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Book: Countermeasures against chemical threats / 1 / editor Jeffrey D. Laskin

Laskin, Jeffrey D.

(Annals of the New York Academy of Sciences ; volume 1374)

2016

Series title	Annals of the New York Academy of Sciences ; volume 1374 Countermeasures against chemical threats
Collection	Countermeasures against chemical threats
Language	English
Size	209 Seiten, Illustrationen
Publishing country	United States
Document type	Book
HBZ-ID	HT019069336
Database	Catalogue ZB MED Medicine, Health

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Book: Countermeasures against chemical threats / 2 / editor Jeffrey D. Laskin

Laskin, Jeffrey D.

(Annals of the New York Academy of Sciences ; volume 1378)

2016

Series title	Annals of the New York Academy of Sciences ; volume 1378 Countermeasures against chemical threats
Collection	Countermeasures against chemical threats
Language	English
Size	179 Seiten, Illustrationen
Publishing country	United States
Document type	Book
HBZ-ID	HT019164186
Database	Catalogue ZB MED Medicine, Health

In stock of ZB MED Cologne/Königswinter

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Article: Mechanisms of Psoralen Action in the Skin.

Laskin, Jeffrey D

Journal of the American College of Toxicology

2023 Volume 8, Issue 5, Page(s) 797–800

Abstract: The combination of psoralens and ultraviolet light (UVA, 320-400 nm), also referred to as PUVA, is a potent modulator of epidermal cell growth and differentiation. Although it has been postulated that PUVA exerts its actions by binding to DNA, our ... ...

Abstract	The combination of psoralens and ultraviolet light (UVA, 320-400 nm), also referred to as PUVA, is a potent modulator of epidermal cell growth and differentiation. Although it has been postulated that PUVA exerts its actions by binding to DNA, our laboratory has obtained evidence that a specific, saturable, high-affinity receptor site independent of the DNA mediates the biologic actions of these drugs. This receptor is a 22,000 molecular weight protein present in membrane and cytoplasmic fractions of responsive cell types. Treatment of cells with psoralens followed by UV light causes activation of the receptor. This leads to specific cell surface membrane alterations, in particular phosphorylation of the receptor for epidermal growth factor (EGF). The EGF receptor is a transmembrane glycoprotein possessing intrinsic tyrosine kinase activity. Modification of the EGF receptor leads to a loss in its ability to bind EGF, as well as an inhibition of its tyrosine kinase activity. These data indicate that the psoralens act at the level of the cell membrane and that their biologic effects in the skin may be mediated by the ability of these drugs to disrupt normal growth factor functions.
Language	English
Publishing date	2023-02-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	604987-4
ISSN	0730-0913
ISSN	0730-0913
DOI	10.3109/10915818909018037
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Article ; Online: Identification of early events in nitrogen mustard pulmonary toxicity that are independent of infiltrating inflammatory cells using precision cut lung slices.

Bellomo, Alyssa / Herbert, Julia / Kudlak, Melissa J / Laskin, Jeffrey D / Gow, Andrew J / Laskin, Debra L

Toxicology and applied pharmacology

2024 Volume 486, Page(s) 116941

Abstract: ... lung cell populations. PCLS were exposed to NM (1-100 μM) for 0.5-3 h and analyzed 1 and 3 d later. NM ...

Abstract	Nitrogen mustard (NM; mechlorethamine) is a cytotoxic vesicant known to cause acute lung injury which can progress to chronic disease. Due to the complex nature of NM injury, it has been difficult to analyze early responses of resident lung cells that initiate inflammation and disease progression. To investigate this, we developed a model of acute NM toxicity using murine precision cut lung slices (PCLS), which contain all resident lung cell populations. PCLS were exposed to NM (1-100 μM) for 0.5-3 h and analyzed 1 and 3 d later. NM caused a dose-dependent increase in cytotoxicity and a reduction in metabolic activity, as measured by LDH release and WST-1 activity, respectively. Optimal responses were observed with 50 μM NM after 1 h incubation and these conditions were used in further experiments. Analysis of PCLS bioenergetics using an Agilent Seahorse showed that NM impaired both glycolytic activity and mitochondrial respiration. This was associated with injury to the bronchial epithelium and a reduction in methacholine-induced airway contraction. NM was also found to cause DNA damage in bronchial epithelial cells in PCLS, as measured by expression of γ-H2AX, and to induce oxidative stress, which was evident by a reduction in glutathione levels and upregulation of the antioxidant enzyme catalase. Cleaved caspase-3 was also upregulated in airway smooth muscle cells indicating apoptotic cell death. Characterizing early events in NM toxicity is key in identifying therapeutic targets for the development of efficacious countermeasures.
Language	English
Publishing date	2024-04-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	204477-8
ISSN	1096-0333 ; 0041-008X
ISSN (online)	1096-0333
ISSN	0041-008X
DOI	10.1016/j.taap.2024.116941
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Article ; Online: Targeting Tumor Necrosis Factor Alpha to Mitigate Lung Injury Induced by Mustard Vesicants and Radiation.

