Tri-n-butyltin Chloride Research Articles

Sonochemical synthesis of bis(tri-n-butylstannyl) aromatic compounds via Barbier-like reactions

This paper reports a study of the synthesis of aryltri-n-butylstannanes via a sonochemical Barbier reaction of aryl- and heteroaryl bromides with bis(tri-n-butyltin) oxide (2) in THF. Our results demonstrate that, despite previous reports on contrary, the aryltributylstannanes can also be obtained under the same reaction conditions via sonicated reactions between aryl monobromides and tri-nbutyltin chloride (2). A comparative study of the reactions of electrophiles 2 and 3 with bromobenzene, 2-bromopyridin, o- and m-bromoanisole, m-bromotoluene, 9-bromophenthrene, and 9-bromoanthracene, indicates that the corresponding aryl- and heteroaryl-tri-n-butylstannyl derivatives are obtained in about the same yields. Best reaction conditions and the results obtained in the investigation of the sonicated reactions between several aromatic and heteroaromatic dibromides are also reported. It was found that the reactions using 1,2-, 1,3-, and 1,4-dibromobenzenes, 4,4′-dibromobiphenyl, 1,4-dibromonaphthalene, 2,5- and 3,5-dibromopyridines, and 2,5-dibromothiophene lead to the corresponding bis(tri-n-butylstannylated) derivatives in many cases in very high yields. Also the excellent results obtained in the sonicated reactions of 1,3,5-tribromobenzene with 2 and 3 are reported.

TBTCl (tri-n-butyltin chloride)과 bisphenol A에 의한 단기노출이 등줄쥐의 번식에 미치는 영향

To investigate the effects of short-term treatment with tri-n-butyltin chloride (TBTCl) and bisphenol A (BPA) on the reproduction of striped field mice, the mice were intramuscularly injected with TBTCl or BPA immediately before the reproductive season and examined in the reproductive season after keeping them for 4 months. As a result, there were no differences between the control and the compound-treated groups regarding body weight in both sexes, the residual levels of the compounds in the adult males, and the gonadosomatic index (GSI) and the histological structures with LM and EM of the testes and epididymides in both the adult and young males. The infant mortality and abortion rate, however, were high in the TBTCl-treated groups and BPA-treated groups respectively, compared to the control group. Conclusively, it was suggested that short-term treatment with TBTCl or BPA in mice in the non-reproductive season might have inhibited the development of the uterine embryos or fetuses, although it did not induce accumulations of these compounds or affect the reproductive organs of adult and young (F1) males.

Participation of the inositol phospholipid signaling pathway in the increase in cytosolic calcium induced by tributyltin chloride intoxication of chlorophyllous protozoa Euglena gracilis Z and its achlorophyllous mutant SM-ZK

Exposure of tri- n-butyl tin chloride (TBTCl) as a stressor to Euglena gracilis Z causes rapid alteration of cell morphology followed by deflagellation. The present study was undertaken to reveal the mechanism of the cell response at a molecular level. Chlamydomonas reinhardtii, in this study E. gracilis Z and its achlorophyllous mutant SM-ZK, gave similar results when subject to the same stressor. Indeed, similar results were obtained with both strains. Next, assuming that the morphological alteration caused by TBTCl is mediated by the inositide phosphate-lipid signaling pathway, the effects of signal transduction and Ca 2+ release reagents (mastoparan as a G-protein activator, neomycin as a phospholipase C inhibitor, verapamil as a Ca 2+ channel blocker, and A23187 as a Ca 2+ ionophore) on morphology and intracellular Ca 2+ levels were examined with or without TBTCl. The data strongly suggest that the morphological alteration is mediated by an increase in Ca 2+ linked to the inositol phosphatide pathway. The cellular response to signal transduction inducing reagents was compared between the E. gracilis chlorophyllous Z strain and its achlorophyllous mutant SM-ZK strain. Significant differences were observed between the Z and SM-ZK strains in terms of the stress response and intracellular Ca 2+ level.

