Sulfhydryl Radical Research Articles

In situ desulfurization mechanism of molten salt thermal treatment for waste tires

Pyrolysis is regarded as a practical way for waste tires to achieve waste-to-resource objectives. However, the environmental risk of pollution emissions in product utilization caused by the migration of sulfur is an important issue in the waste tire disposal industry. This study introduced a solution to using the binary molten salt system (NaOH-Na2CO3) as a heat transfer and desulfurization medium for the thermal utilization of waste tires. The results demonstrated that molten salts had in-situ desulfurization capability at 425 °C −575 °C and inhibited the migration of sulfur to gas–liquid-solid products with the total sulfur ratio reduced by 50 % − 67 %. The sulfur-containing radical intermediates could be extensively consumed by molten salt, leading to a low concentration level of H2S and COS in gaseous products. Simultaneously, molten salt blocked the traditional pathway of the sulfhydryl radical with inorganic additives, weakening the sulfur enrichment to char. Additionally, molten salt enhanced heat transfer during pyrolysis, facilitating the decomposition of thiazole and the polymerization of sulfur-containing benzene ring (2,3-dimethyl-thiophene to benzothiophene). The online monitoring further corroborated that COS release was preceded by H2S at high temperatures (>500 °C) along with the full degradation of the waste tires. Higher desulfurization efficiency of molten salt was achieved with feedstocks of small particle size, as it allows for adequate exposure of the reaction contact sites. This approach provides a new opportunity for in-situ desulfurization of waste tire pyrolysis via molten salt thermal treatment.

H2SIncreases Blood Pressure via Activation of L-Type Calcium Channels with Mediation by HS•Generated from Reactions with Oxyhemoglobin.

Although the gasotransmitter hydrogen sulfide (H2S) is well known for its vasodilatory effects, H2S also exhibits vasoconstricting properties. Herein, it is demonstrated that administration of H2S as intravenous sodium sulfide (Na2S) increased blood pressure in sheep and rats, and this effect persisted after H2S has disappeared from the blood. Inhibition of the L-type calcium channel (LTCC) diminished the hypertensive effects. Incubation of Na2S with whole blood, red blood cells, methemoglobin, or oxyhemoglobin produced a hypertensive product of H2S, which is not hydrogen thioperoxide, metHb-SH- complexes, per-/poly- sulfides, or thiolsulfate, but rather a labile intermediate. One-electron oxidation of H2S by oxyhemoglobin generated its redox cousin, sulfhydryl radical (HS•). Consistent with the role of HS• as the hypertensive intermediate, scavenging HS• inhibited Na2S-induced vasoconstriction and activation of LTCCs. In conclusion, H2S causes vasoconstriction that is dependent on the activation of LTCCs and generation of HS• by oxyhemoglobin.

