Inactivation of bacteriophage T4 by organic and inorganic tin compounds

Summary Butyltins and inorganic tins inactivated bacteriophage T4. The effect was on the phage and not on its host,Escherichia coli. The order of effectiveness was SnCl₄monobutyltin>dibutyltin>tributyltinSnCl₂. For the butyltins and SnCl₄ this was the reverse of the order of effectiveness usually observed for plants, animals, and microorganisms. This pattern suggests that degradation of tributyltin does not always detoxify it. Monobutyltin (MBT), the most effective organotin, was more effective at pH 4 than at higher pH values and it was more eeffective at low strength. Inactivation proceeded more rapidly at 37°C than at 18°C. The results of experiments in which the ratio of phage to MBT was varied suggests that tin compounds may act by flocculating phage particles. Zinc, which is bound by phage short tail fibers (P12), inhibited phage inactivation by MBT, suggesting that MBT may act upon these tail fibers.     

Effects of organotin and organolead compounds on yeasts

Summary Four methods were used to screen nine organotin and two organolead compounds for toxicity to 29 yeasts, representing 10 genera. Center well diffusion plates were useful in comparing the sensitivity of yeasts to the most toxic organometals but were not useful for comparisons between compounds because of differences in diffusion rates and lack of sensitivity. Two-layer diffusion plates (density gradient plates) were also of limited use for comparisons between compounds but provided quantitative information on toxicity and allowed comparisons between organisms. Two-dimensional diffusion plates were useful for estimating the effect of pH on organometal toxicity. Release of K⁺ from cell suspensions measured using a K⁺-electrode provided quantitative information and allowed comparisons between compounds and organisms. The presence of 3% NaCl in cell suspensions decreased the rates and extent of organotin-induced K⁺ release. Yeasts varied in their sensitivity from strain to strain, but tributyltin was the most toxic compound tested. Mono- and dimethyltins were the least toxic. Triphenyltin, dibutyltin, monobutyltin, trimethyltin, triethyltin, diethyllead, diethyltin, and dimethylleads showed intermediate toxicity, but triphenyltin and monobutyltin were the most toxic among the group.     

Microbial transformations of tin and tin compounds

Summary The use of organotins for agricultural and industrial purposes and in the marine environment has been increasing steadily for more than 20 years. Recently, reliable methodologies have been developed to permit quantification of individual molecular species of organotins in cultures and in the environment. Particular attention has been given to methyltins which can be formed abiotically and by microorganisms, and to tributyltins which are toxic components of effective antifouling paints. In the aquatic environment tin, tributyltins and other organotins accumulate in the surface microlayer, in sediments, and on suspended particulates. Tin compounds are toxic to a variety of organisms and some aquatic organisms can bioaccumulate them. When tin compounds, particularly di-or tri-substituted tins, enter an ecosystem, a portion of the microbial population is killed. Among the survivors are organisms which can methylate inorganic or organic tins, but the relative contribution of biotic and abiotic mechanisms is not clear. While many details of methylations and demethylations need to be worked out, it is clear that transformations of tins can influence the toxicity, volatility and mobility of tin in natural ecosystems. Tributyltins can be debutylated by microorganisms, and hydroxybutyl tins may be intermediates, as they are in mammalian systems. Little is known of the potential and probable microbial transformations of other economically important organotins, but the transformations should be studied for they may have industrial and environmental importance.     

Resistance to arsenic compounds in microorganisms

Abstract: Arsenic ions, frequently present as environmental pollutants, are very toxic for most microorganisms. Some microbial strains possess genetic determinants that confer resistance. In bacteria, these determinants are often found on plasmids, which has facilitated their study at the molecular level. Bacterial plasmids conferring arsenic resistance encode specific efflux pumps able to extrude arsenic from the cell cytoplasm thus lowering the intracellular concentration of the toxic ions. In Gram-negative bacteria, the efflux pump consists of a two-component ATPase complex. ArsA is the ATPase subunit and is associated with an integral membrane subunit, ArsB. Arsenate is enzymatically reduced to arsenite (the substrate of ArsB and the activator of ArsA) by the small cytoplasmic ArsC polypeptide. In Gram-positive bacteria, comparable arsB and arsC genes (and proteins) are found, but arsA is missing. In addition to the wide spread plasmid arsenic resistance determinant, a few bacteria confer resistance to arsenite with a separate determinant for enzymatic oxidation of more-toxic arsenite to less-toxic arsenate. In contrast to the detailed information on the mechanisms of arsenic resistance in bacteria, little work has been reported on this subject in algae and fungi.     

