Evidence for the inactivation and repair of the mammalian DNA template after alkylation by mustard gas and half mustard gas.
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The principles of complex, ecologically-safe technology for the destruction of battle gas mustard were worked out. This technology was based on the reaction alkaline detoxication of mustard; the major component of reaction mixture obtained after detoxication was thiodiglycol. Thorough thiodiglycol mineralization was achieved by electrochemical treatment. Electrolysis products were biologically utilized in biosorber.
BACKGROUND: During the Iraq-Iran war (1980-1988), 535 patients who were exposed to mustard gas (one of the chemical warfare agents used by Iraq) were referred to our dermatology department. In this article, we have tried to review the skin manifestations of these patients. OBSERVATIONS: The skin lesions were of early or late onset. The early onset lesions consisted of erythema (76%), bulla (55%), and purpura (1.1%). These lesions were mostly found on the face and skin folds. The late-onset manifestations were pigmentation (20.4%) and desquamation (11.2%). Other complications were ophthalmic (85%), pulmonary (15%), and gastrointestinal (10%). Lymphopenia (7%) was the most serious laboratory disorder reported. Biopsy specimens of the lesions showed subepidermal bullae with mild dermal and epidermal necrosis. CONCLUSIONS: All patients were treated as for burns using sulfadiazine and furacine. All patients were cured in a period of 15 to 45 days. During a 6-month follow-up, no mortality was observed.
Mustard gas (MS) has been used in chemical warfare since World War I. The blistering skin lesions are slow to heal. Secondary inflammation might occur, as well as damage to organs distant from the original wound. Presently there is no specific antidote for burns and poisoning by MS. This study examined treatment modalities with free oxygen radical scavengers, copper-zinc, and manganese superoxide dismutase (SOD), for MS skin burns in an experimental guinea pig model. Each of the SOD compounds reduced dramatically burn lesion area when administered intraperitoneally/intralesionally (i.p./i.l.) before wound infliction. The protective action of the SODs was also evident in the significantly higher histopathological score of biopsies obtained on day 7 from local tissue, caused with the lower dose of MS. When the SOD compounds were administered i.p. 1 hour after burn infliction, and repeated daily for 7 days, no protective effect could be detected under the present experimental conditions.
Mustard gas (MG) is a mutagenic and carcinogenic alkylating agent, and is a known risk factor for occupational lung cancer. Our hypothesis is that lung cancers from MG workers contain mutations (G:C to A:T transitions) as the result of MG-produced DNA promutagenic adducts in the p53 tumor suppressor gene. We analyzed 12 primary lung cancers from Japanese MG factory workers and 12 lung cancers from non-exposed individuals. Genomic DNA was isolated from archival paraffin-embedded tissues. Exons 5-8 were amplified by polymerase chain reaction using p53-specific primers, and sequenced by dideoxy termination methods. Six out of 12 lung cancers from MG workers contained a total of eight somatic point mutations: two cases had double G:C to A:T transitions; one had a G:C to T:A transversion; one case had an A:T to G:C transition; and two cases had single base deletions. Four of the six mutated purines occurred on the non-transcribed, DNA-coding strand. Out of 12 unexposed cases, there were six single base mutations in six cancers, and no double mutations. The p53 mutational frequency in the MG-exposed cases is similar to the non-exposed controls and the usual smoking-related lung cancers reported previously. However, the distinctive double mutations (G:C to A:T transition) observed in two cases are unusual and may be related to MG exposure.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Chemical agents such as mustard gas (or sulfur mustard), which has alkylating characteristics, were used against Iranian combatants in the Iraq-Iran war. Previous studies have not shown a strong link between these chemical agents and the development of chronic myelocytic leukemia (CML). The purpose of this study was to evaluate the increased risk of CML development in Iranian soldiers exposed to mustard gas during the war. Based on a descriptive study of 2,500 cases with documented exposure to various chemical warfare agents, 665 patients had documented exposure to mustard gas. We screened the latter using the leukocyte alkaline phosphatase (LAP) test and performed further cytochemical studies on cases with positive results. From among the 665 cases with documented exposure to mustard gas, 9 cases had LAP scores < 20; 2 of these 9 cases had CML and a score of zero (0.3%). We detected cytogenetic abnormalities in 7 patients with low LAP scores and atypical lymphocytes of 5-11% in 40 patients. The risk ratio of CML developing in victims exposed to mustard gas (cutaneous or respiratory) may be higher in comparison with the normal population, although confounding factors (e.g., the possibility of exposure to combined chemical agents, excluding patients who did not manifest blisters) limited our results. Because the increased development of CML in young patients with a documented history of exposure to mustard gas cannot be disregarded, further studies are needed.