P-23 Insulin autoimmune syndrome possibly induced by Alpha-Lipoic acid

Abstract Introduction Insulin autoimmune syndrome (IAS) is a relative rare cause of hypoglycemia due to the presence of extremely high circulating insulin levels and elevated serum concentrations of autoantibodies to human insulin despite no prior exposure to exogenous insulin, insulin analogues or oral hypoglycemic agents. It is characterized by repeated fasting hypoglycemia or episodes of hypoglycemia late after meals in non-diabetic, non-acutely ill patients. Increasing the titer of insulin autoantibodies and immune reactive insulin occurs owing to both genetic influences and environmental triggers such as medication, genetic instability and other factors. It is associated with the use of drugs comprising sulfhydryl groups, such as methimazole, clopidogrel and alpha lipoic acid, mostly. Insulin autoantibodies appear a few weeks after the exposure of sulfhydryl radicals. Here, we summarize the case of IAS caused by drug administration. Clinical Case A 60-year-old female patient who has a history of migraine for 30 years was referred to our hospital for feeling of hunger, dizziness, sweating, tremor, and palpitations for 1 month. These symptoms had commenced episodically, soon after starting 600 mg/day of alpha lipoic acid. She was diagnosed with hypoglycemia based on a plasma glucose concentration of 31 mg/dL. There was no personal or family history of diabetes mellitus, or previous use of oral hypoglycemic drugs such as sulfonylureas or exogenous insulin. No abnormality was detected in the systemic examination. She had no smoking and alcohol abuse. Her regular medication was tricyclic antidepressant (amitriptyline). Laboratory results are presented in Table 1. On our evalution, the serum levels of insulin, C-peptide, and anti-insulin antibody titers were inappropriately elevated in the presence of hypoglycemia, confirming the diagnosis of hyperinsulinemic hypoglycemia. Thyroid function, human growth hormone, insulin growth factor-1 (IGF-1), and cortisol result were within normal limits. Screening for antinuclear factor, serum protein electrophoresis, serology for viral hepatitis, and other autoimmune diseases were negative. Insulinoma was excluded with computed tomography. In light of the above results, a diagnosis of IAS was made with possible alpha lipoic acid. Because, alpha lipoic acid was the only medication being taken associated with a sulfhydryl group. The patient was prescribed oral methylprednisolone (32 mg once daily), alpha lipoic acid was withdrawn. Hypoglycemia did not occur after methylprednisolone treatment of follow-up. Methylprednisolone treatment was tapered to 4 mg once daily within 2 months. The insulin, and anti-insulin antibody titers had decreased. Conclusion We report a rare case of IAS. Sulfhydryl group containing drugs such as alpha lipoic acid might induce or exacerbate hypoglycemia in patients with a history of IAS. For this reason, the use of alpha lipoic acid should be questioned in patients with IAS. Table 1. Laboratory test results

Influence of Organic Sulfur on Low-Temperature Oxidation of Coal and its Transition Characteristics.

The low-temperature oxidation spontaneous combustion of coal was caused by the active groups in its structure. The oxidation mechanism of carbon and oxygen functional groups in coal had been extensively studied, but there were few reports on the study of sulfur functional groups initiating the coal spontaneous combustion. To investigate the influence of organic sulfur functional groups on the spontaneous combustion of high-sulfur coal and explore its transformation characteristics, the low-temperature oxidation experimental system was used to study the spontaneous combustion tendency of coal with similar metamorphic degrees and different organic sulfur contents. The variations of element forms and organic sulfur functional groups were analyzed by X-ray photoelectron spectroscopy and Fourier transform infrared spectroscopy during low-temperature oxidation of coal and model compounds. The results showed that the forms of organic sulfur in coal mainly included mercaptans, thioethers, thiophenes, sulfones (sulfoxides), and sulfates, and the low-temperature oxidation of coal was not only related to the content of organic sulfur but also related to its type. The coal samples, which possess a low content of total sulfur and a small proportion of active organic sulfur groups such as mercaptans and thioethers, had a lower concentration of indicator gas and a smaller tendency to coal spontaneous combustion. After low-temperature oxidation, the content of mercaptan, thioether, thiophene, methyl(methylene), and pyridine in coal decreased, and the content of oxygen-containing groups such as sulfone (sulfoxide), sulfate, carboxyl, and nitrogen oxide increased. The elements of S, C, and N all changed to a high-valent state. In the oxidation reaction of model compounds, mercaptans were more reactive than thiophenes in the low-temperature region, and the oxidation of thiophene could direct form sulfone (sulfoxide), while the oxidation of mercaptan formed disulfide first. It is speculated that low-valence sulfur migrated to a high-valent state by providing sulfhydryl radicals (•SH) and sulfur radicals (C-S•) combined with active oxygen atoms. After the low-temperature oxidation reaction of model compounds, some organic sulfur existed in the form of aromatic sulfur or sulfur oxides and a small part of sulfur escaped as SO2 and H2S gases in the solid oxidation product.

Radical nucleophilic substitution/cyclization: A novel strategy for selective and ultrafast fluorescence imaging of cysteine levels in ferroptosis process

Diphenylisoindolo[2,1-a]quinoline can be used to detect cysteine among homocysteine, glutathione, and other 19 natural amino acids. Unlike other reported probes, the response mechanism involves sulfhydryl radical nucleophilic substitution and cyclization, and thus the differences in ring-formation kinetics enable high selectivity. After treated with Cys, the response process was completed rapidly and the maximum fluorescence intensity (at 496 nm) was reached extremely fast (<1 s) when excited at 380 nm in MeCN-PBS buffer (10.0 mM, pH = 7.4, 3:7 (v/v)). The quantum yield after the reaction was increased almost 7 times to be 0.02 from 0.003. Fluorescence intensity displayed a good quantitative linear relationship in the range 1–10 μM Cys with a detection limit of 270 nM. Furthermore, the probe was demonstrated for real-time monitoring of intracellular cysteine levels within HepG2 cells in ferroptosis process.

