

[Effect of tin on rats. 1. Inverse voltammetric determination of tin in the presence of lead in biological material after extraction].

By means of inverse polarography, the authors determined tin selectively after double extraction with diethylammonium diethyl dithiocarbamate (DADDTC) in perchloric solution. The recovery rates were: in potatoes, 91.7 +/- 5.8%; in beef kidney, 85.0 +/- 22.7%; in beef liver 79.9 +/- 13.8%; and in milk, 69.8 +/- 11.4%. Possible interferences from other elements with the tin determination are discussed.

Animals↗
PubMedDate not supplied

Cytotoxic activity of bis-[di-n-butyl(4-aminosalicylato)tin] oxide, NSC: 628561, bis-[diphenyl(4-aminosalicylato)tin] oxide, NSC: 628562, and some related compounds, against a series of human tumour cell lines.

Bis[di-n-butyl (4-aminosalicylato)tin] oxide [NSC: 628561] (compound 1), bis [diphenyl(4-aminosalicylato)tin] oxide [NSC: 628562] (compound 2), and six other analogous compounds of the type [n-Bu2 (XYZ-C6H2COO)Sn]2O (compounds 3 to 8), were tested in vitro at the National Cancer Institute, Bethesda, Maryland, USA, for cytotoxic activity against a series of human cell lines. Compounds 1, 6 and 8 score globally satisfactorily since four of the five relevant sensitivity or selectivity parameters, DGI50, DTGI or DLC50, DH and MGDH, are statistically significant. Compounds 3 and 7 are less satisfactory because only three such parameters are statistically significant. For compound 2, only two of the parameters are significant.

Antineoplastic Agents↗
PubMed1977

[Clinical and microstructural comparative studies on fillings made from gallium-tin-nickel alloys and from silver-tin amalgam].

The filling material "Gallodent" has been clinically controlled for a period of one year. Scanning electron microscopic examinnations revealed greater surface porosity with negligible microleakage and better marginal adaptation as compared to amalgam. Early corrosion phenomena required re-polishing every three months. This disadvantage and the brittleness of the gallium-tin-nickel alloys hinder, at present, these alloys from superseding high-silver amalgams.

Dental Amalgam↗
PubMed1992

Comparative effects of tin- and zinc-protoporphyrin on steroidogenesis: tin-protoporphyrin is a potent inhibitor of cytochrome P-450-dependent activities in the rat adrenals.

Synthetic metalloporphyins inhibit formation of bilirubin by the heme oxygenase system, an ability that is of considerable experimental and clinical interest for suppression of jaundice in the newborn. The present investigation compares the consequences of treatment with Sn- and Zn-protoporphyrin on hemoprotein-dependent enzymes of the rat adrenals and corticosterone production and defines Sn-protoporphyrin as a potent toxin to adrenal functions. Treatment of rats with Sn-protoporphyrin (two doses of 50 mumols/kg, in 7 d) resulted in a marked reduction of 30-40% in cytochrome P-450-dependent adrenal microsomal 21 alpha-hydroxylase and mitochondrial 11 beta-hydroxylase activities. In the serum, the levels of corticosterone were reduced to about 70% of the control value. In addition, the mitochondrial cytochrome P-450SCC activity was decreased by about 50%. This decrease, however, could not be attributed to a reduced total heme level or an accelerated heme degradatory activity. Disruption by Sn-protoporphyrin of adrenal hemoprotein-dependent functions was not restricted to steroidogenic activities and encompassed drug metabolism activity of the organ; benzo(a)pyrene hydroxylase activity of both the microsomal and the mitochondrial fractions, as well as the microsomal NADPH-cytochrome P-450 reductase activity, were significantly reduced. Zn-protoporphyrin did not cause significant alterations in the above measured parameters although it too was effective in inhibiting the hepatic microsomal heme oxygenase activity. In light of the presently defined adverse effects of Sn-protoporphyrin on adrenal steroidogenesis, we suggest Zn-protoporphyrin is the agent of choice for potential use in treatment of hyperbilirubinemia in humans.

Adrenal Glands↗
PubMed1975

Studies on energy-linked reactions: isolation, characterisation and genetic analysis of trialkyl-tin-resistant mutants of Saccharomyces cerevisiae.

