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Interaction of quinacrine mustard with mononucleotides and polynucleotides.

1. The interaction between quinacrine mustard and mononucleotides and polynucleotides was investigated by fluorimetry and absorbance spectrophotometry. 2. The fluorescence spectrum of quinacrine mustard is independent of the ionic strength and pH. The dependence of the quinacrine mustard fluorescence intensity on ionic strength, pH and anions is described. 3. The fluorescence intensity of quinacrine mustard was enhanced with the mononucleotide adenylic acid and polynucleotides such as poly(rA), poly(rU) and poly(rA,rU). 4. Quenching of the fluorescence intensity of quinacrine mustard occurred with the mononucleotide guanylic acid and with poly(rG) and poly(rC,rG). 5. The mononucleotide cytidylic acid or poly(rC) showed no effect on the fluorescence intensity of quinacrine mustard. 6. The interaction between the dye and native DNA species was also dependent on the presence of base-specific binding sites in the DNA. The higher the (G+C) content was in the native DNA tested the higher was the quenching effect on the fluorescence intensity of quinacrine mustard. 7. No interaction was found between the dye and methylated DNA. The binding between quinacrine mustard and apurinic DNA was confirmed to be in the phosphate groups of the purines.

Adult↗

Presynaptic effect of the aziridinium ion of acetylcholine mustard (methyl-2-acetoxyethyl-2'-chloroethylamine) on the phrenic nerve--rat diaphragm preparation.

The rat diaphragm has been used to investigate the neuromuscular blocking action of acetylcholine mustard which yields a potent nicotinic agonist, an aziridinium ion, in aqueous medium. Evidence was obtained that the acetylcholine mustard aziridinium ion impaired neuromuscular activity when the phrenic nerve was stimulated and that the ion did not directly inhibit muscle contraction. Impairment of neuromuscular activity was characterized by a latent period and depended both on the concentration of aziridinium ion and the frequency of stimulation of the phrenic nerve. Elevated concentrations of Ca-2+ and choline changed the response of the rat diaphragm to the aziridinium ion, the former increasing the rate of development of neuromuscular block and the latter protecting against neuromuscular block. These results indicated that the aziridinium ion may act either at the site of choline uptake or have an effect on acetylcholine synthesis in the nerve ending and that impairment of neuromuscular transmission in the rat diaphragm involved the availability of acetylcholine. Similar results were obtained with acetylcholine mustard aziridinium ion subjected to alkaline hydrolysis. This substance is thought to be choline mustard aziridinium ion. Although difficult to prove with the rat diaphragm it is possible that acetylcholinesterase of this preparation could hydrolyze acetylcholine mustard aziridinium ion at the neurotransmitter site and the resultant choline mustard aziridinium ion would interfere with the uptake of choline and eventually prevent neuromuscular transmission. This hemicholinium-like hypothesis for the mechanism of action of choline mustard aziridinium ion is compatible with reported date for toxicity of acetylcholine mustard aziridinium ion in the mouse.

Acetylcholine↗

[Mustard--an important food allergen?].

BACKGROUND: The European Parliament and the Council of the European Union have issued a new directive on information on the label about the ingredients present in foodstuffs. Twelve foods causing hypersensitivity are now subject to particularly strict labelling rules. Among these foods is mustard, which until now has been little recognised as a food allergen in Norway. MATERIALS AND METHODS: Literature searches in Medline were performed and supplemented by manual searches of reference lists. RESULTS: Since the first published case of mustard allergy in 1980, a number of case reports and patient series have been published. Most reports come from certain regions of France, and a majority of the studies have been performed by a limited number of investigators. Symptoms triggered by mustard cover the whole range from full-blown systemic anaphylactic reactions to pollen-food allergy syndrome-like local reactions. Frequently, reactions appear to be serious. Mustard allergy has on many instances been found in small children. Cross-reactivity apart from that among different types of mustard does not appear to be a clinical problem. Mustard allergens are resistant to heat and food processing. INTERPRETATION: With more attention being given to mustard as a food allergen because of the new labelling rules, it will most likely soon become apparent whether mustard is a food allergen of importance in Norway. The Norwegian national reporting system and register of severe allergic reactions to food will be an important tool in this context.

Cross Reactions↗

Mustard: a potential agent of chemical warfare and terrorism.