Reductive Stress of Sulfur-Containing Amino Acids within Proteins and Implication of Tandem Protein-Lipid Damage.

Reductive radical stress represents the other side of the redox spectrum, less studied but equally important compared to oxidative stress. The reactivity of hydrogen atoms (H•) and hydrated electrons (e–aq) connected with peptides/proteins is summarized, focusing on the chemical transformations of methionine (Met) and cystine (CysS–SCys) residues into α-aminobutyric acid and alanine, respectively. Chemical and mechanistic aspects of desulfurization processes with formation of diffusible sulfur-centered radicals, such as methanethiyl (CH3S•) and sulfhydryl (HS•) radicals, are discussed. These findings are further applied to biomimetic radical chemistry, modeling the occurrence of tandem protein–lipid damages in proteo-liposomes and demonstrating that generation of sulfur-centered radicals from a variety of proteins is coupled with the cis–trans isomerization of unsaturated lipids in membranes. Recent applications to pharmaceutical and pharmacological contexts are described, evidencing novel perspectives in the stability of formulations and mode of action of drugs, respectively.

A parametric study of the UV-A photocatalytic oxidation of H2S over TiO2

A parametric study of the UV-A H2S photocatalytic oxidation over TiO2 P25 has investigated the influence of the TiO2 coating surface density, the total flow rate, the relative humidity, the temperature and the irradiance as main reaction parameters on the H2S conversion, the SO2 selectivity (targeted as low as possible), the duration without any SO2 release, and thus on the gas phase sulfur removal efficiency. The deepest non-illuminated internal TiO2 layers – even not photocatalytically active – could play a role in adsorbing SO2 and delaying its release into the gas phase, for explaining the behavior of high surface density TiO2 coatings. The Ti4+ surface sites have been proposed to act as active sites for the H2S photocatalytic oxidation, and general reaction pathways leading to the formation of SO2 in the gas phase and to surface sulfates have been hypothesized, involving photogenerated holes, sulfhydryl radicals or hydroxyl radicals. The role of active sulfate radicals has been put forward for explaining the behavior turn with time on stream on sulfate-deactivated TiO2, from a progressive deactivation into a complete H2S conversion to SO2. Finally, effective regeneration treatment with recovering of the initial activity could be performed by weakly basic washing.

Chronic methyl mercury poisoning may trigger endemic pemphigus foliaceus “fogo selvagem”

In endemic pemphigus foliaceus (EPF) or “fogo selvagem” the epidemiological evidence shows that all the described outbreaks occur on the banks of rivers where there is mercury contamination from alluvium gold mining and deforestation.Pathophysiological evidence shows a similarity to pemphigus induced by sulphydryl (SH−) drugs that act by denaturing cadherins at the desmosomal level, which are the pemphigus antigens. The sulfhydryl radical (SH−) call also thiol or mercaptans from the SH-drugs, act at the level of SH-groups of cystein as would the methyl mercury from the contaminated animals and fish in the diet of humans from endemic areas of pemphigus foliaceus. The methyl mercury would join the SH-groups from the cysteines amino acids from cadherin proteins in the skin. The autoimmune disease would only be triggered in genetically susceptible individuals with human leukocyte antigen HLA-DRB 1 haplotypes, just as Brown-Norway (BN) rats which are susceptible to develop Th2-dependent autoimmunity induced by metals. Immunological evidence from all the seroepidemiological studies could also be explained by binding mechanism of the methyl mercury to the SH-groups from the cysteines in the desmosomal cadherins proteins. The conclusion is that chronic methyl mercury poisoning is the most likely trigger of endemic pemphigus foliaceus “fogo selvagem”. To reduce the contamination of methyl mercury in the animals of the polluted rivers is pertinent to the design of campaigns and education programs with the population. Implement reforestation and biological control measures like phytoremediation technologies using decontaminant plants to decrease the methylation, and the process of biomagnifications of the methyl mercury in the Latin-America EPF foci.

