A Combination Drug Treatment Against Ocular Sulfur Mustard Injury

Babin, Michael C.; Ricketts, Karen M.; Gazaway, M; Lee, Robyn B.; Sweeney, Richard E.; Brozetti, J.

doi:10.1081/cus-120027483

Cited by 12 publications

(13 citation statements)

References 12 publications

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“…Management of delayed ocular symptoms is medical and surgical. These treatments are artificial tears and lubricants, anti‐inflammatory drugs, immunomodulatory drugs, human blood‐derived therapy, amniotic membrane transplantation, tarsorrhaphy, stem cell transplantationand corneal transplantation …”

Section: Treatment Protocols In Sm Exposed Victimsmentioning

confidence: 99%

A review on symptoms, treatments protocols, and proteomic profile in sulfur mustard‐exposed victims

Panahi

Abdolghaffari

Sahebkar

2017

J of Cellular Biochemistry

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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.

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Section: Treatment Protocols In Sm Exposed Victimsmentioning

confidence: 99%

A review on symptoms, treatments protocols, and proteomic profile in sulfur mustard‐exposed victims

Panahi

Abdolghaffari

Sahebkar

2017

J of Cellular Biochemistry

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“…Various studies were performed on the rabbit eye to assess the treatment regime in SM-exposed eyes [Amir et al, 2000[Amir et al, , 2003Babin et al, 2004;Kadar et al, 2014] as mentioned above. Various studies were performed on the rabbit eye to assess the treatment regime in SM-exposed eyes [Amir et al, 2000[Amir et al, , 2003Babin et al, 2004;Kadar et al, 2014] as mentioned above.…”

Section: Management Of Acute Ocular Lesionsmentioning

confidence: 99%

Ocular Effects of Sulfur Mustard and Therapeutic Approaches

Panahi

Rajaee

Sahebkar

2017

J of Cellular Biochemistry

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Sulfur mustard (SM) is a strong blistering, highly reactive, lipophilic chemical war agent that causes injury in different organs including the skin, eyes, and respiratory tract. The Eyes are especially susceptible to the consequences of SM poisoning because of the aqueous and mucosal nature of conjunctiva and cornea. DNA alkylation and depletion of glutathione, are the most important mechanisms of SM action in the eye injuries. Acute clinical symptoms are including decrease in visual acuity, dryness, photophobia, blepharospasm, conjunctivitis, and complaints of foreign body sensation and soreness that gradually progress to severe ocular pain. Corneal abrasions, ulcerations, vesication, and perforations are common corneal consequences in SM injured victims. Appearance of chronic symptoms has been reported as chronic inflammation of the corneal and conjunctival vasculature, ischemia, lipid and cholesterol deposition, scarring in cornea, corneal thinning, opacification and perforation of the cornea, limbal stem cell deficiency (LSCD), and neovascularization. Different medical and surgical protocols have been documented in the management of SM-induced ocular injuries, including preservative-free artificial tears, topical steroids and antibiotic, mydriatic, antiglaucoma drops, therapeutic contact lenses, dark glasses and punctal plugs/cauterization, N-acetylcysteine, tarsorrhaphy, amniotic membrane transplantation, stem cell transplantation, and corneal transplantation. New drugs such as resolvin E1, topical form of essential fatty acids, thymosin β4, 43 amino-acid polypeptides, topical form of curcumin, newly formulated artificial tears, diquafosol, rebamipide, tretinoin, and oral uridineseems to be beneficial in the management of ocular lesion associated with sulfur mustard poisoning. Further studies are needed to approve these drugs in SM victims. J. Cell. Biochem. 118: 3549-3560, 2017. © 2017 Wiley Periodicals, Inc.

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“…To date there is no definitive treatment for the delayed keratitis caused by SM. Current therapeutic strategies provide a microenvironment conducive to healing, such as through artificial tears, bandage contact lenses and immunomodulatory drugs, but otherwise depend on the eye's innate ability to self‐repair 12–14 . Although much progress has been made in understanding how the cornea responds to acute insults, the design of SM treatment strategies is complicated by the lack of knowledge regarding the etiology of recurrent corneal dysfunctions.…”

Section: Introductionmentioning

confidence: 99%

“…Current therapeutic strategies provide a microenvironment conducive to healing, such as through artificial tears, bandage contact lenses and immunomodulatory drugs, but otherwise depend on the eye's innate ability to self-repair. [12][13][14] Although much progress has been made in understanding how the cornea responds to acute insults, the design of SM treatment strategies is complicated by the lack of knowledge regarding the etiology of recurrent corneal dysfunctions. Since symptoms of this delayed keratitis are distributed throughout the anterior chamber, we believe an effective therapeutic strategy is likely to require a combination of drugs and delivery method(s) that ensures treatment of multiple corneal tissues.…”

Section: Introductionmentioning

confidence: 99%

Progression of ocular sulfur mustard injury: development of a model system

Milhorn

Hamilton

Nelson

et al. 2010

Annals of the New York Academy of Sciences

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Exposure of tissues to sulfur mustard (SM) results in the formation of protein and nucleotide adducts that disrupt cellular metabolism and cause cell death. Subsequent pathologies involve a significant proinflammatory response, disrupted healing, and long-term defects in tissue architecture. Following ocular exposure, acute corneal sequelae include epithelial erosions, necrosis, and corneal inflammation. Longer term, a progressive injury becomes distributed throughout the anterior chamber, which ultimately causes a profound remodeling of corneal tissues. In many cases, debilitating and vision-threatening injuries reoccur months to years after the initial exposure. Preliminary data in humans suffering from chronic epithelial lesions suggest that thymosin beta4 (Tbeta4) may be a viable candidate to mitigate acute or long-term ocular SM injury. To evaluate therapeutic candidates, we have developed a rabbit ocular exposure model system. In this paper, we report molecular, histological, ultrastructural, and clinical consequences of rabbit ocular SM injury, which can be used to assess Tbeta4 efficacy, including timepoints at which Tbeta4 will be assessed for therapeutic utility.

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A Combination Drug Treatment Against Ocular Sulfur Mustard Injury

Cited by 12 publications

References 12 publications

A review on symptoms, treatments protocols, and proteomic profile in sulfur mustard‐exposed victims

A review on symptoms, treatments protocols, and proteomic profile in sulfur mustard‐exposed victims

Ocular Effects of Sulfur Mustard and Therapeutic Approaches

Progression of ocular sulfur mustard injury: development of a model system

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