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PubMed2002

Samarangenin B from Limonium sinense suppresses herpes simplex virus type 1 replication in Vero cells by regulation of viral macromolecular synthesis.

Inhibitory effects of ethanolic extracts from 10 Chinese herbs on herpes simplex virus type 1 (HSV-1) replication were investigated. By a bioassay-guided fractionation procedure, samarangenin B (Sam B) was isolated from Limonium sinense; Sam B significantly suppressed HSV-1 multiplication in Vero cells without apparent cytotoxicity. Time-of-addition experiments suggested that the inhibitory action of Sam B on HSV-1 replication was not due to the blocking of virus adsorption. In an attempt to further localize the point in the HSV-1 replication cycle where arrest occurred, a set of key regulatory events leading to viral multiplication was examined, including viral immediate-early (alpha), early (beta), and late (gamma) gene expression and DNA replication. Results indicated that levels of glycoprotein B (gB), gC, gD, gG, and infected-cell protein 5 (ICP5) expression and gB mRNA expression in Vero cells were impeded by Sam B. Data from PCR showed that replication of HSV-1 DNA in Vero cells was arrested by Sam B. Furthermore, Sam B decreased DNA polymerase, ICP0, and ICP4 gene expression in Vero cells. Results of an electrophoretic mobility shift assay demonstrated that Sam B interrupted the formation of an alpha-trans-induction factor/C1/Oct-1/GARAT multiprotein complex. The mechanisms of antiviral action of Sam B seem to be mediated, at least in part, by inhibiting HSV-1 alpha gene expression, including expression of the ICP0 and ICP4 genes, by blocking beta transcripts such as DNA polymerase mRNA, and by arresting HSV-1 DNA synthesis and structural protein expression in Vero cells. These results show that Sam B is an antiviral agent against HSV-1 replication.

Animals↗
PubMed1980

Stimulation of yeast ascospore germination and outgrowth by S-adenosylmethionine.

The supplementation of S-adenosylmethionine (SAM) to germination medium stimulated the accumulation of [14C]uracil from the medium into germinating cells, as well as its incorporation into ribonucleic acid during germination and outgrowth of ascospores of Saccharomyces cerevisiae. In addition to uracil, the accumulation of leucine, cytosine, serine, and methionine was also stimulated by the extracellular addition of this sulfonium compound. The SAM-stimulatory effect was dose dependent; half-maximal stimulation was observed at about 50 muM. The effect exerted by SAM supplementation appeared to be specific for SAM and for germination and outgrowth. In the absence of SAM biosynthesis (in the presence of cycloleucine), spores were inhibited in their ability to accumulate label, whereas the supplementation of SAM completely reversed the cycloleucine-induced inhibition of accumulation. In addition to accumulation and incorporation, the kinetics of bud formation during outgrowth were also stimulated by exogenous SAM. The stimulation of budding by SAM was amplified in an ethionine-resistant strain. These observations suggest that SAM may be essential for the initiation of cell division during the breaking of spore dormancy.

Cell Division↗
PubMed2004

Inhibition of lipopolysaccharide-stimulated TNF-alpha promoter activity by S-adenosylmethionine and 5'-methylthioadenosine.

S-adenosylmethionine (SAM) is the principal biological methyl donor and precursor for polyamines. SAM is known to be hepatoprotective in many liver disease models in which TNF-alpha is implicated. The present study investigated whether and how SAM inhibited LPS-stimulated TNF-alpha expression in Kupffer cells (hepatic macrophages). SAM downregulated TNF-alpha expression in LPS-stimulated Kupffer cells at the transcriptional level as suggested by a transfection experiment with a TNF-alpha promoter-reporter gene. This inhibition was not mediated through decreased NF-kappaB binding to four putative kappaB binding elements located within the promoter. The inhibited promoter activity was neither prevented by overexpression of p65 and/or its coactivator p300 nor enhanced by overexpression of coactivator-associated arginine methyltransferase-1, an enzyme that methylates p300 and inhibits a p65-p300 interaction. SAM did not lead to DNA methylation at the most common CpG target sites in the TNF-alpha promoter. Moreover, 5'-methylthioadenosine (MTA), which is derived from SAM but does not serve as a methyl donor, recapitulated SAM's effect with more potency. These data demonstrate that SAM inhibits TNF-alpha expression at the level downstream of NF-kappaB binding and at the level of the promoter activity via mechanisms that do not appear to involve the limited availability of p65 or p300. Furthermore, our study is the first to demonstrate a potent inhibitory effect on NF-kappaB promoter activity and TNF-alpha expression by a SAM's metabolite, MTA.