Iron overload alters glucose homeostasis, causes liver steatosis, and increases serum triacylglycerols in rats

The objective of this study was to investigate the effect of iron overload with a hyperlipidemic diet on the histologic feature of hepatic tissue, the lipid and glycemic serum profiles, and the markers of oxidative damage and stress in a rat model. Twenty-four male Fischer rats, purchased from Experimental Nutrition Laboratory, Federal University of Ouro Preto, were assigned to 4 equal groups, 2 were fed a standard cholesterol-free diet (group C or control and CI or control with iron) containing 8.0% soybean oil and 2 were fed a hyperlipidemic diet (group H or hyperlipidemic and HI or hyperlipidemic with iron) containing 1.0% cholesterol and 25.0% soybean oil. A total of 50 mg of iron was administered to rats in groups CI and HI in 5 equal doses (1 every 3 weeks for a 16-week period) by intraperitoneal injections of 0.1 mL of iron dextran solution (100 g Fe(2+)/L; Sigma, St Louis, Mo). The other rats in groups C and H were treated in a similar manner but with sterile saline (0.1 mL). Irrespective of the diet, iron excess enhanced serum triacylglycerols (P < .05) and reduced serum glucose and glycated hemoglobin levels (P < .05) but did not affect serum cholesterol concentration. Histologic analysis showed steatosis in groups H and to a lesser extent in HI. No significant differences (P > .05) were observed in paraoxonase activities or in serum levels of free or total sulfhydryl radicals, malondialdehyde, or total antioxidants. The findings suggest that iron excess in the rat probably modifies lipid metabolism and, as a consequence, alters glucose homeostasis and increases the level of serum triacylglycerols but not of cholesterol.

The Sulfhydryl Radical (HS./S.−): A Contender for the Isomerization of Double Bonds in Membrane Lipids

The Sulfhydryl Radical (HS^./S^.−): A Contender for the Isomerization of Double Bonds in Membrane Lipids

The Sulfhydryl Radical (HS./S.−): A Contender for the Isomerization of Double Bonds in Membrane Lipids

Das biologisch wichtige Gas Schwefelwasserstoff ist eine Quelle für Radikale, welche die cis-trans-Isomerisierung ungesättigter Lipide in einer Vesikelsuspension katalysieren (siehe Bild). Dieses biomimetische Modell unterstreicht die Bedeutung der Doppelbindungskonfiguration bei Membranlipiden und ist für die Untersuchung der H2S-Aktivität (Schädigung und Signalgebung) in biologischen Systemen nützlich.

Flavin-induced photodecomposition of sulfur-containing amino acids is decisive in the formation of beer lightstruck flavor

Photooxidation of sulfur-containing amino acids and derivatives readily occurs upon visible-light irradiation in the presence of flavins. The sulfur moiety seems pivotal for interaction, as was determined from kinetic analyses using laser flash photolysis spectroscopy. After photooxidation, the resulting radical intermediates were characterized by addition to a spin trap, followed by electron paramagnetic resonance spectroscopy and evaluation of the coupling constants. The presence of the proposed radical intermediates was strongly supported by the identification of the reaction products using mass spectrometry. Accordingly, feasible degradation pathways for various sulfur-containing amino acids and derivatives were proposed. It was finally proven that flavin-induced photoproduction of sulfhydryl radicals and recombination with a 3-methylbut-2-enyl radical, derived from the photodegradation of hop-derived isohumulones, are decisive in the formation of beer lightstruck flavor.

Mechanisms of protection by pantoprazole against NSAID-induced gastric mucosal damage