The influence of tin compounds on the dynamic properties of liposome membranes: A study using the ESR method

The influence of organic and inorganic compounds of tin on the dynamic properties of liposome membranes obtained in the process of dipalmitoylphosphatidylcholine (DPPC) sonication in distilled water was investigated. This was carried out by means of the spin ESR probe method. The probes were selected in such a way as to penetrate different areas of the membrane (a TEMPO probe, 5-DOXYL stearic acid, 16-DOXYL stearic acid). Four compounds of tin were chosen: three organic ones, (CH₃)₄Sn, (C₂H₅)₄Sn and (C₃H₇)₃SnCl, and one inorganic one, SnCl₂. The investigated compounds were added to a liposome dispersion, which was prepared prior to that. The concentration of the admixture was changed within the values from 0 to 10%-mole in proportion to DPPC. The studies indicated that the chlorides of tin display the highest activity in their interaction with liposome membranes. Since these compounds have ionic form in a water solution, the obtained result can mean that this form of admixture has a considerable influence on its activity. Furthermore, it was found that there is a slightly stronger influence of tin compounds with a longer hydrocarbon chain on changes in the probes’ spectroscopic parameters.     

Toxic effects of dichloromethane on the growth of methanotrophic bacteria

Abstract The effect of a range of dichloromethane (DCM) concentrations on the growth of five obligate methanotrophic bacteria of the genera Methylomonas, “Methylosinus” , and Methylocystis was assessed. DCM concentrations of 78 mM were bactericidal for all strains. Concentrations of 7.8 mM–156 μM were bacteriostatic for Methylocystis parvus ACM 3309 and Methylomonas aurantiaca HB2, and partially inhibitory for Methylomonas methanica strains ACM 3307 and HB1. “Methylosinus trichosporium” ACM 3311 grew in the presence of up to 780 μm DCM, but a concentration of 7.8 mM was bacteriostatic.     

Toxic effects of chromium and its compounds

Chromium was discovered in 1797 by Vauquelin. Numerous industrial applications raised chromium to a very important economic element. At the same time, with the development of its uses, the adverse effects of chromium compounds in human health were being defined. Trivalent chromium is an essential trace element in humans and in animals. Chromium as pure metal has no adverse effect. Little toxic effect is attributed to trivalent chromium when present in very large quantities. Both acute and chronic toxicity of chromium are mainly caused by hexavalent compounds. The most important toxic effects, after contact, inhalation, or ingestion of hexavalent chromium compounds are the following: dermatitis, allergic and eczematous skin reactions, skin and mucous membrane ulcerations, perforation of the nasal septum, allergic asthmatic reactions, bronchial carcinomas, gastro-enteritis, hepatocellular deficiency, and renal oligo anuric deficiency. Prevention of occupational risks, biological monitoring of workers, and treatment of poisoning are also reported.     

Synthesis and reactivity of tin amide complexes

A terminal tin amide and a terminal tin anilide complex, (BDI)SnN(iPr₂) and (BDI)SnN(H)Ar (Ar = 2,6-ⁱPr₂C₆H₃), respectively, have been synthesized utilizing the bulky β-diketiminate ligand, [{N(2,6-ⁱPr₂C₆H₃)C(Me)}₂CH]⁻, or BDI, to stabilize the low coordinate divalent tin metal center. Only (BDI)SnN(iPr₂) reacts with phenylacetylene to yield (BDI)SnCCPh, but both species react with methyl triflate to give (BDI)SnOTf and carbon dioxide, resulting in the formation of (BDI)SnOC(O)N(iPr₂) and (BDI)SnOC(O)N(H)Ar.     

Toxicity of organotins towards cyanobacterial photosynthesis and nitrogen fixation

Abstract Inhibition of photosynthesis by a range of organotin compounds in Plectonema boryanum was concentration-dependent and decreased in the order tributyltin (Bu₃SnCl) > tripropyltin (Pr₃SnCl) ≥ dibutyltin (Bu₂SnCl₂) ≥ triphenyltin (Ph₃SnCl) > triethyltin (Et₃SnCl) > trimethyltin (Me₃SnCl) > monobutyltin (BuSnCl₃). IC₅₀ values were determined for the most toxic organotin species and varied from approximately 1.2 μM for Bu₃SnCl to approximately 13 μM for Ph₃SnCl. A similar order of inhibition of photosynthesis was observed in Anabaena cylindrica , although here IC₅₀ values were slightly lower (e.g. approximately 1 μM for Bu₃SnCl and 5 μM for Ph₃SnCl).Nitrogenase activity was generally more sensitive to inhibition by organotin compounds than photosynthesis in A. cylindrica and this was particularlyy evident for Bu₂SnCl₂; approximate IC₅₀ values for Bu₂SnCl₂ were 3 and 9 μM, as estimated by nitrogenase activity and photosynthesis, respectively. These results indicate that organotin compounds have the potential to inhibit cyanobacterial metabolism in aquatic systems.     