Animals↗
PubMed1998

Leaf polarity and meristem formation in Arabidopsis.

Shoot apical meristems (SAMs) of seed plants are small groups of pluripotent cells responsible for making leaves, stems and flowers. While the primary SAM forms during embryogenesis, new SAMs, called axillary SAMs, develop later on the body of the plant and give rise to branches. In Arabidopsis plants, axillary SAMs develop in close association with the adaxial leaf base at the junction of the leaf and stem (the leaf axil). We describe the phenotype caused by the Arabidopsis phabulosa-1d (phb-1d) mutation. phb-1d is a dominant mutation that causes altered leaf polarity such that adaxial characters develop in place of abaxial leaf characters. The adaxialized leaves fail to develop leaf blades. This supports a recently proposed model in which the juxtaposition of ad- and abaxial cell fates is required for blade outgrowth. In addition to the alteration in leaf polarity, phb-1d mutants develop ectopic SAMs on the undersides of their leaves. Also, the phb-1d mutation weakly suppresses the shoot meristemless (stm) mutant phenotype. These observations indicate an important role for adaxial cell fate in promoting the development of axiallary SAMs and suggest a cyclical model for shoot development: SAMs make leaves which in turn are responsible for generating new SAMs.

Arabidopsis↗
PubMedDate not supplied

Antidepressant activity of S-adenosyl-L-methionine in mice and rats.

S-Adenosyl-L-methionine (SAM), main methyl donor, was tested in mice and rats in several models which are predictive of possible antidepressant activity. In the forced swimming test in rats the effect of SAM was compared with that of the tricyclic antidepressant amitriptyline. SAM decreased dose-dependently immobility time in the forced swimming test in mice and rats, these effects being antagonized by haloperidol and prazosin (the latter only in rats). Locomotor or exploratory activity in mice and rats was not increased by SAM. D-Amphetamine-induced locomotor hyper-activity in rats was increased by repeated (14 days, twice daily) treatment with SAM. Behavioural stimulation induced by D-amphetamine or L-dopa (given with benserazide) in mice was not changed by a single dose of SAM. The drug reduced hypothermia induced by apomorphine in mice. Hypothermia induced by reserpine or clonidine in mice was not antagonized. SAM increased the amplitude of the acoustic startle reflex. The above results indicate that the psychopharmacological profile of SAM resembles that of antidepressants in only some tests. The mechanism by which SAM produces its antidepressant effect needs further investigation.

Amphetamine↗
PubMed2005

Strong repulsive forces between protein and oligo (ethylene glycol) self-assembled monolayers: a molecular simulation study.

Restrained molecular dynamics simulations were performed to study the interaction forces of a protein with the self-assembled monolayers (SAMs) of S(CH2)4(EG)4OH, S(CH2)11OH, and S(CH2)11CH3 in the presence of water molecules. The force-distance curves were calculated by fixing the center of mass of the protein at several separation distances from the SAM surface. Simulation results show that the relative strength of repulsive force acting on the protein is in the decreasing order of OEG-SAMs > OH-SAMs > CH3-SAMs. The force contributions from SAMs and water molecules, the structural and dynamic behavior of hydration water, and the flexibility and conformation state of SAMs were also examined to study how water structure at the interface and SAM flexibility affect the forces exerted on the protein. Results show that a tightly bound water layer adjacent to the OEG-SAMs is mainly responsible for the large repulsive hydration force.

Adsorption↗
PubMed1999

Molecular characterization of Plasmodium falciparum S-adenosylmethionine synthetase.