The use of nonsteroidal anti-inflammatory drugs (NSAIDs) can be associated with severe adverse digestive effects. In clinical settings, proton pump inhibitors have proven to be effective in preventing and healing NSAID-induced gastroduodenal lesions. The present study investigates the mechanisms of protection afforded by pantoprazole against gastric injury induced by different NSAIDs in rats. Animals were orally treated with indomethacin (100 micromol/kg), diclofenac (60 micromol/kg), piroxicam (150 micromol/kg) or ketoprofen (150 micromol/kg). Thirty minutes before NSAIDs, animals received pantoprazole 6 or 60 micromol/kg orally. Four hours after NSAIDs, the following parameters were assessed: histomorphometric evaluation of gastric mucosal damage; gastric mucosal levels of myeloperoxidase (MPO), malondialdehyde (MDA), reduced glutathione as an index of non-proteic sulfhydryl compounds (GSH), and prostaglandin E2 (PGE2); mucosal cyclooxygenase-1 and -2 (COX-1, COX-2) mRNA expression by reverse transcription-polymerase chain reaction (RT-PCR). Separate experiments were carried out to assay the effects of pantoprazole on gastric acid secretion in pylorus-ligated rats. The in vitro influence of pantoprazole (1-10 microM) on the oxidation of low density lipoproteins (LDLs) induced by copper sulphate was also examined. All NSAIDs elicited mucosal necrotic lesions associated with neutrophil infiltration and reduction of PGE2 levels. Increments of MPO and MDA contents, as well as a decrease in GSH levels, were detected in the gastric mucosa of indomethacin-, piroxicam- or ketoprofen-treated animals. Indomethacin enhanced mucosal COX-2 expression, while not affecting COX-1. At the oral dose of 6 micromol/kg pantoprazole did not affect NSAID-induced mucosal damage, whereas at 60 micromol/kg it markedly reduced injuries provoked by all test NSAIDs. Pantoprazole 60 micromol/kg also reversed the effects of NSAIDs on MPO, MDA, and GSH mucosal contents, without interfering with the decrease in PGE2 levels or indomethacin-induced COX-2 expression. However, at both doses, pantoprazole inhibited acid secretion in pylorus-ligated rats. Furthermore, pantoprazole concentration dependently reduced the in vitro oxidation of LDLs. Our results suggest that besides inhibiting acid secretion, the protection afforded by pantoprazole against NSAID-induced gastric damage depends on a reduction in mucosal oxidative injury, which may also account for an increment of sulfhydryl radical mucosal bioavailability. It is also suggested that pantoprazole does not influence the down-regulation of gastric prostaglandin production associated with NSAID treatment.

Lansoprazole prevents experimental gastric injury induced by non-steroidal anti-inflammatory drugs through a reduction of mucosal oxidative damage

This study investigated the mechanisms of protection afforded by the proton pump inhibitor lansoprazole against gastric injury induced by different non-steroidal anti-inflammatory drugs (NSAIDs) in rats. Male Sprague-Dawley rats were orally treated with indomethacin (100 micromol/kg), diclofenac (60 micromol/kg), piroxicam (150 micromol/kg) or ketoprofen (150 micromol/kg). Thirty minutes before NSAIDs, animals were orally treated with lansoprazole 18 or 90 micromol/kg. Four hours after the end of treatments, the following parameters were assessed: gastric mucosal PGE2, malondialdehyde (MDA), myeloperoxidase (MPO) or non-proteic sulfhydryl compounds (GSH) levels; reverse transcription-polymerase chain reaction (RT-PCR) of mucosal COX-2 mRNA; gastric acid secretion in pylorus-ligated animals; in vitro effects of lansoprazole (1-300 micromol/L) on the oxidation of low density lipoproteins (LDLs) induced by copper sulphate. All NSAIDs elicited mucosal necrotic lesions which were associated with neutrophil infiltration and reduction of PGE2 levels. Increments of MPO and MDA contents, as well as a decrease in GSH levels were detected in the gastric mucosa of indomethacin- or piroxicam-treated animals. Indomethacin enhanced mucosal cyclooxygenase-2 expression, while not affecting cyclooxygenase-1. At the oral dose of 18 micromol/kg lansoprazole partly counteracted diclofenac-induced mucosal damage, whereas at 90 micromol/kg it markedly prevented injuries evoked by all test NSAIDs. Lansoprazole at 90 micromol/kg reversed also the effects of NSAIDs on MPO, MDA and GSH mucosal contents, without interfering with the decrease in PGE2 levels or indomethacin-induced cyclooxygenase-2 expression. However, both lansoprazole doses markedly inhibited acid secretion in pylorus-ligated rats. Lansoprazole concentration-dependently reduced the oxidation of LDLs in vitro. These results suggest that, besides the inhibition of acid secretion, lansoprazole protection against NSAID-induced gastric damage depends on a reduction in mucosal oxidative injury, which is also responsible for an increment of sulfhydryl radical bioavailability. It is also suggested that lansoprazole does not influence the down-regulation of gastric prostaglandin production associated with NSAID treatment.