Identification by DNA Macroarray of nur77 as a Gene Induced by Di-n-butyltin Dichloride: Its Role in Organotin-Induced Apoptosis

The thymotoxic organotin compounds di-n-butyltin dichloride (DBTC) and tri-n-butyltin chloride (TBTC) are known to induce apoptosis in vitro in rat thymocytes. They also affect macromolecular synthesis, inhibiting DNA synthesis and increasing RNA synthesis. Since these RNA molecules, likely to be involved in the initiation of the apoptotic process, have not been identified yet, the purpose of this research was to characterize by a cDNA macroarray the expression of genes involved in DBTC-induced apoptosis. We found that nur77 was rapidly transcripted in vitro following exposure of freshly isolated rat thymocytes to 3 μM DBTC. nur77 induction has also been observed in vivo after treatment of rats with apoptotic doses (60 mg/kg body wt) of DBTC. The products of nur77 are known to be involved in the apoptotic process, as nur77 is a transcription factor expressed in response to T-cell receptor-mediated apoptosis in immature T cells. Antisense oligonucleotide inhibition of nur77 expression prevented apoptosis induced by DBTC, supporting a role for nur77 in organotin-induced apoptotic cell death.

Organotin-induced apoptosis occurs in small CD4 +CD8 + thymocytes and is accompanied by an increase in RNA synthesis

The organotin compounds di- n-butyltin dichloride (DBTC) and tri- n-butyltin chloride (TBTC) induce thymus atrophy in rats. At low doses they inhibit immature thymocyte proliferation, whereas at higher doses in particular TBTC induces apoptotic cell death. In vitro, a similar concentration–effect relationship was observed, i.e. low concentrations inhibit DNA and protein synthesis and higher concentrations induce apoptosis. The mechanism of apoptosis by organotins has been partly investigated, but their capacity to inhibit protein synthesis seems to contradict with the idea that macromolecular synthesis is required for organotin-induced apoptosis. Therefore, we aimed to evaluate the relation between apoptosis and the synthesis of RNA and proteins, with a focus on the apoptosis-sensitive thymocyte subset. Results showed that DBTC increases RNA synthesis in particular in the subset of small CD4 +CD8 + thymocytes, which normally shows a high incidence of DNA fragmentation. Moreover, the RNA synthesis inhibitor actinomycin D or the protein synthesis inhibitor cycloheximide protected cells from apoptosis by DBTC or TBTC. Although organotin compounds increase synthesis of the heat shock protein HSC73/HSP72, heat shock treatment did not initiate apoptosis in thymocytes, neither antagonized organotin-induced apoptosis. This indicates that synthesis of heat shock proteins is not related to organotin-induced increase of RNA synthesis, and that other RNA-molecules are probably involved.

Sediment-associated tri- n-butyltin chloride and its effects on osmoregulation of freshwater-adapted 0-group European flounder, Platichthys flesus (L.)

The disruption of osmoregulatory processes was examined in European flounders exposed to environmental concentrations (150 ng TBTCl g −1 dry weight sediment) of sediment-associated tri- n-butyltin chloride (TBTCl), by using radiotracers to measure changes in hydromineral fluxes and water balance. The water permeabilities of TBTCl-exposed fish varied during the course of the experiment and were significantly lower than those of the corresponding controls that did not change significantly with time. It was found that the maximum decrease in water permeability of TBTCl-exposed fish occurred after 14 days; thereafter there was an increase towards control values. However, there was a differential reduction of the diffusional ( P d) and osmotic ( P os) permeability coefficients, where the former decreased more rapidly than the latter, reflecting the reduction of diffusional membrane permeability and the increasing importance of osmotic permeability. In fish exposed to TBTCl sodium efflux and drinking rates were significantly increased but Na +/K +-ATPase activities and urine production rates were not affected. The effects of TBTCl exposure are also manifested at the level of the whole organism by a reduction in the increase of the body length of exposed fish, when compared to controls. It was concluded that tributyltin- n-chloride in sediments is capable of significantly disrupting the osmoregulatory functions of a benthic estuarine fish, at concentrations found in the sediments of Southampton Water and the River Itchen.