S-Adenosylmethionine (AdoMet) synthetase (SAMS: EC 2.5.1.6) catalyses the formation of AdoMet from methionine and ATP. We have cloned a gene for Plasmodium falciparum AdoMet synthetase (PfSAMS) (GenBank accession no. AF097923), consisting of 1209 base pairs with no introns. The gene encodes a polypeptide (PfSAMS) of 402 amino acids with a molecular mass of 44844 Da, and has an overall base composition of 67% A+T. PfSAMS is probably a single copy gene, and was mapped to chromosome 9. The PfSAMS protein is highly homologous to all other SAMS, including a conserved motif for the phosphate-binding P-loop, HGGGAFSGKD, and the signature hexapeptide, GAGDQG. All the active-site amino acids for the binding of ADP, P(i) and metal ions are similarly preserved, matching entirely those of human hepatic SAMS and Escherichia coli SAMS. Molecular modelling of PfSAMS guided by the X-ray crystal structure of E. coli SAMS indicates that PfSAMS binds ATP/Mg(2+) in a manner similar to that seen in the E. coli SAMS structure. However, the PfSAMS model shows that it can not form tetramers as does E. coli SAMS, and is probably a dimer instead. There was a differential sensitivity towards the inhibition by cycloleucine between the expressed PfSAMS and the human hepatic SAMS with K(i) values of 17 and 10 mM, respectively. Based on phylogenetic analysis using protein parsimony and neighbour-joining algorithms, the malarial PfSAMS is closely related to SAMS of other protozoans and plants.

Amino Acid Sequence↗
PubMed2000

Determination of S-adenosylmethionine and S-adenosylhomocysteine in plasma and cerebrospinal fluid by stable-isotope dilution tandem mass spectrometry.

BACKGROUND: Available methods for the determination of nanomolar concentrations of S:-adenosylmethionine (SAM) and S:-adenosylhomocysteine (SAH) in plasma and cerebrospinal fluid (CSF) are time-consuming. We wished to develop a method for their rapid and simultaneous measurement. METHODS: We used tandem mass spectrometry (MS/MS) for the simultaneous determination of SAM and SAH, with stable-isotope-labeled internal standards. The (13)C(5)-SAH internal standard was enzymatically prepared using SAH-hydrolase and [(13)C(5)]adenosine. The method comprises a weak anion-exchange solid-phase extraction procedure serving as clean-up step for the deproteinized plasma and CSF samples. After clean-up, samples were injected on a C(18) HPLC column, which was connected directly to the tandem mass spectrometer, operating in MS/MS mode. RESULTS: In plasma samples, the intraassay CVs for SAM and SAH were 4.2% and 4.0%, respectively, and the interassay CVs were 7.6% and 5. 9%, respectively. In CSF, the intraassay CVs for SAM and SAH were 6. 8% and 6.9%, respectively, and the interassay CVs were 4.2% and 5.5%, respectively. Mean recovery of SAM and SAH for both matrices at two concentrations was 93%. Detection limits for SAM and SAH in samples were 7.5 and 2.5 nmol/L, respectively. Concentrations of SAM and SAH in plasma from healthy subjects were within the previously reported ranges. In 10 CSF samples, the mean concentrations (range) were 248 (137-385) nmol/L for SAM and 11.3 (8.9-14.1) nmol/L for SAH. CONCLUSIONS: SAM and SAH can be analyzed by MS/MS, taking optimal advantage of the speed and high sensitivity and specificity of this relatively new analytical technique.

Carbon Isotopes↗
PubMed2003

[Application of synthetic aperture magnetometry for epilepsy surgery].

Recently developed synthetic aperture magnetometry (SAM) is a new MEG signal analysis introducing a high performance spatial filtering technique. SAM is not an inverse solution like dipole analysis, but rather an adaptive beamformer for estimating source activity at each selected voxel inside of the brain. SAM can estimate source changes as a function of time, or power changes subjected to statistical analysis from the non-averaged raw MEG data. Thus this method enables to display the regional currentodensitogram of the arbitrary selected brain tissue as if depth electrodes were inserted (SAM virtual sensor), and to detect the origin of epileptic discharges and their spread. By applying statistical discrimination, SAM can also demonstrate the spatial distribution of event-related changes of brain rhythm (SAM statistical method), in other words activated cerebral cortex during task performance. We will present the usefulness of noninvasive SAM methods in epilepsy surgery detecting the epileptogenic zone by SAM virtual sensor method as well as eloquent brain by SAM statistical method.

Cerebral Cortex↗
PubMed1989

Autoimmune abnormalities in a murine model of accelerated senescence.

