Analysis of interleukin-8 release from normal human epidermal keratinocytes exposed to aliphatic hydrocarbons: delivery of hydrocarbons to cell cultures via complexation with α-cyclodextrin

While inhalation exposures represent the predominant route for jet fuel toxicity, increased concern has been placed on topical exposures due to reports of severe contact dermatitis among military personnel. All three of the predominant aviation fuels currently used by the commercial and military sec...

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Bibliographic Details
Published in:Toxicology in vitro 2001-12, Vol.15 (6), p.663-669
Main Authors: Allen, D.G, Riviere, J.E, Monteiro-Riviere, N.A
Format: Article
Language:English
Subjects:
alpha-Cyclodextrins
Biological and medical sciences
Cells, Cultured
Chemical and industrial products toxicology. Toxic occupational diseases
Cyclodextrin
Cyclodextrins - chemistry
Cytokine
Dose-Response Relationship, Drug
Drug Carriers - chemistry
Humans
Hydrocarbon
Hydrocarbons - chemistry
Hydrocarbons - toxicity
Interleukin-8 - secretion
Jet fuel
Keratinocyte
Keratinocytes - drug effects
Keratinocytes - secretion
Keratinocytes - ultrastructure
Kerosene - toxicity
Medical sciences
Solubility
Toxicology
Various organic compounds
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Summary:While inhalation exposures represent the predominant route for jet fuel toxicity, increased concern has been placed on topical exposures due to reports of severe contact dermatitis among military personnel. All three of the predominant aviation fuels currently used by the commercial and military sectors have been demonstrated experimentally to induce the production of interleukin-8 (IL-8), a proinflammatory cytokine, in normal human epidermal keratinocytes (NHEK). The objective of this study was to examine the effects of individual hydrocarbon components found in these fuels on IL-8 production by NHEK. In order to circumvent the extreme hydrophobicity of these compounds, inclusion complexes were formed between α-cyclodextrin/aliphatic hydrocarbons by adding 2 m m hydrocarbons to 4 m m α-cyclodextrin. NHEK were exposed to four aliphatic hydrocarbons (undecane, dodecane, tridecane, hexadecane) for 24 h at concentrations of 7.8–500 μ m. These hydrocarbons caused a peak in IL-8 release at a concentration of 31.2 μ m, with the exception of dodecane which peaked at 62.5 μ m. Subtoxic concentrations of the aliphatic hydrocarbons were those
ISSN:0887-2333
1879-3177
DOI:10.1016/S0887-2333(01)00075-3