Tri- n-butyltin delays the cell death induced by hydrogen peroxide in rat thymocytes

Tri- n-butyltin (TBT), one of environmental pollutants accumulated in mollusks, at nanomolar concentrations decreases cellular content of glutathione (GSH), suggesting that TBT increases cell vulnerability to oxidative stress because GSH has a role in catabolizing hydrogen peroxide (H 2O 2). In order to examine this possibility, the effect of tri- n-butyltin chloride (TBTCl) on rat thymocytes suffering from oxidative stress induced by H 2O 2 was examined using a flow cytometer with four fluorescent probes; ethidium bromide, 2′,7′-dichlorofluorescin diacetate, 5-chloromethylfluorescein diacetate and annexin-V-FITC. TBTCl at concentrations ranging from 100 nM to 1 μM attenuated H 2O 2-induced decrease in cell viability in a dose-dependent manner. It was unlikely that TBTCl reduced H 2O 2-induced oxidative stress because TBTCl failed to affect H 2O 2-induced oxidation of intracellular molecule (2′,7′-dichlorofluorescin) and H 2O 2-induced decrease in cellular content of GSH. Results suggest that TBTCl may inhibit the pathway of cell death induced by H 2O 2 or that TBTCl may induce a protective substance against the oxidative stress produced by H 2O 2.

Environmental levels of sediment-associated tri- n -butyltin chloride (TBTCl) and ionic regulation in flounders during seawater adaptation

The effects of exposure to sediment-associated tri-n-butyltin chloride (TBTCl) were examined in the euryhaline European flounder, Platichthys flesus (L.). The effects were quantified by measuring the changes in sodium efflux; Na+/K+-ATPase activity; and the numbers, areas, and distribution of chloride cells in the gills of freshwater-adapted fish, following a rapid transfer to seawater. Following the transfer to seawater, the Na+/K+-ATPase activity and the sodium efflux were significantly increased in the control group but remained unchanged in the TBTCl-exposed group. The normal morphological changes to the gill epithelium associated with seawater adaptation, which involve chloride cell distribution, took place in the control group but were significantly inhibited or delayed in the TBTCl group. The results presented in this study lead to the conclusion that environmental concentrations of tri-n-butyltin chloride in sediments are capable of significantly disrupting both the physiological and the morphological components of iono-regulatory functions of an estuarine flatfish.

Organotin and osmoregulation: quantifying the effects of environmental concentrations of sediment-associated TBT and TPhT on the freshwater-adapted European flounder, Platichthys flesus (L.).

Chronic (5 weeks) exposure of freshwater-adapted European flounder, Platichthys flesus (L.), to environmental concentrations of sediment-associated tri-n-butyltin chloride (TBTCl) and triphenyltin chloride (TPhTCl) caused significant changes to hydromineral fluxes and membrane permeability, mechanisms that maintain osmotic homeostasis. The half-time of exchange of tritiated water (THO) in TBTCl- and TPhTCl-exposed fish was significantly increased during the first 2 weeks of the experiment and then decreased steadily, eventually reaching the level that the control group had constantly maintained throughout the experiment. This change in apparent water permeability was accompanied by a significant decrease in diffusional water flux across the membranes. Passive Na(+)-efflux across the gills was increased significantly but effluxes in the control group were near constant over the same time span. Drinking rates in the organotin groups increased significantly while the rate of urine production did not change. This lead to an increased net water balance in the organotin groups and consequently to a significant reduction of the blood osmolality of both organotin groups when compared to a control. There would appear to be a metabolic cost attached to the changes produced by exposure to environmental levels of organotin compounds which are manifested as a minimal increase in body length compared to the controls.