Immunopathological abnormalities in senescence-accelerated mice (SAM) were studied by comparison of senescence-prone (SAM-P/1) and senescence-resistant (SAM-R/1) mice. Sera from SAM-P/1 mice contained a number of autoantibodies, including natural thymocytotoxic autoantibody (NTA), anti-nuclear antibodies (ANA) and IgG anti-single-stranded and anti-double-stranded (ss and ds) DNA antibodies. Furthermore, an earlier increase in serum IgG2 levels and an earlier appearance of IgG circulating immune-complexes (CIC) associated with low C3 levels, were observed in SAM-P/1 mice. These serological findings were distinctive features in SAM-P/1 mice, which could almost discriminate these mice from SAM-R/1 mice. In addition, age-associated glomerular mesangial and capillary lesions with granular IgG and C3 deposition were frequently observed in SAM-P/1 mice, whereas SAM-R/1 mice even at 10 months of age showed only mild mesangial lesions. These findings suggest that autoimmune abnormalities may contribute to the accelerated senescence in these mice.

Aging↗
PubMed1988

Metabolism of senile amyloid precursor and amyloidogenesis. Age-related acceleration of apolipoprotein A-II clearance in the senescence accelerated mouse.

Serum clearance kinetics of murine senile amyloid-related high-density lipoprotein (HDL) apoprotein A-II (apo A-II) was examined in the senescence-accelerated mouse, prone (SAM-P/1) and resistant (SAM-R/1), with 125I-HDL purified from both strains. In SAM-R/1, with 125I-HDL purified from both strains. In SAM-R/1, the serum half-life of apo A-II was not altered with increasing age and was practically identical to that of apo A-I. In 2-month old SAM-P/1, the serum half-life of both apo A-I and apo A-II was generally the same as observed in SAM-R/1. However, at age 6 and 12 months, in SAM-P/1, the serum half-life of apo A-II decreased significantly and was less than that of apo A-I. These age-related changes in apo A-II clearance kinetics were observed regardless of the HDL donor. The authors also examined the tissue distribution of injected apo A-II, using 125I-apo A-II reconstituted HDL, and found that several organs trapped more 125I radioactivity in old SAM-P/1 than in young mice. This evidence strongly suggests that age-related changes in the metabolic environment of apo A-II might affect senile amyloidogenesis in SAM-P/1.

Aging↗
PubMed1988

[Anterolateral papillary muscle motion before and after septal myotomy in hypertrophic obstructive cardiomyopathy].

The left ventricular outflow pressure gradient in hypertrophic cardiomyopathy results from systolic anterior motion of the mitral valve (SAM). This abnormal orientation of the valve was previously proposed to be caused by inappropriately hypertrophied papillary muscles which protrude to the interventricular septum (IVS). Septal myotomy can alter the orientation of the papillary muscles and resolve the pressure gradient, without myectomy. Recently, we have experienced two instructive cases to prove our previously advocated hypothesis. Case 1: This 54-year-old man complained of effort dyspnea, and his echocardiogram disclosed marked SAM, and a thickened IVS (28 mm) and left ventricular posterior wall (16 mm). The intraventricular pressure gradient was 134 mmHg, and there was mitral regurgitation of grade 2/4. A longitudinal incision via the aorta on the anterior portion of the IVS, toward the base of the anterolateral papillary muscle, resolved the pressure gradient and mitral regurgitation, and two-dimensional echocardiography demonstrated that the SAM resolved at the lateral aspect of the valve, but it remained on the medial side. Case 2: This 57-year-old man complained of dyspnea during effort. He had marked SAM. The intraventricular pressure gradient was 65 mmHg, and there was grade 3/4 mitral regurgitation. Longitudinal incisions on the anterior, medial and posterior parts of the IVS abolished the SAM and reduced mitral regurgitation to grade 1/4. In both cases, during systole, the anterolateral papillary muscle protruded into the left ventricular ontflow tract, causing SAM. After surgery, the direction of the muscle axis moved toward the mitral orifice during systole, resulting in alleviation of SAM on the same side of the location of septotomy. This further confirmed our concept that disoriented papillary muscles play essential roles in causing SAM. If the Venturi forces previously stressed by other investigators cause SAM, the latter should resolve on both the medial and lateral aspects, even by septotomy. Thus, the Venturi theory seems untenable.

Cardiomyopathy, Hypertrophic↗
PubMed1995

Segmental arterial mediolysis: a precursor to fibromuscular dysplasia?