As one of the most important vesicant agents, the destructive properties of mustards on the skin, eyes and respiratory system, combined with a lack of antidote, makes them effective weapons. Such weapons are inexpensive, easily obtainable and frequently stockpiled. Sulphur mustard (mustard gas) has been used as a chemical warfare agent in at least 10 conflicts. In this article, the use of mustard as a potential agent of chemical warfare and terrorism is outlined. The dose-dependent effects of acute sulphur mustard exposure on the skin, eyes, and respiratory system are described, as well as the possible extents of injuries, the mechanisms of action and the long-term complications. Prevention and management of mustard exposure are briefly discussed. The need for awareness and preparedness in the dermatological community regarding mustard exposure is emphasized.

Adult↗

Topical nitrogen mustard in the management of mycosis fungoides: update of the Stanford experience.

OBJECTIVE: To evaluate and update the response and survival outcomes and toxic effects in patients treated with topical nitrogen mustard (mechlorethamine hydrochloride) as primary therapy. DESIGN: A single-center, retrospective cohort analysis. SETTING: Academic referral center for cutaneous lymphoma. PATIENTS: A total of 203 patients with mycosis fungoides (clinical stages I-III) treated with topical nitrogen mustard as initial therapy. MAIN OUTCOME MEASURES: Long-term actuarial survival, freedom-from-relapse, and freedom-from-progression results as calculated by the Kaplan-Meier method. RESULTS: The overall response rate for the 203 patients was 83%, with a complete response rate of 50%. The median time to achieve complete response was 12 months (T1, 10 months; T2, 19 months), and the median time to relapse was 12 months. The duration of complete response increased with longer maintenance therapy; however, after completion of therapy, the response duration or relapse rate was similar regardless of maintenance regimen. Patients with T1 disease had better response and survival outcomes than those with T2 disease, with overall and complete response rates in T1 of 93% and 65%, respectively, and in T2, 72% and 34%, respectively. A similar clinical response was seen for patients with stage IIA vs IB. Sixty-eight percent of 203 patients received only topical nitrogen mustard therapy throughout their follow-up course, including most of the patients who achieved an initial complete response. The clinical response to topical nitrogen mustard as salvage therapy was similar to initial response rates. The efficacy results were similar in patients treated with aqueous vs ointment preparations. Freedom-from-progression rates in T1 disease (no progression to higher T classification or worse clinical stage) at 5 and 10 years were 92% and 85%, respectively, and in T2, 83% at 5 and 10 years. Fewer than 10% of patients experienced contact hypersensitivity reactions when topical nitrogen mustard was used as an ointment preparation. Only 8 patients (4%) developed secondary cutaneous malignancy, none attributable to topical nitrogen mustard monotherapy. Pediatric patients experienced no significant toxic effects with topical nitrogen mustard therapy. CONCLUSIONS: Topical nitrogen mustard remains an effective primary initial or salvage therapy in mycosis fungoides for patients with T1 and T2 disease. Long-term follow-up results confirm its safety.

Administration, Topical↗

Cholinergic but not GABAergic neuronal markers are decreased in primary neuronal cultures treated with choline mustard.

Nitrogen mustard analogues of choline are potent irreversible inhibitors of high-affinity choline transport at the cholinergic presynaptic nerve terminal in vitro. Ethylcholine mustard aziridinium ion, and to a lesser extent choline mustard aziridinium ion, have been used as tools to chemically lesion cholinergic neurons in the central nervous system. The selectivity of these compounds as neurotoxins for cholinergic neurons in vivo has been questioned and the mechanism by which they mediate neuronal death has not been elucidated. The objective of the present study was to investigate the selectivity of choline mustard aziridinium ion on embryonic rat brain neurons maintained in primary culture. The effect of choline mustard aziridinium ion on levels of cholinergic neuronal markers was compared with markers for GABAergic neurons as a measure of neuronal specificity. Choline mustard aziridinium ion at 10 and 30 microM irreversibly inhibited hemicholinium-sensitive, high-affinity choline transport into the cultured neurons without altering sodium-dependent, high-affinity GABA transport. Similarly, incubation of the neurons for 30 min in the presence of 10 microM choline mustard aziridinium ion led to a decrease in choline acetyltransferase activity of the cultures which was maintained for 72 h; glutamic acid decarboxylase activity was not altered under the same experimental conditions. Protein and DNA content and DNA-to-protein ratios of the choline mustard aziridinium ion-treated cultures were monitored as indicators of generalized cellular damage.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Cardiac rhythm after Mustard repair and after arterial switch operation for complete transposition.

