DNA fragmentation pattern induced in thymocytes by sulphur mustard

Michaelson, Samantha

doi:10.1016/s0009-2797(99)00155-6

Cited by 15 publications

(7 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One important reason of this toxicity is the reaction of SM with DNA, forming both DNA monoadducts and inter-strand cross links. These damages can lead to cell death by apoptosis [10][11][12]. Indeed, cells react to genotoxic damage by activation DNA damage signaling cascades and using specific DNA repair pathways for repairing it.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of JAK2 (V617F) Mutation in Iranian Veterans with Delayed Complications of Sulphur Mustard Poisoning

Reza

Hadi

Ayatollahi

et al. 2016

IJT

View full text Add to dashboard Cite

Background: Sulfur mustard was the most widely applied chemical warfare agent by the Iraqi army in Iran–Iraq war (1983-1988). Considering the role of sulfur mustard toxicity in hematopoietic neoplasms and also new role of JAK2 mutation in these neoplasms, we assessed this mutation and delayed hematologic complications in veterans exposed to sulfur mustard. Methods: This case control study was performed in Mashhad University of Medical Sciences, Mashhad, Iran in collaboration with Janbasan Foundation of Khorasan Razavi, Iran in 2012. The case group consists of 42 patients who exposed to sulfur mustard about 30 yr ago and the control group includes 30 healthy persons. For all subjects complete blood counts and ARMSpolymerase chain reaction for JAK2 (V617F) mutation was carried out. Data were analyzed by statistical software using independent sample t-testand Mann- Whitney U test. Results: JAK2 (V617F) mutation was detected, neither in the sulfur mustardveterans nor in the control group. Moreover no significant difference was detected in hematologic parameters between the two groups. Conclusion: Despite sulfur mustard can increase risk of tumor genesis especially hematologic neoplasms but this is probablyas result of other genetic mechanism apart from JAK2 mutation. Considering the health and importance of preventive measure for the sulfur mustard victims, we suggest other genetic aspects of tumor genesis to be assessed in these patients.

show abstract

Section: Discussionmentioning

confidence: 99%

Evaluation of JAK2 (V617F) Mutation in Iranian Veterans with Delayed Complications of Sulphur Mustard Poisoning

Reza

Hadi

Ayatollahi

et al. 2016

IJT

View full text Add to dashboard Cite

show abstract

“…Basal keratinocytes are cellular targets of SM (21). In vitro studies have demonstrated morphological characteristics of apoptosis in SM-exposed keratinocytes (22), endothelial cells (4), and thymocytes (15). However, less information is available regarding in vivo apoptosis of BC following SM cutaneous toxicity.…”

Section: Discussionmentioning

confidence: 99%

Sulfur Mustard-Induced Apoptosis in Hairless Guinea Pig Skin

Kan¹,

Pleva²,

Hamilton³

et al. 2003

Toxicol Pathol

View full text Add to dashboard Cite

The present study was aimed to examine whether apoptosis is involved in the pathogenesis of sulfur mustard (SM)-induced basal cell death. Skin sites of the hairless guinea pig exposed to SM vapor for 8 minutes were harvested at 3, 6, 12, 24, and 48 hours postexposure. Immunohistochemical detection of basal cell apoptosis was performed using the ApopTag in situ apoptosis labeling kit. Only occasional apoptotic basal cells (BC) were observed in nonexposed and perilesional control sites. At lesional sites, apoptosis of BC was not detected at 3 hours postexposure. However, at 6 hours and 12 hours postexposure, 18% and 59% of BC were apoptotic, respectively. At 24 and 48 hours postexposure, individual apoptotic basal cells were not clearly recognizable due to necrosis. At the ultrastructural level, degenerating BC exhibited typical apoptotic morphology including nuclear condensation and chromatin margination. The results suggest that apoptotic cell death is a cytotoxic mechanism with the number of BC undergoing apoptosis significantly increasing from 6 to 12 hours postexposure. In addition, because necrosis is preferential at 24 hours postexposure, we believe that SM-induced cell death involves early apoptosis and late necrosis, which temporally overlap to produce a single cell death pathway along an apoptotic-necrotic continuum.

show abstract

“…Apoptotic cells were also demonstrated after chemical stimuli. Apoptosis was observed, upon exposure to mustard gas and its derivatives, in cultured keratinocytes (24), endothelial cells (8) and cytoplasts (14), and thymocytes (13,17). In vivo studies have shown the appearance of apoptotic cells in mustard gas-exposed skin of weanling pigs (26).…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Topical Iodine Preparations Upon Heat-Induced and Hydrofluoric Acid-Induced Skin Lesions

et al. 2002

View full text Add to dashboard Cite

In this study, the protective prophylactic and post-exposure effects of novel topical iodine preparations were demonstrated upon heat- and hydrofluoric acid-induced skin lesions in the haired guinea pig. Prophylactic treatment of thermal bums with a liquid iodine preparation resulted in statistically significant reductions of 39% and 30%, respectively, in acute inflammation and hemorrhage-microscopic dermal parameters indicative of acute tissue damage. A clear trend of iodine-induced reduction in dermal necrosis occurred, and the epidermal healing markers, acanthosis and hyperkeratosis, were increased. Postexposure treatment of thermal burns with an iodine ointment preparation immediately after occurrence also conferred significant therapeutic reduction in parameters of tissue damage such as epidermal ulceration (87%), acute inflammation (58%), and hemorrhage (30%). Gross pathological evaluation showed that prophylactic and postexposure treatments with the liquid iodine preparation significantly reduced the heat-induced ulceration area by 97% and 65%, respectively. In addition, immediate treatment with an ointment iodine formulation significantly decreased the ulceration area by 98%; its tetraglycol vehicle also had a beneficial effect. Postexposure treatment with the iodine ointment proved efficacious upon hydrofluoric acid-induced skin burns. We observed statistically significant reductions of 76% and 68% in ulceration areas at intervals of 5 and 10 minutes between exposure and treatment, whereas a weaker effect was observed at a longer time interval of 15 minutes. Our findings suggest the therapeutic usage of these newly developed iodine preparations for thermally induced and hydrofluoric acid-induced skin burns.

show abstract

DNA fragmentation pattern induced in thymocytes by sulphur mustard

Cited by 15 publications

References 45 publications

Evaluation of JAK2 (V617F) Mutation in Iranian Veterans with Delayed Complications of Sulphur Mustard Poisoning

Evaluation of JAK2 (V617F) Mutation in Iranian Veterans with Delayed Complications of Sulphur Mustard Poisoning

Sulfur Mustard-Induced Apoptosis in Hairless Guinea Pig Skin

Protective Effect of Topical Iodine Preparations Upon Heat-Induced and Hydrofluoric Acid-Induced Skin Lesions

Contact Info

Product

Resources

About