Gastroprotective effects of pantoprazole against experimental mucosal damage

The present study investigated the gastroprotective effects of the proton pump inhibitor pantoprazole on gastric mucosal damage induced by ethanol-HCl in rats. Omeprazole was used as reference drug. The morphometric analysis of gastric histological sections revealed that pantoprazole and omeprazole dose-dependently prevented the necrotic mucosal injury evoked by ethanol-HCl (ED50 = 14.1 and 21.6 micromol/kg, respectively). These effects were associated with a marked increment of Alcian blue recovery from gastric bound mucus (ED50 = 18.8 and 29.3 micromol/kg, respectively). In addition, both pantoprazole and omeprazole inhibited gastric acid secretion in pylorus-ligated rats (ED50 = 1.5 and 3.3 micromol/kg, respectively). Further experiments indicated that the protective effects of pantoprazole were not modified by L-365,260 (a gastrin receptor antagonist), suramin (a drug able to interfere with endogenous growth factors), N(G)-nitro-L-arginine (an inhibitor of nitric oxide synthase) or systemic ablation of capsaicin-sensitive sensory nerves, whereas they were partly blocked by indomethacin (an inhibitor of prostaglandin synthesis) and fully prevented by N-ethylmaleimide (a potent blocker of sulfhydryl compounds). The present data provide histomorphometric evidence that: 1) pantoprazole is endowed with gastroprotective properties and is more active than omeprazole in preventing the necrotic mucosal damage induced by ethanol-HCl; 2) according to the rank order of ED50 values, the protective effects of both drugs appear to depend mainly on the enhancement of the gastric mucosal barrier rather than on the inhibition of acid secretion; 3) an increased production of prostaglandins, as well as an increased availability of sulfhydryl radicals at the level of the gastric mucosa may account for the gastroprotective effects of pantoprazole.

Reduction Potential of the Sulfhydryl Radical: Pulse Radiolysis and Laser Flash Photolysis Studies of the Formation and Reactions of ·SH and HSSH·- in Aqueous Solutions

Formation and reactions of the ·SH/·S- and HSSH·-/HSS·2- radicals in aqueous solutions have been studied by excimer laser flash photolysis and by pulse radiolysis. Acidic H2S solutions can be photolyzed with 193 nm laser pulses and produce a transient species with λmax at 240 nm, ascribed to the ·SH/·S- radical. Solutions of SH- can be photolyzed also with 248 nm laser pulses to produce the ·SH/·S- radical. The same radical is formed by oxidation of SH- ions with SO4·- and CO3·- radicals. At pH > 5, ·SH/·S- reacts with SH- (kf = 4 × 109 L mol-1 s-1, kr = 5 × 105 s-1) to form HSSH·-/HSS·2-, with λmax at 380 nm. Both ·SH/·S- and HSSH·-/HSS·2- react rapidly with O2; the former produces SO2·- (k = 5 × 109 L mol-1 s-1), and the latter produces O2·- (k = 4 × 108 L mol-1 s-1). Both radicals react with olefinic compounds. The monomeric radical oxidizes Fe(CN)64-, SO32-, ClO2-, and chlorpromazine. The dimeric radical is a weaker oxidant toward ferrocyanide but reduces N-methylpyridinium compounds. The reduction potential for the dimeric radical at pH 7 was determined from one-electron transfer equilibria with Mo(CN)83- and with the 4-methoxyaniline radical cation and found to be 0.69 V vs NHE. From the equilibrium constant K = [HSS·2-]/[SH-][·S-] = 8 × 103 L mol-1, the reduction potential for (·S-,H+/SH-) is calculated to be 0.92 V.