RATIONALE: Mustard gas primarily affects the eyes, skin, and particularly the respiratory tract. Tracheobronchomalacia (TBM) and air trapping are often observed in high-resolution computerized tomography (HRCT) scans of the chest of mustard gas-exposed patients. OBJECTIVES: To examine the frequency and severity of TBM in a group of Iranian wartime mustard gas-exposed victims, and to investigate the correlation between TBM and air trapping in these cases. MATERIALS AND METHODS: Chest HRCT films obtained from 300 randomly selected subjects who had been exposed to mustard gas 15.5 yr previously were reviewed to determine the existence of TBM and air trapping. The HRCT films of a healthy control group were also analyzed for comparison. RESULTS: Out of 300 reviewed cases, 13 had TBM. From these 13 TBM cases, 11 (85%) showed air trapping with mean score of 5.5. In the control group, 5 (25%) of 20 subjects showed air trapping, with mean score of 0.6. The total air trapping was significantly higher in the TBM group (p < 0.001). There was an association between the severity of tracheomalacia and air trapping in the TBM group (p = 0.01, r = 0.69), but no association was observed between severity of bronchomalacia and air trapping. CONCLUSION: The results show that air trapping and TBM are correlated, both as long-term sequelae in mustard gas-exposed cases. Because air trapping is highly suggestive of bronchiolitis obliterans, we conclude that both bronchiolitis obliterans and TBM are caused by a single underlying process affecting small and large airways, respectively, in this group of patients.
Explore the source record for details and available documents.
Mustard gas induces inactivation and mutation in yeast. Both effects are dose-proportional, indicating single-hit events. Induction of both effects is influenced by the cell's capacity for DNA dark-repair, whereby the probability of reversion is highest in repair-proficient cells. Binding of mustard gas to cells and probably to DNA is independent of DNA-repair systems. The number of inter-strand cross-links, as determined by assaying for renaturability of alkalidenatured DNA, increases in a dose-proportional manner. At 37% survival an excision-deficient strain contains 55 inter-strand cross-links. Chromatographic analysis yields several alkylation products of DNA. Their relative frequencies resemble the values reported for E. coli and bacteriophage T7.
BACKGROUND: Mustard agents are of the major chemical agents used during Iran-Iraq war. There are no reports concerning long-term cardiac effects. The aim was to assess the scintigraphic pattern of myocardial perfusion in patients intoxicated with blistering gases. METHOD: We analyzed myocardial perfusion scans of 22 consecutive intoxicated patients (21 male and 1 female, all < 44 years) and compared results with 14 controls. Only those patients and controls were entered whose 10-year risk of coronary artery disease (Framingham criteria) was <5%. Also only those patients were experimented upon that had currently other confirmed complications of intoxication (respiratory, cutaneous and ocular complications). All patients underwent a 1-day stress and rest protocol using (99m)Tc-MIBI. Images were assessed visually and quantitatively using Cedars Sinai program. RESULTS: The prevalence of nonhomogeneity of uptake and left and right ventricular enlargement in both visual and quantitative analyses were higher in the mustard exposed patients than unexposed controls. The prevalence of ischemia was higher in the exposed patients (P < 0.05). Cavity to myocardium ratio, as an established and validated measure of ejection fraction, was also significantly lower in the warfare patients than the controls. CONCLUSION: In so far it lies in our knowledge, this is the first report concerning the scintigraphic pattern of myocardial perfusion in mustard intoxicated patients. Based on the results, the pattern of myocardial perfusion in these patients is significantly different from normal controls, which could resemble either coronary artery disease or mild cardiomyopathic changes.
Sulfur mustard is a chemical warfare agent which was widely used during World War I and more recently in conflicts in the Middle East. This highly toxic compound causes severe dermal, gastrointestinal, respiratory and ocular injuries. It acts as an alkylating agent that induces structural changes and, hence, destruction of nucleic acids and proteins, impairing the cell's normal homeostasis and eventually causing its death. Sulfur mustard reacts rapidly with ocular tissues, and after a latent period of a few hours the patient starts suffering from severe eye pain, photophobia, excessive lacrimation and blindness. The injury, which is restricted to the anterior segment of the eye, may cause long-lasting incapacity in large numbers of casualties. Approximately 0.5% of the severely wounded victims may develop late complications which require prolonged ophthalmologic observation and therapy. In light of the ever-present threat of mustard chemical warfare against military and civilians, physicians worldwide should be aware of its grave effects and know how to care for its victims.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.