Malaviya, Rama / Laskin, Jeffrey D / Businaro, Rita / Laskin, Debra L

Disaster medicine and public health preparedness

2023 Volume 17, Page(s) e553

Abstract: Pulmonary injury induced by mustard vesicants and radiation is characterized by DNA damage, oxidative stress, and inflammation. This is associated with increases in levels of inflammatory mediators, including tumor necrosis factor (TNF)α in the lung and ... ...

Abstract	Pulmonary injury induced by mustard vesicants and radiation is characterized by DNA damage, oxidative stress, and inflammation. This is associated with increases in levels of inflammatory mediators, including tumor necrosis factor (TNF)α in the lung and upregulation of its receptor TNFR1. Dysregulated production of TNFα and TNFα signaling has been implicated in lung injury, oxidative and nitrosative stress, apoptosis, and necrosis, which contribute to tissue damage, chronic inflammation, airway hyperresponsiveness, and tissue remodeling. These findings suggest that targeting production of TNFα or TNFα activity may represent an efficacious approach to mitigating lung toxicity induced by both mustards and radiation. This review summarizes current knowledge on the role of TNFα in pathologies associated with exposure to mustard vesicants and radiation, with a focus on the therapeutic potential of TNFα-targeting agents in reducing acute injury and chronic disease pathogenesis.
MeSH term(s)	Humans ; Inflammation ; Irritants/toxicity ; Lung Injury/drug therapy ; Lung Injury/etiology ; Lung Injury/prevention & control ; Mustard Plant ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Irritants ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2023-10-18
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2375268-3
ISSN	1938-744X ; 1935-7893
ISSN (online)	1938-744X
ISSN	1935-7893
DOI	10.1017/dmp.2023.178
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Menthol flavoring in e-cigarette condensate causes pulmonary dysfunction and cytotoxicity in precision cut lung slices.

Herbert, Julia / Kelty, Jacklyn S / Laskin, Jeffrey D / Laskin, Debra L / Gow, Andrew J

American journal of physiology. Lung cellular and molecular physiology

2023 Volume 324, Issue 3, Page(s) L345–L357

Abstract: E-cigarette consumption is under scrutiny by regulatory authorities due to concerns about product toxicity, lack of manufacturing standards, and increasing reports of e-cigarette- or vaping-associated acute lung injury. In vitro studies have demonstrated ...

Abstract	E-cigarette consumption is under scrutiny by regulatory authorities due to concerns about product toxicity, lack of manufacturing standards, and increasing reports of e-cigarette- or vaping-associated acute lung injury. In vitro studies have demonstrated cytotoxicity, mitochondrial dysfunction, and oxidative stress induced by unflavored e-cigarette aerosols and flavoring additives. However, e-cigarette effects on the complex lung parenchyma remain unclear. Herein, the impact of e-cigarette condensates with or without menthol flavoring on functional, structural, and cellular responses was investigated using mouse precision cut lung slices (PCLS). PCLS were exposed to e-cigarette condensates prepared from aerosolized vehicle, nicotine, nicotine + menthol, and menthol e-fluids at doses from 50 to 500 mM. Doses were normalized to the glycerin content of vehicle. Video-microscopy of PCLS revealed impaired contractile responsiveness of airways to methacholine and dampened ciliary beating following exposure to menthol-containing condensates at concentrations greater than 300 mM. Following 500 mM menthol-containing condensate exposure, epithelial exfoliation in intrabronchial airways was identified in histological sections of PCLS. Measurement of lactate dehydrogenase release, mitochondrial water-soluble-tetrazolium salt-1 conversion, and glutathione content supported earlier findings of nicotine or nicotine + menthol e-cigarette-induced dose-dependent cytotoxicity and oxidative stress responses. Evaluation of PCLS metabolic activity revealed dose-related impairment of mitochondrial oxidative phosphorylation and glycolysis after exposure to menthol-containing condensates. Taken together, these data demonstrate prominent menthol-induced pulmonary toxicity and impairment of essential physiological functions in the lung, which warrants concerns about e-cigarette consumer safety and emphasizes the need for further investigations of molecular mechanisms of toxicity and menthol effects in an experimental model of disease.
MeSH term(s)	Animals ; Mice ; Nicotine/toxicity ; Electronic Nicotine Delivery Systems ; Menthol/toxicity ; Respiratory Aerosols and Droplets ; Lung ; Flavoring Agents/toxicity
Chemical Substances	Nicotine (6M3C89ZY6R) ; Menthol (1490-04-6) ; Flavoring Agents
Language	English
Publishing date	2023-01-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00222.2022
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: SYNTHETIC APPROACHES TO 4,8-DIMETHYL-4'- (