Carbonyl sulfide (OCS) and carbon monoxide (CO) in natural waters: evidence of a coupled production pathway

The mechanisms for the photoproduction of carbonyl sulfide (OCS) and carbon monoxide (CO) in natural waters were studied by evaluating experimental results from different aqueous systems. A coupled photoproduction mechanism was observed operating on CO and OCS. For CO photoproduction, the presence of a carbonyl group is necessary, while for OCS, a source of reduced sulfur in addition to the carbonyl is required. An acyl radical is postulated to be the key intermediary for OCS and CO photoproduction while a sulfur-centered radical (thiyl or sulfhydryl radical) is likely to be the key species that reacts with acyl radicals to produce OCS. Laboratory experiments indicated that addition of reduced sulfur to seawater and subsequent irradiation leads to a decrease in CO and an increase in OCS photoproduction rates relative to original water. Furthermore, treatment of Suwannee fulvic acid (SFA) or Aldrich humic (AH) aqueous solutions with sodium borohydride (NaBH4) decreased photoproduction of CO compared to untreated samples. A metal redox system (Ce(IV)/Ce(III)) was also used to generate radicals in solution and demonstrate radical participation in the production processes of OCS and CO. Based on these results, potential pathways are proposed for the photoproduction of both gases in natural waters involving the formation of free radicals. In natural waters, the anti-correlation CO/OCS is likely to be seen in areas with high biological productivity in which reduced sulfur compounds and dissolved organic matter are abundant. This study furthers our understanding of sulfur chemistry in aqueous systems and provides another demonstration of the complex link of the biogeochemical cycles of carbon and sulfur.

An Active Amide Group in the Molecule of Drugs That Induce Pemphigus: A Casual or Causal Relationship?

Traditionally, drugs that are capable of inducing pemphigus are divided into two main groups according to their chemical structure, in particular, the existence of a sulfhydryl group in their molecule. Thus, two groups are formed: (1) drugs containing a sulfhydryl radical (thiol drugs or SH drugs) and (2) nonthiol or other drugs. Much emphasis has been put on the role of the sulfhydryl group in the pathogenesis of drug-induced pemphigus. The effects of this group have been extensively studied, and a logical paradigm on the mode of its action has been created. However, no attempt has been made to search for other biochemical radicals which might have an influence on the activation/triggering of this disease. The aim of the present report is to draw attention to a chemical group common to the molecule of several drugs that have been associated with the induction of pemphigus. Careful analysis of the chemical structure of nonthiol drugs known to induce pemphigus revealed that several of them share an active amide group in their molecule. We believe that this group might be responsible for the induction of the disease; thus, a third group of drugs capable of triggering pemphigus can be formed, namely drugs containing an active amide group. Several drugs of this group are discussed.

Theoretical estimate of the enthalpy of formation of sulfhydryl radical (HSO) and HSO-SOH isomerization energy

The thermochemistry of HSO is of importance because this species is involved in the atmospheric oxidation of HS, one of the chemical processes that leads to acid rain. The enthalpy of formation of HSO is estimated to be [minus]5.4 [plus minus] 1.3 kcal/mol through a series of multireference configuration interaction (MR-CI) calculations that systematically expand the orbital basis set. The estimated value of [Delta]H[sub f][degrees] suggests that HSO may well be involved in a catalytic cycle that depletes ozone in the atmosphere. In contrast to all earlier theoretical studies, the computed energy difference between the HSO and SOH isomers is estimated to be 5.4 kcal/mol, with the HSO isomer being more stable. 21 refs., 2 figs., 1 tab.

Drug-Induced versus Drug-Triggered Pemphigus

112 cases of induced pemphigus were reviewed. The causative drugs were divided into three groups according to their chemical structure, and the clinical, prognostic and laboratory characteristics were analyzed and compared. Our literature screening indicates that the biological progress and clinical course of the disease depend upon the type of the inducing/triggering drug in the majority of patients. Patients with penicillamine-induced pemphigus or with pemphigus induced by SH drugs (drugs containing a sulfhydryl radical) showed spontaneous recovery in 39.4 and 52.6%, respectively, once the drug was discontinued. Patients whose pemphigus was induced by other drugs showed spontaneous recovery in only 15% of the cases. These results indicate that in patients with pemphigus induced by penicillamine (or SH drugs), the drug plays a major role in the pathogenesis of the disease, as compared to patients with pemphigus induced by other drugs. It seems that penicillamine (and SH drugs) actually induces pemphigus in most of the cases, whereas other drugs only trigger the disease in patients with a previous predisposition.