We compared the prevalence of arrhythmias among the first consecutive 45 patients with complete transposition (concordant atrioventricular and discordant ventriculo-arterial connexions) after arterial switch operation and the last 47 patients after Mustard repair in infancy. Both groups had 24-hour Holter electrocardiographic studies at similar periods of follow up (24 +/- 14 and 25 +/- 18 months). A second group of patients undergoing the Mustard procedure had been repaired at an older age before 1981. They were studied to determine the frequency of disturbances of rhythm during later postoperative follow-up (85 +/- 24 months). Symptomatic brady-/tachyarrhythmia syndrome never occurred after the arterial switch and only once in the group of patients repaired by the Mustard procedure in infancy, but developed at a late stage (69 +/- 28 months); five times in the group of patients having Mustard's repair at an older age. In addition, Holter monitoring did not detect bradyarrhythmias indicating sinus node dysfunction in a single patient after the arterial switch, but did so to a similar extent in both groups having the Mustard procedure (recent: n = 14; older: n = 18). Three cases of the group of older patients undergoing a Mustard operation developed complete atrioventricular block during follow-up. Normal findings were present in 93% of the cases after arterial switch, but in only 51% of the cases with a similar follow-up repaired by the Mustard procedure, and in 29% of the group having the Mustard repair at an older age.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗

Is ethylcholine mustard aziridinium ion a specific cholinergic neurotoxin?

The histopathologic effects of different doses of ethylcholine mustard aziridinium ion infused into the caudate-putamen complex or nucleus basalis were evaluated in rats. Although no non-specific tissue damage was observed at the lowest doses of ethylcholine mustard aziridinium ion examined--0.01 nmol in 1-microliter vehicle and 0.02 nmol in 2-, 5-, and 10-microliters vehicle in both the striatum and nucleus basalis--minimal but definite non-selective pathology, characterized by gliosis and loss of all neuronal elements in the region affected by the nitrogen mustard, was observed in both targets at a dose of 0.02 nmol 1 microliter and more severely at all doses containing 0.05 and 0.1 nmol ethylcholine mustard aziridinium ion. At doses of ethylcholine mustard aziridinium ion containing 0.2 nmol of the cytotoxin and greater amounts, non-specific cell loss in intact tissue and extensive cavitation became increasingly the most prominent histologic features of drug action. No statistically significant effects of ethylcholine mustard aziridinium ion on striatal choline acetyltransferase activities were found until doses of 0.4 nmol/1 microliter or greater were injected, concentrations of the cytotoxin at which appreciable non-specific pathology was also observed. Levels of dopamine in the caudate-putamen nucleus were reduced by comparatively greater amounts than choline acetyltransferase at doses of 2.5 nmol/2 microliters, 5.0 nmol/2 microliters and 10 nmol/2 microliters cytotoxin, but a significant effect of ethylcholine mustard aziridinium ion on striatal L-glutamate decarboxylase activity was found only at a dose of 10 nmol/2 microliters. As no dose of ethylcholine mustard aziridinium ion was found that reduced choline acetyltransferase without producing considerable non-specific tissue destruction, the usefulness of the cytotoxin in studying the behavioral and physiological consequences of selective cholinergic hypofunction in the brain must be questioned.

Animals↗

Intermediate outcome after Mustard and Senning procedures: A study by the Congenital Heart Surgeons Society.