Effects of endocrine disrupting chemicals on the microtubule network in Chinese hamster V79 cells in culture and in Sertoli cells in rats

The effects of ten endocrine disrupting chemicals, i.e., bisphenol A (BPA), p-nonylphenol (NP), p-octylphenol (OP), p-pentylphenol (PP), butyl benzyl phthalate (BBP), dicyclohexyl phthalate (DCHP), di-n-butyl phthalate (DBP), tetrabutyltin (TBT), tri-n-butyltin chloride (TBC), and di-n-butyltin dichloride (DBD), as well as 17 beta-estradiol (E(2)) as a positive control on the microtubule network in Chinese hamster V79 cells in culture were examined by the indirect immunofluorescence method using anti-beta-tubulin antibody. In the whole-animal system, the effects of BPA, NP, OP, BBP, DBD, and E(2) as well as vinblastine sulfate (VB) as a positive control on microtubules in the cytoplasm of Sertoli cells in rats were examined by electron microscopy. In Chinese hamster V79 cells, TBC and DBD showed higher microtubule-disruptive activity than E(2), while other chemicals had less activity than E(2). The ranking for efficiency on microtubule disruption was (TBC falling dots DBD) > (E(2) = TBT) > (BPA = alkylphenols, NP and OP) >> (phthalate esters, BBP, DHP, and DBP). In rats as a whole-animal system, no disrupting effects on the microtubule network in the cytoplasm of Sertoli cells were observed under any environmental chemicals tested, whereas exposure to VB resulted in marked disruption of the microtubule network. The results of this study suggested that some endocrine disrupting chemicals have disrupting effects on the microtubule network in vitro, but no such effects in vivo.

Organotins Induce Apoptosis by Disturbance of [Ca2+]i and Mitochondrial Activity, Causing Oxidative Stress and Activation of Caspases in Rat Thymocytes

Di-n-butyltin dichloride (DBTC) and tri-n-butyltin chloride (TBTC) cause thymus atrophy in rodents. At low doses, antiproliferative modes of action have been shown to be involved, whereas at higher doses apoptosis seems to be the mechanism of thymotoxicity by these chemicals. In vitro, a similar concentration-dependency has been observed. The purpose of the present research was to investigate the mechanisms underlying DNA fragmentation induced by these organotin compounds in freshly isolated rat thymocytes. As previously shown for TBTC, DBTC is also able to significantly increase intracellular Ca2+ level ([Ca2+]i). The rise in [Ca2+]i, already evident 5 min after treatment, was followed by a dose- and time-dependent generation of reactive oxygen species (ROS) at the mitochondrial level. Simultaneously, organotins induced the release of cytochrome c from the mitochondrial membrane into the cytosol. ROS production and the release of cytochrome c were reduced by BAPTA, an intracellular Ca2+ chelator, or rotenone, an inhibitor of the electron entry from complex I to ubiquinone, indicating the important role of Ca2+ and mitochondria during these early intracellular events. Furthermore, we demonstrated that rotenone prevents apoptosis induced by 3 μM DBTC or TBTC and, in addition, that both BAPTA and Z-DEVD FMK (mainly a caspase-3 inhibitor) decreased apoptosis by DBTC (already shown for TBTC). Taken together these data show the apoptotic pathway followed by organotin compounds starts with an increase of [Ca2+]i, then continues with release of ROS and cytochrome c from mitochondria, activation of caspases, and finally results in DNA fragmentation.

Some sulfur-containing metabolites of tri-n-butyltin chloride in male rats.

In an attempt to elucidate metabolic destination of TBTO, sulfur-containing metabolites were investigated in the urine. Tri-n-butyltin chloride (TBTC), tri-n-butyltin oxide (TBTO), and their in vitro metabolites in rat liver microsomal enzyme systems, di-n-butyl(3-hydroxybutyl)tin chloride (T3OH), di-n-butyl(3-oxobutyl)tin chloride (T3CO), dibutyltin dichloride (DBTC), and monobutyltin trichloride (MBTC), were intraperitoneally administered to rats. In particular, administration of T3OH and T3CO gave higher amounts of mercapturic acid derivatives, such as N-acetyl-S-(3-oxobutyl)-L-cysteine (3CO-MA) and N-acetyl-S-(3-hydroxybutyl)-L-cysteine (3OH-MA), than TBTC or TBTO. On the other hand, DBTC and MBTC did not yield measurable amounts of 3CO-MA and/or 3OH-MA. The appearance of organotin metabolites in urine indicates that T3OH, T3CO, and hypothesized secondary metabolites, such as n-butyl(3-hydroxybutyl)(3-oxobutyl)tin chloride, n-butyl(3-hydroxybutyl)(4-hydroxybutyl)tin chloride, etc., are subject to the action of glutathione S-transferase to give mercapturic acid derivatives. These sulfur-containing metabolites (3CO-MA and 3OH-MA) were also found in control rat urine.