We describe five cases of segmental arterial mediolysis (SAM), formerly known as segmental mediolytic arteritis. SAM occurs in epicardial coronary arteries and in the abdominal splanchnic arteries. Patients with abdominal SAM are generally elderly, whereas coronary SAM presents in neonates, children, and young adults. SAM is initiated by mediolysis of the outer media, which can expand to involve the mid- and inner media. Accompanying alterations include fibrinous linear deposits at the medial adventitial junction and replacement of the lysed muscle fibers by fibrin, erythrocytes, and granulation tissue. Transmural mediolysis results in arterial wall gaps frequently complicated by dissecting hematomas and aneurysms. Abdominal hemorrhages stem from these complications. SAM involving abdominal splanchnic arteries clinically presents with abdominal pain and distension, falling hematocrit, and shock. Simultaneous involvement of more than one abdominal artery is frequent, and branches of the celiac axis are most commonly affected. Various disease states that provoke pathologic stimuli for endothelial mediated vasoconstriction occur in the immediate clinical background of patients with SAM. Certain morphologic features of SAM suggest that this arterial lesion is due to vasospasm, which we putatively ascribe to focal endothelial paracrine dysfunction. Organization of uncomplicated SAM lesions could resemble certain types of fibromuscular dysplasia, suggesting that the genesis of such arterial lesions is related to vasospasm.

Abdomen↗
PubMed1997

Importance of leaflet elongation in causing systolic anterior motion of the mitral valve.

BACKGROUND AND AIMS OF THE STUDY: There is growing evidence for mitral leaflet elongation in patients with hypertrophic cardiomyopathy. Such elongation could predispose to systolic anterior motion (SAM) of the mitral valve by increasing leaflet mobility and providing a geometry that promotes this condition. METHODS: To test this postulate, five porcine mitral valves were studied in a physiologic left heart pulsatile flow duplicator. They were elongated with patches sutured to the basal posterior leaflet (three sizes per valve) or anterior leaflet (basal, middle, or distal). Each geometry was studied with normal papillary muscle position and with anterior and inward displacement, as seen in hypertrophic cardiomyopathy, to shift the leaflets into the outflow stream. RESULTS: Four points became clear. 1) Leaflet elongation promoted the development of SAM in response to papillary muscle displacement by creating long overlapping residual leaflets capable of moving anteriorly. 2) Posterior leaflet elongation also promoted SAM by shifting leaflet coaptation anteriorly, with progressive increases in SAM. 3) Basal and mid-anterior leaflet elongation caused SAM with prolapse; distal anterior leaflet elongation created SAM with a mobile flap (leaflet elongation without papillary muscle displacement created prolapse). 4) Residual leaflet length correlated well with total leaflet length (r = 0.87-0.98 for each valve), and the degree of SAM in turn correlated well with residual leaflet length (r = 0.62-0.98 for individual valves). CONCLUSIONS: Mitral leaflet elongation, by increasing the residual leaflet length and leaflet mobility, can play an important role in promoting SAM in response to outflow forces, as demonstrated by prospectively altering leaflet length. These findings are consistent with recent observations that reducing leaflet redundancy and posterior leaflet height can reduce obstructive SAM following mitral valve repair in patients with mitral valve prolapse and help relieve obstruction in patients with hypertrophic cardiomyopathy and enlarged leaflets.

Cardiomegaly↗
PubMed1998

Differential expression of methionine adenosyltransferase genes influences the rate of growth of human hepatocellular carcinoma cells.

Methionine adenosyltransferase (MAT) catalyzes the formation of S-adenosylmethionine (SAM), the principal methyl donor, and is essential to normal cell function. The two forms of MAT, liver specific and non-liver specific, are products of two genes, MAT1A and MAT2A, respectively. We have reported a switch from MAT1A to MAT2A gene expression in human liver cancer cells. In the current work, we examined whether the type of MAT expressed by the cell influences cell growth. HuH-7 cells were stably transfected with MAT1A and were subsequently treated with antisense oligonucleotides directed against MAT2A. MAT2A antisense treatment reduced the amount of MAT2A mRNA by 99% but had no effect on MAT1A mRNA. Cell growth and DNA synthesis rates were reduced by approximately 20-25% after transfection with MAT1A and by an additional 30-40% after MAT2A antisense treatment. SAM level and SAM:S-adenosylhomocysteine (SAH) ratio increased by 50-75% after MAT1A transfection and by an additional 60-80% after MAT2A antisense treatment. DNA methylation changed in parallel to changes in SAM level and SAM:SAH ratio. Supplementing untransfected HuH-7 cells with SAM in the culture medium increased SAM level, SAM:SAH ratio, and DNA methylation and decreased cell growth and DNA synthesis. In conclusion, cell growth is influenced by the type of MAT expressed. The mechanism likely involves changes in SAM:SAH ratio and DNA methylation.