Toxic effects of catecholamines on skin

The purpose of this study was to examine the effects of catecholamines on skin necrosis independent of their vasoactive effects. Rat abdominal or human breast skin was excised, pinned flat, and incubated at 37 degrees C for 6 hours in a buffered salt solution containing catecholamine. At 0.1 and 6 hours the lactate dehydrogenase (LDH) released from the skin and appearing in the buffer was determined spectrophotometrically. All groups showed similar LDH levels at 0.1 hour. Rat skin treated with greater than or equal to 10(-7) M epinephrine (33 times less than the 1:200,000 used clinically) or greater than or equal to 10(-5) M norepinephrine showed a significant increase in the LDH released at 6 hours versus controls (18.75 +/- 1.25 versus 13.75 +/- 1.25 and 29.25 +/- 2.96 versus 22.00 +/- 1.96 IV, respectively). Total tissue LDH levels were not significantly different at 0.1 or 6 hours. The toxic effect of epinephrine was eliminated by the addition of propranolol or selective beta 2 blockade, but not by alpha or beta 1 blockade. Therefore, this effect appears to be mediated largely by beta 2 receptors. Similar toxic effects were seen in human breast skin treated with 1:200,000 epinephrine and were blocked with propranolol. Phenylephrine at 1:20,000 demonstrated toxicity, but angiotensin II and vasopressin did not. These studies indicate that addition of catecholamine to ischemic rat or human skin accelerates skin death within 6 hours, but that the toxicity can be reversed with beta blockade.     

Synthesis of one dimensional tin selenides in supercritical amines

Three new crystalline tin selenide salts have been prepared from the reactions of [PPh₄]₂[Sn(Se₄₃] in supercritical solvents. The starting material pyrolyzes in supercritical acetonitrile to form [PPh₄]₄[Sn₆Se₂₁] (I), and it also reacts with SnSe in supercritical ammonia leading to a mixture of [PPh₄]₄[Sn₃Se₁₁]₂ (II). and [PPh₄]₂[Sn(Se₄)(Se₆)₂] (III). All three compounds have been characterized by single crystal X-ray diffraction. Crystallographic data: for I, C₉₆H₉₀P₄Se₂₁Sn₆, space group triclinic, P-1, A = 18.763(3), B = 24.600(4), C = 13.137(1) Å, = 102.63(1), β = 93.66(1), γ = 108.72(1)°, V = 5544(1) ų, Z = 2, R = 0.0350, R_W = 0.0317: for II, C₉₆H₈₀P₄Se₂₂Sn₆, space group monoclinic P2₁/c, A = 31.500(4), B = 16.572(3), C = 22.352(3) Å, β = 103.53(1)°, V = 11344(3) ų, Z = 4, R = 0.0771, R_W = 0.0664: for III, C₄₈H₄₀P₂Se₁₆Sn, space group monoclinic, C2/c, A = 25.381(2), B = 13.934(4), C = 19.465(3) Å, β = 121.587(8)°, V = 5867(2) ų, Z = 4, R = 0.0807, R_W = 0.0650. One of the compounds, [PPh₄]₂[Sn(Se₄(Se₆₂], is a molecular cluster while the other two complexes [PPh₄]₄[Sn₃Se₁₁]₂ and [PPh₄]₄[Sn₆Se₂₁], are one dimensional tin selenide chains. The structures of the two chains are related and consits of tetrahedral and distorted trigonal bipyramidal tin(IV) centers bridged by Se²⁻, Se₂²⁻ and Se₃²⁻ chains.     