Although atrial switch is rarely performed today except as part of a "double switch" operation, there continues to be interest in the long-term outcome of the procedure because of the many Mustard and Senning survivors who are in follow-up. In contrast to most other reported series on atrial switch, this study by the Congenital Heart Surgeons Society (CHSS) is a prospective multiinstitutional study of patients encountered in a relatively short time frame during the late 1980s. Between 1985 to 1989, 20 centers with surgeons belonging to the CHSS prospectively registered patients <15 days of age presenting with simple or complex transposition of the great arteries (TGA). The patients were assigned to protocol groups based on intent to treat (arterial switch, Mustard, or Senning). Data were abstracted in the Data and Analysis Center, which in most cases, conducted the annual follow-up. Among the 281 patients who had an atrial switch, there were 108 Mustard and 173 Senning procedures. For the combined atrial switch population, the survival at 1 month, 5 years and 10 years was 90%, 85%, and 84%, respectively. Results for the Mustard were better than for the Senning with survival at 1 month, 5 years, and 10 years being 96% versus 86%, 95% versus 80%, 93% versus 78%; (P <.001) for Mustard versus Senning. While the major mortality risk occurred in the first postoperative month for both groups, thereafter, the late rate of death from 1 to 10 years after operation was 0.78%/year Senning versus 0.23%/year Mustard (P <.05). TGA/ventricular septal defect (VSD), lower weight, younger age, cardiac positional anomalies, and procedures on the left ventricle (LV) outflow all correlated significantly with poor outcome. There were 19 reoperations including 2 for right ventricle (RV) failure, 12 for pathway obstruction, and 5 for baffle leak with a 36% overall mortality. Freedom from any pathway obstruction at 10 years was 95%. A permanent pacemaker was required in 21 patients with the significant risk factors including TGA/VSD and a Senning, and previous atrial septectomy. Freedom from a pacemaker insertion at 10 years was 91%. For both Mustard and Senning, 60% of patients were in New York Heart Association (NYHA) functional Class I with the remaining in Class II. This study of atrial switch outcomes by the CHSS suggests that the subgroup undergoing a Mustard procedure had better early and late survival than those undergoing a Senning operation. The overall incidence of baffle pathway obstruction was low though reoperation for this complication carried high risk. Serious arrhythmia requiring medication and the need for a permanent pacemaker were both relatively uncommon. The incidence of severe right heart failure was very low, although only 60% of patients are unrestricted in their activity. Copyright 2000 by W.B. Saunders Company

Journal Article↗

Bioassay of Estradiol Mustard for Possible Carcinogenicity (CAS No. 22966-79-6).

A bioassay of the experimental anticancer drug estradiol mustard for possible carcinogenicity was conducted by administering the chemical by gavage to Sprague-Dawley rats and B6C3F1 mice. Groups of 35 rats and 34-36 mice of each sex were administered estradiol mustard at one of the following doses, either 0.62 or 1.25 mg/kg body weight for rats and either 15 or 30 mg/kg body weight for mice. The vehicle used for the test chemical consisted of 0.05% polysorbate 80 in phosphate-buffered saline. The rats and mice were dosed three times per week for 52 weeks, then observed for an additional 30-34 weeks. Controls consisted of groups of 10 rats and 15 mice of each sex that were not administered the chemical (untreated controls) and also of groups of 10 rats of each sex, 14 male mice, and 16 female mice administered the vehicle alone (vehicle controls). Pooled controls were also used. All surviving rats were killed at 84-86 weeks and all surviving mice at 82-86 weeks. Mean body weights of male rats and male and female mice administered estradiol mustard were lower throughout the greater part of the study than those of corresponding vehicle or untreated controls; mean body weights of dosed female rats were unaffected. Administration of the test chemical had no significant effect on the survival of either male or female rats. A large number of dosed mice died prior to the end of the study. The numbers of dosed male mice which were at risk as long as 52 weeks were sufficient, however, for development of tumors appearing up to that time. Time-adjusted analysis and life-table analyses were applied to data obtained with the mice. In rats, no tumors were observed in a statistically significant incidence in the animals administered estradiol mustard. In mice, lymphoma or lymphocytic leukemia occurred at significant incidences in low-dose (P=0.018) and high-dose (P<0.001) groups of males compared with those in the pooled vehicle controls (controls 0/28, low-dose 6/32, high-dose 17/29) and at significant incidences in low-dose (P=0.020) and high-dose (P=0.002) groups of females compared with those in the corresponding vehicle controls (controls 0/14, low-dose 9/30, high-dose 11/23). In addition, the incidences of lymphoma were statistically significant for dose-related trend for both the males (P<0.001) and the females (P=0.003). Since lymphoma was observed in male mice as early as 25 weeks, life-table analyses of the incidence in each sex were performed. The results indicated a dose association (P=0.001) between the administration of estradiol mustard and the time of observation of lymphoma in either sex of mice. In mice, alveolar/bronchiolar adenoma or carcinoma occurred at a significant incidence (P=0.004) in the low-dose group of males compared with the pooled vehicle controls (controls 2/28, low-dose 12/30, high-dose 5/24) and at a significant incidence (P=0.022) in the low-dose group of females compared with the pooled vehicle controls (controls 1/28, low-dose 7/27, high-dose 1/18). Sarcoma of the myocardium similarly occurred at a significant incidence (P=0.015) in the low-dose group of males compared with the pooled vehicle controls (controls 0/28, low-dose 6/30, high-dose 2/24) and at a significant incidence (P=0.002) in the low-dose group of females compared with the pooled vehicle controls (controls 0/28, low-dose 8/27, high-dose 1/12). The survival of both high-dose males and high-dose females was slightly lower than that of the respective low-dose groups and may account for the higher numbers of pulmonary tumors and myocardial sarcomas among low-dose mice of both sexes. The association of myocardial sarcoma with administration of the chemical in both dosed groups of each sex is strengthened by the fact that these tumors of the myocardium have not occurred in the more than 500 male and 500 female historical-control mice of this strain at the laboratory. Squamous cell carcinoma of the stomach occurred in the dosed male mice (high-dose 2/29) and in the dosed female mice (low-dose 2/26, high-dose 2/14) but was absent in all controls. Although the incidences in this bioassay were too low to be statistically significant, the fact that no squamous-cell carcinomas of the stomach have occurred in the more than 500 male and 500 female historical-control mice of this strain at this laboratory indicates that these gastric tumors were related to the administration of the estradiol mustard. It is concluded that under the conditions of this bioassay, estradiol mustard administered in a buffered saline vehicle was not carcinogenic in Sprague-Dawley rats. Estradiol mustard was carcinogenic in both male and female B6C3F1 mice, inducing lymphoma, sarcoma of the myocardium, alveolar adenoma or carcinoma, and squamous-cell carcinoma of the stomach. Levels of Evidence of Carcinogenicity: Male Rats: Negative Female Rats: Negative Male Mice: Positive Female Mice: Positive Synonym: estradiol, bis((p-bis(2-chloroethyl)-amino)phenyl)acetate