Whittemore, Marilyn S / Heindel, Ned D / Guillon, Christophe D / McNeel, Thomas E / Rapp, Robert D / Mariano, Thomas M / Heck, Diane E / Laskin, Jeffrey D

Heterocycles

2024 Volume 55, Issue 6, Page(s) 1081–1093

Abstract: Synthetic approaches to novel 4,8-dimethyl-4'-halomethyl-4',5'-dihydropsoralens as synthetic precursors to 4,8-dimethyl-4'-( ...

Abstract	Synthetic approaches to novel 4,8-dimethyl-4'-halomethyl-4',5'-dihydropsoralens as synthetic precursors to 4,8-dimethyl-4'-(
Language	English
Publishing date	2024-01-07
Publishing country	Japan
Document type	Journal Article
ISSN	0385-5414
ISSN	0385-5414
DOI	10.3987/com-01-9197
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Article: Optimizing Nanosuspension Drug Release and Wound Healing Using a Design of Experiments Approach: Improving the Drug Delivery Potential of NDH-4338 for Treating Chemical Burns.

Roldan, Tomas L / Li, Shike / Guillon, Christophe / Heindel, Ned D / Laskin, Jeffrey D / Lee, In Heon / Gao, Dayuan / Sinko, Patrick J

Pharmaceutics

2024 Volume 16, Issue 4

Abstract: ... concentration (DC), and drug/stabilizer ratio (D/S) were the critical sonoprecipitation factors that control ...

Abstract	NDH-4338 is a highly lipophilic prodrug comprising indomethacin and an acetylcholinesterase inhibitor. A design of experiments approach was used to synthesize, characterize, and evaluate the wound healing efficacy of optimized NDH-4338 nanosuspensions against nitrogen mustard-induced skin injury. Nanosuspensions were prepared by sonoprecipitation in the presence of a Vitamin E TPGS aqueous stabilizer solution. Critical processing parameters and material attributes were optimized to reduce particle size and determine the effect on dissolution rate and burn healing efficacy. The antisolvent/solvent ratio (A/S), dose concentration (DC), and drug/stabilizer ratio (D/S) were the critical sonoprecipitation factors that control particle size. These factors were subjected to a Box-Behnken design and response surface analysis, and model quality was assessed. Maximize desirability and simulation experiment optimization approaches were used to determine nanosuspension parameters with the smallest size and the lowest defect rate within the 10-50 nm specification limits. Optimized and unoptimized nanosuspensions were prepared and characterized. An established depilatory double-disc mouse model was used to evaluate the healing of nitrogen mustard-induced dermal injuries. Optimized nanosuspensions (A/S = 6.2, DC = 2%
Language	English
Publishing date	2024-03-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527217-2
ISSN	1999-4923
ISSN	1999-4923
DOI	10.3390/pharmaceutics16040471
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Article ; Online: Skin Models Used to Define Mechanisms of Action of Sulfur Mustard.

Laskin, Jeffrey D / Ozkuyumcu, Kevin / Zhou, Peihong / Croutch, Claire R / Heck, Diane E / Laskin, Debra L / Joseph, Laurie B

Disaster medicine and public health preparedness

2023 Volume 17, Page(s) e551

Abstract: Sulfur mustard (SM) is a threat to both civilian and military populations. Human skin is highly sensitive to SM, causing delayed erythema, edema, and inflammatory cell infiltration, followed by the appearance of large fluid-filled blisters. Skin wound ... ...