Chemical species of organotin compounds in sediment at a marina.

A bottom sediment collected in a marina was analyzed for organotin species, and >20 organotin compounds including biodegraded ones were confirmed by comparison with the synthesized standards using gas chromatography (GC)/mass spectrometry and a GC/atomic emission detection system. Their structures were also determined in comparison with those in a technical grade of tri-n-butyltin chloride (TBTC). Eleven organotin compounds were found in the technical TBTC. Among them, unexpected organotin compounds, such as di-n-butyl(2-ethylhexyl)tin chloride and di-n-butyloctyltin chloride, were identified, although the levels were low. These compounds were also found in the sediment sample. The relationship between organotin compounds in the technical TBTC and those in marine products was also discussed.

Macrophage secretory function is enhanced by low doses of tributyltin-oxide (TBTO), but not tributyltin-chloride (TBTCl).

Numerous studies suggest that tributyltin (TBT) is a potent immunotoxicant in nontarget organisms with lymphoid atrophy being a hallmark response. Two of the most common formulations of TBT are bis (tri-n-butyl)-tin oxide (TBTO) and tri-n-butyl-tin chloride (TBTCl). Most of studies investigating TBT-related immunotoxicity have used relatively high doses of both compounds, but little is known about the effects of very low doses. In addition, no studies have directly compared the effects of both formulations on immune function(s). We exposed female B6C3F1 mice to a single dose of TBTO or TBTCl at 0.3, 3.0, 30 mM/kg or corn oil as a carrier control. Forty-eight h later mice received a 4% solution of thioglycolate intraperitoneally to elicit peritoneal macrophages. Ninety-six h later macrophages were harvested and stimulated with a mixture of gamma-interferon (IFN-gamma) and lipopolysaccharide (LPS). Nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha), transforming growth factor beta-1 (TGF-beta1), and phorbol ester-stimulated oxidative burst activity were then measured. Nitric oxide and TNF-alpha production were significantly elevated in the 0.3 and 3.0 mM TBTO/kg-treated groups but not in those treated by TBTCl. Background TNF-alpha production (without stimulation) was also elevated at these two doses but suppressed in TBTCl-treated animals. Oxidative burst activity was elevated at 0.3 mM TBTO/kg but not by TBTCl. TGF-beta1 production was not altered by either treatment, nor were body wts and organ-body wt ratios. To further evaluate the difference between the effects of TBTO and TBTCl on macrophage function, the in vitro toxicity of the two was determined using elicited peritoneal macrophages from untreated mice. Following a 24-h exposure to increasing concentrations of TBTO or TBTCl, functional viability was evaluated using the MTT assay. There were no differences between the two compounds in terms of treatment-related viability except that at the very highest concentrations (10(-6) M) TBTO was more toxic than TBTCl.