Journal Article↗

The effects of a benzoic acid mustard derivative of distamycin A (FCE 24517) and related minor groove-binding distamycin analogues on the activity of major groove-binding alkylating agents.

The distamycin derivative FCE 24517 is a potent antitumour agent. Efforts have been made towards elucidating the mechanism of action of this compound which, to date, have highlighted a high level of DNA sequence specificity for covalent adduct formation. Compared to classical alkylating agents, FCE 24517 forms very few covalent adducts with double-stranded DNA, and thus appears to be a weak alkylating agent. Examination of the effects of this minor groove-binding agent on the major groove of DNA have been facilitated by use of the alkylating agents mustine, melphalan, dabis maleate, quinacrine mustard and uracil mustard. Pretreatment of plasmid DNA with FCE 24517 followed by reaction with any one of these mustards gave rise to a marked abolition of N-7 guanine adduct formation, as assayed by Maxam and Gilbert sequencing gels. The smallest effect was seen for quinacrine mustard, whereas total abolition of N-7 guanine alkylation was seen with uracil mustard. Using related structural analogues of FCE 24517 in the same experiments, it was not possible to reproduce this effect, with very few exceptions. Some effects were seen when using distamycin A itself in these experiments, although these were marginal compared to those seen for FCE 24517. We were able to extrapolate our findings to a whole cell system using murine L-1210 leukaemia cells. Alkaline elution experiments showed that treatment of cultured cells with FCE 24517 followed by either mustine or uracil mustard caused a marked inhibition of DNA interstrand crosslink formation, compared to treatment with mustine or uracil mustard alone. The present study has demonstrated the marked effect that FCE 24517 has upon the reactivity of double-stranded DNA, an effect possibly separate from that of its alkylating function. This study has highlighted the complex nature of the DNA interactive compound FCE 24517 which possess potent and broad spectrum antitumour activity.

Alkylating Agents↗

Mustard gas: clinical, toxicological, and mutagenic aspects based on modern experience.