Abstract	Sulfur mustard (SM) is a threat to both civilian and military populations. Human skin is highly sensitive to SM, causing delayed erythema, edema, and inflammatory cell infiltration, followed by the appearance of large fluid-filled blisters. Skin wound repair is prolonged following blistering, which can result in impaired barrier function. Key to understanding the action of SM in the skin is the development of animal models that have a pathophysiology comparable to humans such that quantitative assessments of therapeutic drugs efficacy can be assessed. Two animal models, hairless guinea pigs and swine, are preferred to evaluate dermal products because their skin is morphologically similar to human skin. In these animal models, SM induces degradation of epidermal and dermal tissues but does not induce overt blistering, only microblistering. Mechanisms of wound healing are distinct in these animal models. Whereas a guinea pig heals by contraction, swine skin, like humans, heals by re-epithelialization. Mice, rats, and rabbits are also used for SM mechanistic studies. However, healing is also mediated by contraction; moreover, only microblistering is observed. Improvements in animal models are essential for the development of therapeutics to mitigate toxicity resulting from dermal exposure to SM.
MeSH term(s)	Humans ; Mice ; Rats ; Animals ; Guinea Pigs ; Rabbits ; Mustard Gas/toxicity ; Skin
Chemical Substances	Mustard Gas (T8KEC9FH9P)
Language	English
Publishing date	2023-10-18
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2375268-3
ISSN	1938-744X ; 1935-7893
ISSN (online)	1938-744X
ISSN	1935-7893
DOI	10.1017/dmp.2023.177
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Article ; Online: Nitrogen Mustard Alkylates and Cross-Links p53 in Human Keratinocytes.

Jan, Yi-Hua / Heck, Diane E / An, Yunqi / Laskin, Debra L / Laskin, Jeffrey D

Chemical research in toxicology

2022 Volume 35, Issue 4, Page(s) 636–650

Abstract: Cytotoxic blistering agents such as sulfur mustard and nitrogen mustard (HN2) were synthesized for chemical warfare. Toxicity is due to reactive chloroethyl side chains that modify and damage cellular macromolecules including DNA and proteins. In ... ...

Abstract	Cytotoxic blistering agents such as sulfur mustard and nitrogen mustard (HN2) were synthesized for chemical warfare. Toxicity is due to reactive chloroethyl side chains that modify and damage cellular macromolecules including DNA and proteins. In response to DNA damage, cells initiate a DNA damage response directed at the recruitment and activation of repair-related proteins. A central mediator of the DNA damage response is p53, a protein that plays a critical role in regulating DNA repair. We found that HN2 causes cytosolic and nuclear accumulation of p53 in HaCaT keratinocytes; HN2 also induced post-translational modifications on p53 including S15 phosphorylation and K382 acetylation, which enhance p53 stability, promote DNA repair, and mediate cellular metabolic responses to stress. HN2 also cross-linked p53, forming dimers and high-molecular-weight protein complexes in the cells. Cross-linked multimers were also modified by K48-linked ubiquitination indicating that they are targets for proteasome degradation. HN2-induced modifications transiently suppressed the transcriptional activity of p53. Using recombinant human p53, HN2 alkylation was found to be concentration- and redox status-dependent. Dithiothreitol-reduced protein was more efficiently cross-linked indicating that p53 cysteine residues play a key role in protein modification. LC-MS/MS analysis revealed that HN2 directly alkylated p53 at C124, C135, C141, C176, C182, C275, C277, H115, H178, K132, and K139, forming both monoadducts and cross-links. The formation of intermolecular complexes was a consequence of HN2 cross-linked cysteine residues between two molecules of p53. Together, these data demonstrate that p53 is a molecular target for mustard vesicants. Modification of p53 likely mediates cellular responses to HN2 including DNA repair and cell survival contributing to vesicant-induced cytotoxicity.
MeSH term(s)	Chromatography, Liquid ; Cysteine ; Humans ; Keratinocytes ; Mechlorethamine/chemistry ; Tandem Mass Spectrometry ; Tumor Suppressor Protein p53
Chemical Substances	Tumor Suppressor Protein p53 ; Mechlorethamine (50D9XSG0VR) ; Cysteine (K848JZ4886)
Language	English
Publishing date	2022-03-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	639353-6
ISSN	1520-5010 ; 0893-228X
ISSN (online)	1520-5010
ISSN	0893-228X
DOI	10.1021/acs.chemrestox.1c00420
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