Carcinoma, Hepatocellular↗
PubMedDate not supplied

6R-L-erythro-5,6,7,8-tetrahydrobiopterin is involved in brain vulnerability of senescence-accelerated mouse during the processes of aging.

The effects of age on the dopamine (DA) turnover and 6R-L-erythro-5,6,7,8-tetrahydrobiopterin (6R-BH4), a cofactor for monooxygenases, were investigated in the striatum and midbrain of the senescence accelerated mouse (SAM) at 6, 12 and 15 months old. 6R-BH4 and DA levels were decreased significantly in the striatum of 15-month-old SAM-P/1 (senescence accelerated prone) mice. At 12 months old, DA level was decreased significantly in the striatum of SAM-P/1 compared with SAM-R/1 (senescence accelerated resistant) mice. The reduction of striatal DA level was shown to be related to the depletion of 6R-BH4 in the striatum during the processes of aging. Age-related decreases in striatal dopamine function occurred in SAM-P/1 mice earlier than in the SAM-R/1 mice. The striatal [DOPAC]/[DA] ratio, as the index of DA turnover, was increased significantly in the 15-month-old SAM-P/1 mice. On the other hand, the DA, 6R-BH4 levels and the ratio of [DOPAC]/[DA] did not show any changes in the midbrain of SAM-P/1 and SAM-R/1 during the processes of aging. It was suggested that brain vulnerability with aging may be associated with the levels of 6R-BH4.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2000

Cation recognition by self-assembled monolayers of oriented helical peptides having a crown ether unit.

Cation recognition of self-assembled monolayers (SAMs) of helical peptides having a crown ether unit was investigated by the impedance spectroscopy and cyclic voltammetry. Lipo-(Ala-Aib)8-Ala-Cr and Boc-Glu(Cr)-(Ala-Aib)8-Lipoa (Lipo, Lipoa, and Cr represent lipoic acid, lipoamide, and amidobenzo-18-crown-6, respectively) were synthesized and the helix SAMs were prepared. The peptides having a crown ether unit formed SAMs oriented nearly vertically to the substrate. The capacitance of the Lipo-(Ala-Aib)(8)-Ala-Cr SAM changed specifically with the addition of cations, and the binding constants of the SAM were larger than those of the crown ether in aqueous solution because of a large dipole moment of the helical peptide. In the case of the Boc-Glu(Cr)-(Ala-Aib)8-Lipoa SAM, the cation binding to the SAM showed a drastic decrease in the peak current of the cyclic voltammetry around 10(-5)M of K+ ion. In either capacitance measurement or cyclic voltammetry, the helical peptide SAM played an important role in the sensitive response to cations.

Cations↗
PubMed2000

Synthesis, surface characterization, and platelet reactivity evaluation for the self-assembled monolayer of alkanethiol with sulfonic acid functionality.

Owing to the capability of fabricating a well-defined chemical structure on the surface, self-assembled alkanethiols with a variety of terminal functionalities were prepared on the gold substrate for investigating the interactions between the biological environment and synthetic surface. In this study, we report the synthesis of the sulfonic acid terminated long-chain alkanethiol, 10-mercaptodecane-sulfonic acid, for direct preparation of a self-assembled monolayer (SAM) with -SO(3)H functionality. Nuclear magnetic resonance (NMR) and elemental analysis studies indicated that a high purity of sulfonic acid terminated alkanethiol was obtained. Surface characterization results showed that the -SO(3)H terminated SAM is hydrophilic and has a slightly higher hysteresis value, possibly because of the slower chain mobility of the bound sulfonic acid alkanethiol. Electron spectroscopy for chemical analysis (ESCA) analysis demonstrated that the -SO(3)H terminal group is situated in the outermost layer of the monolayer, as previous alkanethiol SAM structure models proposed. The platelet reactivity of the -SO(3)H SAM was higher than that of -OH SAM but less than the -CH(3) terminated one in vitro, whereas similar platelet reactivity was noticed between the -SO(3)H and -COOH SAMs. The higher platelet reactivity found on the -SO(3)H SAM could be caused by the higher surface functional group density inherent in the SAM structure and/or the composition and conformation state of the adsorbed protein layer.

Alkanesulfonic Acids↗