Based on a study of the literature and our own experience treating fisherman poisoned by mustard gas, this article outlines the clinical effects, and toxicological and mutagenic properties of the agent. Mustards are very persistent chemical agents that easily penetrate clothing. Mustard gas usually causes clinical symptoms after the liquid penetrates the skin or the vapor is inhaled. Skin lesions are similar to first- or second-degree burns and usually heal spontaneously in 4 to 6 weeks. Eye symptoms are photophobia and reduced vision. Following inhalation of the agent, pulmonary edema and long-term dyspnea may be seen. As mustard gas is an alkylating substance, it is conceivable that the risk of developing cancer may be increased, as observed in people who were involved with the production of mustard gas and in animals exposed to the gas. Also, transient significantly increased sister chromatid exchange rates have been found in fishermen exposed to mustard gas. Patients exposed to mustard gas must be treated immediately after exposure. Treatment should consist of cleaning of the exposed skin and clothes with an antigas powder and water and soap. The skin lesions should be treated as burns. Eye lesions and respiratory problems should be treated symptomatically.

Eye Diseases↗

Results of a randomized study comparing DTIC with TIC mustard in malignant melanoma.

This prospective randomized Eastern Cooperative Oncology Group (ECOG) study (1071) was designed to compare a new and promising cytotoxic agent TIC Mustard (triazeno imidazole carboxamide mustard, NSC 82196) with DTIC (dimethyl triazeno imidazole carboxamide, NSC 45388) in the treatment of inoperable melanoma. One hundred and seventy-eight patients were randomized to receive either DTIC (150 mg/m2/day X 5) or TIC Mustard (800 mg/m2/day X 5). Of this group 145 patients were evaluable for tumor response at the completion of the study. Objective responses were seen in 15/79 (19.0%) DTIC patients and 4/66 (6.1%) TIC Mustard patients. Adjustment of crude response rates yielded final response rates of 18.2% for DTIC patients and 5.8% for TIC Mustard. These differences were significant at the p less than or equal to .03 level. Median response duration was 15 weeks for the DTIC responders and 4 weeks for the TIC Mustard responders. Responders and nonresponders did not differ significantly in any of the standard prognostic categories. However, responders had a significantly longer median survival (47.5 weeks) compared to that for nonresponders (17.8 weeks). Toxicity was tolerable for either drug and no deaths were ascribed to either. We conclude that TIC Mustard has limited usefulness in the treatment of malignant melanoma and is less effective than DTIC.

Clinical Trials as Topic↗

Utilization of mustard waste isolates for improved production of astaxanthin by Xanthophyllomyces dendrorhous.

Astaxanthin production in the wild strain Xanthophyllomyces dendrorhous TISTR 5730 was investigated using different mustard waste media, including mustard waste residue extract (MRE), mustard waste residue hydrolysate (MRH), mustard waste precipitated extract (MPE), and mustard waste precipitated hydrolysate (MPH). The growth of X. dendrorhous and the production of astaxanthin were dependent on the type and initial concentrations of mustard waste media. The MPH medium was the best substrate resulting in yields of biomass and astaxanthin of 19.6 g/L and 25.8 mg/L, respectively, under optimal conditions. MPH medium improved astaxanthin production 11-fold compared to the commonly used commercial yeast malt medium, and 1.3-2.1-fold compared to other mustard waste media.

Basidiomycota↗

Quantification of sulfur mustard-induced DNA interstrand cross-links and single-strand breaks in cultured human epidermal keratinocytes.

The induction of DNA interstrand cross-links and their repair has been studied in cultured human epidermal keratinocytes exposed to sulfur mustard, bis-(beta-chloroethyl)sulfide. Alkaline elution is the most sensitive method to determine the number of DNA interstrand cross-links quantitatively. However, in the case of sulfur mustard the reliability of these data will be less since sulfur mustard also induces DNA single-strand breaks (SSB) and/or alkali-labile sites (ALS). The frequency of SSB and/or ALS induced by sulfur mustard is determined immunochemically. Correction for the induction of SSB and/or ALS induced by sulfur mustard resulted in a substantial increase in the calculated number of cross-links. Our results indicate that per microM sulfur mustard approximately 0.05 SSB (and/or ALS)/10(9) Da of DNA and approximately 0.12 cross-links/10(9) Da of DNA were induced immediately after exposure. Most of the DNA interstrand cross-links are removed during the first 24 h post exposure, but a small number of lesions seem to be persistent. In cells exposed to sulfur mustard concentrations as low as 1 microM, repair seems to occur not at all.

Cells, Cultured↗

Optimisation of solvent desorption conditions for chemical warfare agent and simulant compounds from Porapak Q using experimental design. Part 2: Extraction of sulphur mustard from steel and glass Porapak tubes.

