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Results for “sulfur mustard”

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PubMed2026

Proteomic characterization of ocular tear fluid reveals preclinical markers of sulfur mustard toxicity.

Sulfur mustard (SM) vapor causes ocular injury after a short latent period, when molecular damage has occurred, but clinical signs are not yet apparent. Characterizing ocular responses during this early phase is important for understanding SM pathogenesis, identifying molecular readouts of injury progression, and developing biomarkers of exposure. Tear fluid is well-suited for this purpose because it can be collected noninvasively and captures responses from injured ocular tissues. We tested whether temporal changes in the tear fluid proteome reflect cellular and molecular responses to corneal SM exposure. Rabbits were exposed to SM vapor using a corneal vapor cap, and tear fluid was collected at baseline, 4 h, 1 d, and 5 d, corresponding to the latent period, acute lesion, and early recovery. A large proteomic response was detected at 4 h, involving extracellular injury signaling, epithelial injury, and innate immune activation. By 1 d, the tear fluid proteome transitioned to inflammatory cell activation with metabolic, redox, and proteostasis stress. By 5 d, evidence of acute injury response was reduced but the proteome retained a residual signature of immune, epithelial, and stress responses. This temporal progression is consistent with the molecular mechanisms of SM toxicity and provides insight into acute ocular vesicant injury. These findings establish tear fluid as a noninvasive molecular reporter of ocular SM injury progression. They also reveal a molecular signature of vesicant exposure, which emerges prior to clinical signs, and provide foundational data for developing tear-based biomarkers of chemical exposure, injury assessment, and therapeutic testing.

Animals↗

PubMed1979

[Treatment of psoriasis vulgaris with external sulfur mustard gas with particular reference to its potential carcinogenic risk. III. Clinical and experimental studies on the extent of percutaneous and inhalational uptake of sulfur mustard gas].

Concerning the often discussed carcinogenic risk of psoriasis treatment with 0.005% S-mustard-vaseline (so-called Russian Ointment) -- especially by inhalation -- 19 patients were treated with a radioactive labeled S-mustard-ointment and examined. The patients' whole bodies were inuncted for 1--2 days with about 50 g of radioactive S-mustard vaseline (U14C, 3 muCi/g). Afterwards the radioactivity was determined in the patients' expired air, blood, urine, and in their surrounding air. In three patients punch biopsy material from normal and psoriatic skin was assayed for radioactivity after combustion. In the skin, radioactivity distinctly decreased from the epidermis (13.1 pCi/mg) to the subcutis (0.77 pCi/mg) without significant differences between normal skin and psoriatic lesions as confirmed by autoradiography. In all samples of air, body fluids and tissue, definitive amounts of radioactivity were found, which, however, were far below the US-American MAK-values. Between skin surface and shirt, the values varied from 1.5 to 13.7 nCi/20 l air, at a distance of 2 meters by 0.3 nCi/100 l air, in the breath by 0.5 nCi/20 l. The radioactivity decreased to 1/10 of the maximum values after 1--2 hours. In blood the activity was at the limit of detection and was parallelled by the activity of the urine. Generally, 1--7% of the radioactivity applied to the skin was eliminated with the urine within one week. Thus, the carcinogenic risk may be very low in the external S-mustard therapy of psoriasis and other skin diseases.

Air↗

PubMed1975

Involvement of separate pathways in the repair of mutational and lethal lesions induced by a monofunctional sulfur mustard.

The mutagenic and lethal effects of a monofunctional sulfur mustard, 2-chloro-ethylethylsulfide (CEES), have been studied in a number of repair deficient variants of Escherichia coli K12, B/r and B. The results indicate that CEES induces a (pre)mutational lesion which is subject to Uvr+-excision-repair. Extensive CEES-induced mutagenesis can occur in exrA- uvrA- and recA- uvrB- variants suggesting that the majority of the mutations in Uvr-bacteria do not arise from error-prone repair. These findings are similar to results previously reported with a volatile degradation product of captan and with ethyl methanesulfonate (EMS) but differ from those reported with methyl methanesulfonate (MMS). It is hypothesized that CEES alkylates guanine at the O-6 position (R-O-6-G) and that this R-O-6-G which is Uvr+-excisable is directly mutagenic by producing G-C to A-T transitions during replication. Reduced levels of induced mutation frequencies observed in an endonuclease II-deficient variant lead us to postulate that, in constrast to Uvr- bacteria, CEES-induced mutation in wild-type cells arise from error-prone repair of apurinic sites. Analysis of the lethal actions of CEES indicates that the lesion produced is largely unexcisable by the Uvr+ system. Host-cell reactivation of CEES-treated TI bacteriophage shows that the production of the (pre)ethal lesion is dependent on both the initial dose and post-treatment incubation. The efficient repair of the (pre)ethal lesion requires both endonuclease II and polymerase I. Moreover, deficiencies of these two enzymes rendered bacteria more sensitive to the cytotoxic action of CEES. It is postulated that the lethal mechanism of CEES involves: (I) alkylation at the N-3 position of adenine and the N-7 position of guanine; (2) spontaneous depurination of these alkylated bases; and (3) production of apurinic sites which are lethal unless repaired by the endonuclease II-polymerase I excision-repair system.

Adenine↗

PubMed2026

Sulfonic Ion-Exchange Resins as Versatile Tools for the Oxidative Degradation of Chemical and Biological Hazardous Agents.