Degradation of arylarsenic compounds by microorganisms

Microorganisms were not directly accumulated when soil contaminated to about 0.5 mM with diphenylarsinic acid (DPAA) was used as the sole source of carbon. However, using toluene as the carbon source yielded several isolates, which were then used in cultivation with DPAA as the sole source of carbon. By these methods, Kytococcus sedentarius strain NK0508, which can grow in up to 0.038 mM DPAA, was isolated. The toxicity of DPAA retarded the growth of K. sedentarius and the direct accumulation of DPAA-utilizing microorganisms from environmental samples. This strain can utilize about 80% of DPAA and phenylarsonic acid as the sole source of carbon for 3 days. Degradation products of DPAA were determined to be cis, cis, muconate and arsenic acid. When K. sedentarius was cultivated with methylphenylarsinic acid and diphenylmethylarsine, about 90% and 10% degradation of the two compounds, respectively, were observed. Diphenylmethylarsine oxide, possibly synthesized by methylation of DPAA, was detected as one of the transformation products. These results suggest that degradation is initiated by splitting of the phenyl groups from the arylarsenic compounds with subsequent hydroxylation of the phenyl groups and ring opening to yield cis, cis, muconate.     

Degradation of dioxin-like compounds by microorganisms

Polychlorinated dibenzo-p-dioxins (PCDD) and polychlorinated dibenzofurans (PCDF; PCDD/F, dioxins) have not been commercially produced in bulk amounts, as were polychlorinated biphenyls and other haloaromatic organics. Within the past two decades a lot␣of information has accumulated on the biodegradation of PCDD/F and other dioxin-like compounds because of their toxicity and because of significant environmental concern about many congeners of this class of chemicals. PCDD/F are subjected to reductive dehalogenations leading to less halogenated congeners, which can be attacked efficiently by fungal and bacterial oxidases and dioxygenases. In several cases these compounds can be utilized as carbon and energy sources. Pathways for their enzymatic degradation and the organisation of the corresponding degradative genes have been elucidated. Consequently, biotechnological applications will exploit the degradative potential of such microorganisms for bioremediation of contaminated sites. Received: 29 August 1997 / Received revision: 6 January 1998 / Accepted: 8 January 1998     

Toxic Concentrations of Exogenously Supplied Methylglyoxal in Hybridoma Cell Culture

Concentrations at which methylglyoxal, a by-product of cellular metabolism, can be toxic to hybridoma cell cultures were determined using exogenously supplied doses. Trypan blue cell counts of 6-well cultures incubated for 24 h with various methylglyoxal concentrations revealed inhibition of cell growth at 300 μM and higher, with a median inhibitory concentration of 490±20 μM. The primary mode of death was apoptosis, as assessed by chromatin condensation, and the effects of methylglyoxal were observed to be complete by approximately eight hours. Yet, the impact of methylglyoxal was a function of the rate of dosing; stepwise addition of MG during the first 6 h of incubation inhibited growth but caused much less cell death than a comparable bolus dose. Inhibition of cellular metabolism by MG was found to coincide with inhibition of cell growth, with a comparable median inhibitory concentration of 360±20 μM. The effects on viable cell density and metabolism were both linear at doses approaching zero, with lowest observable effect levels of 54 and 77 μM, respectively. These results provide quantitative estimates for concentrations of methylglyoxal that may be inhibitory to biopharmaceutical-producing cell lines.     

Malnutrition interferes with the unique lymphadenopathy induced in lewis rats by metallic tin

Metallic tin powder injected into Lewis rats caused marked enlargement of draining lymph nodes with prominent hyperplasia of plasma cells. A low level of dietary protein (8%) or deficiency of choline interfered with the cellular proliferation and reduced the size of the nodes by nearly onethird compared to a normal protein diet (20%). A high level of protein in the diet (50%) did not augment the effect of metallic tin powder beyond that achieved by a level usually considered adequate (20%).     

Toxic effects of resazurin on cell cultures

Resazurin, introduced as a cell viability indicator under the trade name alamarBlue^®, is generally regarded as nontoxic when used according to manufacturer’s suggested shorter-term incubation time specifications. However, problems arise when exposure times are extended to longer-term cultures on the order of days. To assess the effect of resazurin over longer incubation times, MCF7 (HTB-22), MCF10A (CRL-10317), 3T3-L1 (CL-173), and D1 (CRL-12424) cultures were tested with varying amounts of resazurin over 4- and 8-day periods. MCF7, 3T3-L1, and D1 cells cultured for 8 days with 20 % alamarBlue^® had significantly less cell survivability. Specifically, levels of metabolic activity, deoxyribonucleic acid (DNA) concentration, and glucose consumption of the cell lines cultured for 8 days in medium with 20 % alamarBlue^® were significantly lower (p < 0.05) than metabolic activity, DNA concentration, and glucose consumption of MCF7 cells cultured for 8 days in medium with no alamarBlue^®. MCF7, 3T3-L1, and D1 cells used less glucose at concentrations as low as 5 %. Data also suggests the toxic effects are more pronounced in the cancerous cell line as compared to the noncancerous cells.