The vesicant chemical warfare (CW) agent sulphur mustard remains a hazard to personnel involved in demilitarisation activities. Sampling tubes containing Porapak Q are used to measure personal exposure to sulphur mustard vapour. Presented here is an evaluation of the solvent desorption parameters employed to remove sulphur mustard from steel and glass tubes containing Porapak Q. Statistical experimental design was used to elucidate the influence of solvent type, tube type, solvent volume and sonication time on sulphur mustard recovery. The order of increasing recovery was established as iso-octane < hexane = isopropyl alcohol. The same degree of sulphur mustard is recovered on both steel and glass tubes using hexane or isopropyl alcohol, with hexane exhibiting quantitative recovery. The sorbent mass (50 mg) should be increased when using steel tubes as breakthrough has been demonstrated. Given the inert nature of hexane towards sulphur mustard, its favourable chromatographic properties for splitless injection, and its greater recoveries, this solvent should be used for elution of Porapak Q tubes for quantitative analysis of sulphur mustard.

Chemical Warfare Agents↗

Ca2+ homeostasis and Ca2+ signalling in sulphur mustard-exposed normal human epidermal keratinocytes.

To investigate the role of increased cytoplasmic free calcium levels ([Ca]i) in sulphur mustard-induced cellular toxicity, the [Ca]i of human epidermal keratinocytes exposed to sulphur mustard concentrations between 50 and 800 microM were measured. No early increase in [Ca]i was observed during the first 20 min after application of the agent. Furthermore, at 3, 6 and 24 h after exposure to sulphur mustard, the [Ca]i of sulphur mustard-exposed cells differed only slightly from that of control cells. However, sulphur-mustard exposed cells responded with a weaker rise of [Ca]i upon stimulation with histamine and ATP than control cells. These results suggest that sulphur mustard can induce small increases in [Ca]i, which reflect abnormal cellular physiology rather than acute toxicity. In addition, it has been shown that sulphur mustard disturbs cellular Ca2+ signalling in human epidermal keratinocytes.

Calcium↗

Involvement of excitatory amino acid receptors and nitric oxide in the rostral ventromedial medulla in modulating secondary hyperalgesia produced by mustard oil.

We have recently reported a model of secondary hyperalgesia in which facilitation of the thermal nociceptive tail-flick reflex following topical mustard oil is largely dependent on descending influences from the rostral ventromedial medulla (RVM). The current study was designed to examine a potential role for excitatory amino acid receptors and nitric oxide in the RVM in modulating this hyperalgesia. Topical application of mustard oil (100%) to the lateral surface of the hind leg of awake rats produced a short-lived (60 min) facilitation of the tail-flick reflex that was dose-dependently attenuated by microinjection of the selective N-methyl-D-aspartate (NMDA) receptor antagonist APV (1-100 fmol) into the RVM. Microinjection of a greater dose of APV (1000 fmol) into the RVM produced a significant inhibition of the tail-flick reflex in the presence, but not absence, of mustard oil. In contrast, microinjection of the non-NMDA receptor antagonist DNQX (10 nmol) into the RVM further enhanced the magnitude and duration of the hyperalgesic response, and produced a facilitation of the tail-flick reflex following injection into the RVM of naive animals. Similar to APV, microinjection of the nitric oxide synthase inhibitor L-NAME (100-1000 nmol) into the RVM attenuated mustard oil hyperalgesia, while the greatest dose (1000 nmol) produced a significant inhibition of the tail-flick reflex in the presence, but not absence, of mustard oil. A role for nitric oxide synthase in the RVM in mustard oil hyperalgesia was further demonstrated by a significant increase in the number of NADPH-d labeled cells in the RVM at the time of maximal hyperalgesia. Involvement of NMDA receptors and nitric oxide in the RVM in descending nociceptive facilitation was supported by the observation that microinjection of either NMDA or the NO* donor GEA 5024 into the RVM of naive animals dose-dependently facilitated the tail-flick reflex. The hyperalgesia produced by NMDA injection into the RVM was blocked by prior intra-RVM injection of either APV or L-NAME. These results support the notion that secondary hyperalgesia produced by mustard oil involves concurrent activation of dominant descending facilitatory, as well as masked inhibitory systems from the RVM. Additionally, the data suggest that descending facilitation involves activation of NMDA receptors and production NO* in the RVM, whereas inhibition involves activation of non-NMDA receptors in the RVM.

Animals↗