Organotin-Induced Apoptosis as Observed in VitroIs Not Relevant for Induction of Thymus Atrophy at Antiproliferative Doses

The organotin compounds di- n-butyltin dichloride (DBTC) and tri- n-butyltin chloride (TBTC) selectively cause thymus atrophy. Previously, DBTC and TBTC were shown to inhibit proliferation of immature thymocytes, but other studies demonstrated that TBTC but not DBTC increased apoptosis in vitroand also in vivo.In this study, we examined whether apoptosis is increased in vitroby DBTC and TBTC at various concentrations and periods of incubation and whether apoptosis is involved in the induction of thymus atrophy at selective antiproliferative doses. In vitro,DBTC or TBTC at a concentration of 3 μ msignificantly increased DNA fragmentation in freshly isolated rat thymocytes after preincubation for 10 min followed by a 22-hr culture period. After continuous exposure for 22 hr, apoptosis was observed to be optimum at 1 μ mTBTC and 0.3 μ mDBTC and lower or absent at higher concentrations. Apparently, apoptosis induced by organotins in vitrodepends on both duration and concentration of exposure. Selective antiproliferative doses of DBTC nor TBTC increased apoptosis on day 1 or 2 after single oral exposure. In contrast, the corticosteroid dexamethasone caused a depletion of both small and large thymocytes and a marked increase of apoptosis on both days 1 and 2 after dosing. Thus, although apoptosis is involved in the in vitrocytotoxic effects of both organotin compounds, it seems not involved in thymus atrophy at a dose that selectively inhibits immature thymocyte proliferation.

活性汚泥微生物の生物吸着，ＣＯＤ除去および酸素吸収速度に及ぼす有害化学物質の影響

The effects of ten hazardous chemicals on biosorption behavior, COD removal rate (CODR) and oxygen uptake rate (OUR) of activated sludge microorganisms were studied.The IC50 values, 50% inhibition of the OUR, determined to be 2.3mg·l-1, 4.5mg·l-1, 7.3mg·l-1, 9.8mg·l-1, >2,500mg·l-1, >12,500mg·l-1, 950mg·l-1, 2,800mg·l-1, 9,500mg·l-1 and 460mg·l-1, respectively, for HgCl2, CUCl2, (CH3COO)2Hg, (CH3COO)2Cu, phenol, paraquat (PQ), gramoxone 100® (24% PQ), tri-n-butyltin chloride (TBTC), tri-n-butyltin oxide (TBTO) and SnCl2.As the IC50 value of Hg (II) and Cu (II) low, CODR low while biosorption behavior high. Conversely, when the IC50 value of phenol, PQ, gramoxone 100&reg, TBTC, TBTO and SnCl2 high, CODR high and biosorption behavior low.It has been shown that these findings are related to the IC50 values or CODR and biosorption behavior on activated sludge microorganisms of the ten hazardous chemicals tested.

Acute toxicity of tri-n-butyltin chloride (TBTC) in the Syrian golden hamster.

The effects of tri-n-butyltin chloride (TBTC) on Syrian golden hamsters were studied. TBTC in single doses of 0, 29.6, 44.4, 66.7, 100 or 150 mg/kg were given to 10 male hamsters in each group and the mortality rates were determined two weeks thereafter. They were 0% (0/10), 0% (0/10), 10% (1/10), 10% (1/10), 30% (3/10) and 70% (7/10) for 0, 29.6, 44.4, 66.7, 100 and 150 mg/kg groups, respectively. In the case of females, seven groups consisting of 10 animals each were given TBTC at doses of 0, 29.6, 44.4, 66.7, 100, 150, or 225 mg/kg. The mortality rates determined two weeks after the TBTC treatment were 0% (0/10), 10% (1/10), 10% (1/10), 0% (0/10), 40% (4/10), 30% (3/10) and 90% (9/10) for 0, 29.6, 44.4, 66.7, 100, and 225 mg/kg groups, respectively. Based on these mortality data, the LD50s via oral administration were determined as 146.9 mg/kg (95% C.I. 111.8-193.3 mg/kg) for the male and 172 mg/kg (95% C.I. 127.2-233.4 mg/kg) for the female. Regarding pathological changes, animals experienced lesions in the bile duct, such as the dilatation of the common bile duct and cholestasis, and/or adhesion of the bile duct to the liver, gallbladder, pancreas and duodenum. In a separate experiment, a single dose of 44.4 mg/kg TBTC was administered orally to 12 male hamsters, then the concentrations of TBTC and its metabolite, di-n-butyltin chloride (DBTC), in the liver were analyzed by means of gas chromatography for 14 days after the treatment. The maximum concentrations of TBTC and DBTC appeared one day after the administration, and decreased rapidly thereafter. The concentration of DBTC was found to be higher than that of TBTC throughout the experimental period.

