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A review on symptoms, treatments protocols, and proteomic profile in sulfur mustard-exposed victims
Yunes Panahi1, Amir H Abdolghaffari2,3, Amirhossein Sahebkar4
1Chemical Injuries Research Centre, Baqiyatallah University of Medical Sciences, Tehran, Iran.
Abstract:
Sulfur mustard (SM) as an alkylating and vesicating agent was used for 100 years as a chemical weapon. SM as bi-functional mustard can attacks and alkylates lots of biomolecules. Different cellular mechanism and molecular pathways are responsible for damages to body tissues. Such as DNA damages, oxidative stress, Apoptosis, and inflammation. Sulfur mustard penetrated body organs and induces long term eye, skin, lung, gastrointestinal, urogenital damages and can cause carcinogenic and mutagenic consequences. Currently there is no definitive treatment protocol for SM exposed patients. The goal of treatment is relieving the symptoms with fast healing rate and retrieval of damaged tissues to normal function and appearance in short period of time. Evaluation of proteomics profile in SM-exposed victims has been performed in animal model and human patients. These studies revealed that different protein were involved in the patients with SM damages to skin and lungs. Apolipoprotein A1, type I cytokeratins K14, K16 and K17, S100 calcium-binding protein A8, α1 haptoglobin isoforms, Amyloid A1, albumin, haptoglobin, and keratin isoforms, immunoglobulin kappa chain are defined expressed proteins in the damaged tissues.
Insights
Sulfur mustard (SM) exposure causes severe tissue damage through alkylation. Proteomics studies identified key proteins like Apolipoprotein A1 and keratins involved in skin and lung injuries, aiding in understanding treatment needs.
Area of Science:
- Toxicology
- Proteomics
- Biochemistry
Background:
- Sulfur mustard (SM) is a potent alkylating and vesicating chemical warfare agent with a history of use.
- SM causes widespread cellular damage via DNA alkylation, oxidative stress, apoptosis, and inflammation.
- Long-term health consequences include chronic damage to eyes, skin, lungs, and other organs, with carcinogenic and mutagenic potential.
Purpose of the Study:
- To investigate the proteomic alterations in tissues affected by sulfur mustard exposure.
- To identify specific proteins indicative of SM-induced damage in skin and lung tissues.
- To inform the development of targeted treatments for SM-exposed individuals.
Main Methods:
- Proteomic analysis of tissue samples from animal models and human patients exposed to sulfur mustard.
- Comparative analysis of protein expression profiles in damaged versus healthy tissues.
- Identification and quantification of differentially expressed proteins.
Main Results:
- Proteomic profiling revealed significant changes in protein expression in SM-affected tissues.
- Key proteins identified include Apolipoprotein A1, cytokeratins (K14, K16, K17), S100 calcium-binding protein A8, haptoglobin, Amyloid A1, albumin, and immunoglobulin kappa chain.
- These proteins are implicated in the inflammatory and tissue repair responses following SM exposure.
Conclusions:
- Proteomic analysis provides valuable insights into the molecular mechanisms underlying sulfur mustard toxicity.
- Identification of specific biomarkers can aid in assessing damage severity and guiding therapeutic strategies.
- Further research into the role of these proteins may lead to effective treatments for SM injuries.