Mutants of Saccharomyces cerevisiae resistant to triethyl tin sulphate have been isolated and are cross-resistant to other trialkyl tin salts. Triethyl-tin-resistant mutants fall into two general phenotypic classes: class 1 and class 2. Class 1 mutants are cross-resistant to a variety of inhibitors and uncoupling agents which affect mitochondrial membranes (oligomycin, ossamycin, valinomycin, antimycin, erythromycin, chloramphenicol, '1799', tetrachlorotrifluoromethyl benzimidazole carbonylcyanide-m-chlorophenylhydrazone and cycloheximide). Class 2 mutants are specifically resistant to trithyl tin and the uncoupling agent "1799' [bis-(hexafluoroacetonyl)-acetone]. Triethyl tin at neutral pH values is a specific inhibitor of mitochondrial energy conservation reactions and prevents growth on oxidisable substrates such as glycerol and ethanol. Triethyl-tin-resistant mutants grow normally on glucose and ethanol in the presence of triethyl tin (10 muM). Biochemical studies indicate that the mutation involves a modification of the triethyl tin binding site on the mitochondrial inner membrane, probably the ATP-synthetase complex. Triethyl tin resistance/sensitivity in yeast is determined by cytoplasmic (mitochondrial) and nuclear genes. The mutants fall into a nuclear and a cytoplasmic (mitochondrial) class corresponding to the phenotypic cross-resistance classes 1 and 2. In the cytoplasmic mutants the triethyl tin resistance segregates mitotically and the resistance determinat is deleted by the action of ethidium bromide during petite induction. Recombination studies indicate that the triethyl tin mutations are not allelic with the other mitochondrial mutations at the loci RI, RIII and OLI. This indicates that the binding or inhibitory sites of oligomycin and triethyl tin are not identical and that the triethyl tin binding site is located on a different mitochondrial gene product to those which are involved in oligomycin binding. Interaction and cooperative effects between different binding sites on the mitochondrial inner membrane have been demonstrated in studies of the effect of the insertion of the TETr phenotype into mitochondrial oligomycin-resistant mutants and provide an experimental basis for complementation studies at the ATP-synthetase level.

Adenosine Triphosphatases↗
PubMed1991

Anti-nutritive effects of dietary tin.

Tin is usually present in foods at levels of less than 4 micrograms/g. Higher levels may be found in some processed foods due to the addition of tin-based preservatives and stabilizers or to corrosion and leaching of the metal from unlacquered cans or from tin foils used in packaging. Estimates of dietary intake range from about 0.2 to greater than 5 mg Sn/day. Diets including a high proportion of canned vegetables and fish could supply greater than 30 mg Sn/day. Although intakes from dietary sources are generally considered to be harmless, a variety of adverse effects of tin have been reported, including effects on serum and bone alkaline phosphatase, lactic dehydrogenase, heme oxygenase, and 5-aminolevulinic acid dehydratase. Perturbations in glutathione metabolism have been reported, as have adverse effects on metabolism of essential trace minerals such as copper, zinc, and iron. Specific effects on calcium content of bone, serum, and kidney have also been described. Reported effects vary with the chemical form, dose of tin, and route and frequency of administration. Effects of tin in animal systems and on essential trace mineral absorption and excretion in human volunteers are reviewed. A summary of recent investigations on dietary tin-copper interactions and effects of tin on rat hepatocellular antioxidant protection are also presented.

Animals↗
PubMed1976

Accumulation of calcium in kidney and decrease of calcium in serum of rats treated with tin chloride.

Effect of tin on the kidney calcium and serum calcium concentration was studied in rats intraperitoneally administered with tin chloride. The calcium concentration in kidney was significantly increased by administration of tin (1.0 mg/100 g), and this increase was dose dependent. A significant increase in the level of kidney calcium was not exhibited by the administration of zinc, manganese, or lead. The increased calcium after the administration of tin predominantly accumulated in the cortex of kidney. The administration of tin did not show a significant alteration of sodium and potassium concentration in the kidney. The level of serum calcium was significantly decreased by the administration of tin (2.0 mg/100 g), and this reduction was dose dependent. The decrease of serum calcium by the administration of tin was associated with the accumulation of calcium in the kidney by treatment with tin.

Animals↗
PubMed1990

The effect of tin on the corrosion behavior of the Ag-Hg phase of dental amalgam and dissolution of mercury.

The anodic polarization behavior of the Ag-Hg matrix phase of dental amalgam (gamma 1) and the rate of mercury dissolution were examined as a function of the tin content. The objectives were to determine the effect of tin on the electrochemical behavior and dissolution of mercury and to provide evidence on whether tin dissolves in the gamma 1 phase or precipitates as a tin-rich phase. Anodic polarization curves were recorded for specimens of the gamma 1 phase containing 0-1.5% Sn and for the gamma 2 phase and a gamma 2-containing dental amalgam, in synthetic saliva. Mercury dissolved in synthetic saliva in 24 h was determined for the gamma 1 phase containing 0-1.0% Sn, with cold-vapor Atomic Absorption Spectrophotometry used for mercury analysis. Tin induced passive behavior of the gamma 1 phase and suppressed mercury dissolution. The passive gamma 1 phase did not exhibit a breakdown of passivity occurring at the gamma 2 phase. The results were consistent with the tin presence in gamma 1 in a solid solution, rather than in tin-rich precipitates, and indicated that at least 1.5% Sn can be dissolved in gamma 1 at 37 degrees C.

Corrosion↗
PubMed1976

Toxicologic studies of tin needles at the intrathoracic site of mice.

Male Marsh mice which received a single intrathoracic injection of 4 mg of tin needles at 3 months of age were compared with controls given isotonic saline. The form and size of most of the tin needles were similar to those of asbestos needles which produced mesotheliomas and lung neoplasms in rodents. Water and food intake was markedly reduced for 24 hrs after the injection of tin. Survival rates (followed for 19 months), pathology of the bladder, liver, and kidney, as well as local and general cancer development were not adversely associated with the tin treatment as compared with the tin treatment as compared with controls. The local reaction to the tin included giant cell phagocytosis, nodular fibroplasia, and capillary formation. The failure of the tin needles to induce local neoplasms may relate to their high density as compared with silicates and/or their lack of the unique potential of the silicate particles to stimulate avascular fibrosis.

Animals↗