Immunotoxicity of tri‐n‐butyltin oxide (TBTO) and tri‐n‐butyltin chloride (TBTC) in the rat

In a 1-month feeding trial, pure and commercial tri-n-butyltin oxide (TBTO) and tri-n-butyltin chloride (TBTC) were fed to rats at concentrations of 5 ppm and 25 ppm. At all times, the mean body weight gain and the food consumption was significantly less in rats treated with 25 ppm pure TBTO or pure TBTC as compared to control rats or rats receiving commercial TBTO. Histological examination of the thymus of rats treated for 7 days with TBTO showed atrophy with severe lymphocytic depletion in the cortex. After 28 days of exposure, most of the lesions reversed and the thymus became markedly smaller than in control rats, both in absolute terms and in relation to body weight. Seven days of exposure to TBTO increased liver weight but this change was reversed during a further 3-week exposure. Tin concentrations were the highest in livers and kidneys. Concentrations in the thymus were less than one-fifth of hepatic values. Changes in the rats treated with the commercial TBTO were very similar. Rats treated with TBTC showed lower tin levels and less immunotoxicity as compared to those treated with TBTO.

Effect of the fungicides tributyltin acetate and tributyltin chloride on multilamellar liposomes: fluorescence studies

The influence of tri- n-butyltin acetate (TBTA) and tri- n-butyltin chloride (TBTC) on the physico-chemical state of charged and neutral phospholipids was investigated using multilamellar liposomes. The thermal dependence of steady state fluorescence polarization of DPH and its charged derivative TMA-DPH was recorded. The two fungicides lowered DPPC phase transition temperature and broadened the temperature range of the transition in different ways. The effects were concentration-dependent. The results show that TBTC interacts more effectively with DPPC model membranes rather than TBTA. Moreover, TBTC broadens and shifts the main phase transition ( T m) more effectively in DPPC rather than in DMPC liposomes. Below T m, TBTC decreases fluorescence polarization (P) in all phospholipids used. Above T m P is almost constant in phospholipids with saturated acyl chains, except for DMPG. In fact, an increase of P is detectable in this lipid as in PLs with unsaturated acyl chains. It is suggested that the effects of TBT on liposomal membranes are dependent on the anion moiety and phospholipids characteristics.

Determination of mono‐, di‐ and tri‐substituted butyltin, phenyltin and methyltin compounds as free halides using gas chromatography with flame photometric detection

AbstractA simple chromatographic procedure has been developed for the sensitive determination of mono‐, di‐ and tri‐substituted butyltin, phenyltin, and methyltin compounds as halides. The organotin compounds were separated on a DB‐1 capillary column and detected by flame photometric detection (FPD) equipped with a 611.5 nm filter.Pretreatment of the capillary column with an ethyl acetate solution of hydrobromic acid, or doping of standard solutions with hydrobromic acid, was found to be necessary if reproducibly sharp peaks of organotin halides were to be obtained. Column treatment and acid doping did not cause any background problems or undesirable degradation of the organotin compounds.Three different standard solutions in ethyl acetate had to be Jrepared, because undesirable degradation of the organotin halides was observed when all the compounds were dissolved in the same solution. The first, standard solution I, contained tri‐n‐butyltin chloride (TBTCI) and trimethyltin chloride (TMTCI), the second, standard solution II, contained triphenyltin chloride (TPTCI), and the third, standard solution III, contained hydrogen bromide and the other organotin compounds: di‐n‐butyltin chloride (DBTCI), mono‐n‐butyltin chloride (MBTCI), dimethyltin chloride (DMTCI), monomethyltin chloride (MMTCI), diphenyltin chloride (DPTCI), and monophenyltin chloride (MPTCI). An ethyl acetate solution containing hydrobromic acid (20 × 10−3 mol/I) was used for column treatment.