Commercial sulfonic styrene-divinylbenzene ion-exchange resins are activated with aqueous H2O2 to generate metal-free decontamination systems that combine strong Brønsted acidity with immobilized oxidizing capability. Among five tested materials, Amberlyst 15 dry showed the best performance in terms of oxidant immobilization capacity and promoting the oxidative degradation of the sulfur mustard simulant (2-chloroethyl)ethyl sulfide, CEES, and the organophosphorus pesticide malathion under very mild conditions. Control experiments with K2CO3-exchanged resin demonstrate that efficient decontamination requires the synergy between surface acidity and peroxide functionality. The activated resins also display rapid biocidal activity, strongly reducing viable Escherichia coli and Staphylococcus aureus and completely suppressing the infectivity of HSV-1 and SARS-CoV-2 within min. These findings identify peroxide-activated sulfonic resins as simple, sustainable, regenerable, and versatile tools for efficient combined hazardous chemical and biological decontamination.

Oxidation-Reduction↗

PubMed1976

[The importance of clinical observations for medical research].

Medical progress owes a great deal to the fundamental medical sciences and to the application of chemistry, physics and mathematics to medical problems. However, clinical observations and investigations are still of decisive importance in any field of medicine. By a feed-back mechanism they may even stimulate and fertilize fundamental medical sciences. Thus, our knowledge of the blood coagulation mechanism has been considerably enlarged by clinical analysis of hereditary bleeding disorders. - Chemotherapy of neoplastic diseases started from clinical observations during World War I (production of leucopenia by sulfur mustard gas). - Surgical procedures and their consequences have contributed greatly to our knowledge of thyroid function, of the segmental anatomy of the lung, and of the conduction system of the heart. - Observations of side effects of drugs have often enlarged or completely changed their primary clinical indications: from antibacterial sulfonamides, anti-diabetic, antihypertensive and powerful diuretic drugs have been developed, and from histaminics the modern neuroleptics and antidepressants. - Fundamental immunology has been enormously activated by clinical transplantation of kidney and bone marrow. Selective immunological defects in men, real experiments of nature, contributed much to our knowledge of the various types of allergic response. The quality of clinical investigations, particularly of controlled clinical trials, has been considerably improved during the last two decades. Although it is an applied science the reliability of its results is to-day comparable with that of "pure" natural sciences. However, medicine is more than a natural science: examples of outstanding scientists who at the same time were great and human physicians are presented.

Adrenal Cortex Hormones↗

PubMed1979

Mutagenicity and cytotoxicity of nineteen heterocyclic mustards (ICR compounds) in cultured mammalian cells.

The mutagenicity and cytotoxicity of 19 ICR compounds, including 6 reported previously, have been determined in the Chinese hamster ovary/hypoxanthine-guanine phosphoribosyltransferase system. As with other physical and chemical agents, ICR 170 and 191 exhibit a phenotypic expression time of 7 to 9 days, independent of concentrations tested. Thirteen of these compounds are mutagenic. At equimolar concentrations, the compounds with the tertiary amine-type side chain (ICR 217, 340, 355, 368, 170, and 292) are more mutagenic than the compounds with the secondary amine-type side chain (ICR 449, 371, 191, and 372). All secondary amine types show a "plateau" in their concentration-dependent mutagenesis curves at 3 to 4 microM. Shortening of the side chain by one carbon (ICR 171) results in a reduced mutagenicity. Substitution of a sulfur atom for a nitrogen in the side chain (ICR 342) increases both mutagenicity and cytotoxicity. The presence of two 2-chloroethyl groups on the side chain (ICR 220) also results in greatly increased cytotoxicity and mutagenicity. When the 2-chloroethyl group of ICR 340, 372, 292, 191, or 170 is replaced by a 2-hydroxyethyl group (ICR 340-OH, 372-OH, 292-OH, 191-OH, or 170-OH), a mutagenically inactive compound results which remains toxic. Replacement of the amine linkage with an ether linkage (ICR 283) also yields a mutagenically inactive compound.

Animals↗

PubMed1976

Effects of alkylation by dimethyl sulfate, nitrogen mustard, and mitomycin C on DNA structure as studied by the ethidium binding assay.

The extent of alkylation of DNA by dimethyl sulfate, nitrogen mustard, and the antibiotic mitomycin C is related to the resulting decrease in the fluorescence of intercalated ethidium. The fluorescence losses due to the first two types of reagents show a marked pH dependence, with greater losses of fluorescence being observed at alkaline pH values. At pH 11.6 the fluorescence shows a slow recovery, so that with low levels of methylation (4% deoxyguanosine residues modified) one observes complete return of fluorescence. We postulate that these phenomena are due to conversion of 7-methyldeoxyguanosine to the zwitterionic form, and partial denaturation of the DNA duplex with loss of ethidium binding sites. Hydroxide-ion-catalyzed imidazole ring opening, and the removal of the positive charge permits reannealing with concomitant return of the ethidium intercalation sites. This conclusion is substantiated by enzymatic hydrolysis of 14C-labelled methylated DNA and identifiions of the ethidium assay. The distinctly different behavior of mitomycin C confirms previous conclusions that its alkylation, preferentially on guanine, does not take part at the N-7 position.

Alkylating Agents↗