The Induction of Ornithine Decarboxylase in Human Epidermis Is Independent of Lipoxygenase and Cyclo‐oxygenase Pathways

  title={The Induction of Ornithine Decarboxylase in Human Epidermis Is Independent of Lipoxygenase and Cyclo‐oxygenase Pathways},
  author={W. P. Arnold and B J Pennings and P. Kerkhof},
  journal={The Journal of Dermatology},
In vivo studies in rodents suggest that prostaglandins and/or leukotrienes are involved in the epidermal induction of ornithine decarboxylase (ODC). Recently, we have shown that, in human epidermis, prostaglandins are not involved in this process. Here we report the role of leukotrienes in epidermal ODC induction in human skin. Topical flufenamic acid (DignodolinR), vehicle, or nothing was applied under plastic occlusion to three sites on the backs of healthy volunteers. This was followed 1 h… 
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Direct and indirect modulation of ornithine decarboxylase and cyclooxygenase by UVB radiation in human skin cells.
UVB radiation can activate cyclooxygenase gene expression in human skin cells both by direct activation pathways or indirectly by inducing a paracrine mechanism.
The immunohistochemical effects of a single challenge with an intermediate dose of ultravilet B on normal human skin
D dose-dependent effects of UVB on normal human skin were assessed using histology and immunohistochemistry, and this model might be a promising approach to evaluate the effect of drugs on epidermal proliferation and differentiation in vivo.
Response of mouse skin to tattooing: use of SKH-1 mice as a surrogate model for human tattooing.
It is demonstrated that mice substantially recover from the tattooing insult by 14 days, leaving behind pigment in the dermis and the regional lymph nodes, suggesting that the murine model might be a suitable surrogate for investigating the toxicological and phototoxicological properties of ingredients used in tattooing.
Ultraviolet light induced alteration to the skin.
The endogenous and exogenous mechanisms of skin photoprotection are discussed, where the UV light is absorbed by endogenous sensitizers that are excited and their further reactions lead to formation of reactive oxygen species (ROS).


Cyclo‐oxygenase products do not participate in the induction of ornithine decarboxylase in human epidermis
The data indicate that the cyclo‐oxygenase products in human epidermis do not contribute to the induction of ODC, and they are not involved in the epidermal induction of ornithine decarboxylase.
Inhibition by prostaglandin synthesis inhibitors of the induction of epidermal ornithine decarboxylase activity, the accumulation of prostaglandins, and tumor promotion caused by 12-O-tetradecanoylphorbol-13-acetate.
The findings that the application of indomethacin prior to TPA treatment inhibits the accumulation of prostaglandins, the induction of ODC activity, and the formation of skin papillomas suggest that TPA-induced O DC activity may be an important component of the mechanism of skin tumor promotion.
Ultraviolet radiation induction of ornithine decarboxylase in rat keratinocytes.
Studying the regulation of ornithine decarboxylase (ODC) gene expression in response to UVB radiation shows that the UVB-induced increase in ODC activity is due, at least in part, to an increase inODC gene expression and they provide a useful model for the analysis of the molecular effects of UVB Radiation.
Inhibition of ultraviolet-B epidermal ornithine decarboxylase induction and skin carcinogenesis in hairless mice by topical indomethacin and triamcinolone acetonide.
Modulation of ultraviolet-B (UVB) skin carcinogenesis by topical treatment with two antiinflammatory drugs expected to have different mechanisms of action has been studied in the hairless mouse.
Prostaglandins and skin tumor promotion: inhibition of tumor promoter-induced ornithine decarboxylase activity in epidermis by inhibitors of prostaglandin synthesis.
Application of 12-O-tetradecanoylphorbol-13-acetate to mouse skin led to a dramatic induction of epidermal ornithine decarboxylase activity, and the degree of induction was remarkably depressed by prior treatment of skin with indomethacin, acetylsalicylic acid or flufenamic acid, inhibitors of prostaglandin synthesis.
Inhibition of teleocidin-caused epidermal ornithine decarboxylase induction by phospholipase A2-, cyclooxygenase- and lipoxygenase-inhibitors.
The present results suggest that arachidonate metabolites, i.e., not only cyclooxygenase product but also lipoxygenases product, are involved in the mechanism of ODC induction by teleocidin.
Antiinflammatory drug effects on ultraviolet light-induced epidermal ornithine decarboxylase and DNA synthesis.
Topical triamcinolone acetonide and indomethacin were found to significantly inhibit the UV-B induction of epidermal ornithine decarboxylase in hairless mice when applied following ultraviolet light irradiation.
Inhibition by lipoxygenase inhibitors of 7-bromomethylbenz[a]anthracene-caused epidermal ornithine decarboxylase induction and skin tumor promotion in mice.
Results indicate that a mechanism susceptible to lipoxygenase inhibitors plays a role not only in the TPA-caused but also in the BrMBA-causes epidermal ODC induction, skin inflammation and tumor promotion.
Induction of mouse epidermal ornithine decarboxylase activity and DNA synthesis by ultraviolet light.
It is shown that irradiation with UVB, the most carcinogenic region of ultraviolet light, induces mouse epidermal ornithine decarboxylase activity, and the elevated enzyme activity precedes increasedEpidermal DNA synthesis.
Inhibition of 12-O-tetradecanoylphorbol-13-acetate-induced epidermal ornithine decarboxylase activity by phospholipase A2 inhibitors and lipoxygenase inhibitor.
The results strongly indicate that the stimulation of phospholipase A2 activity is a crucial process in inducing mouse epidermal ODC by TPA and not only cyclooxygenase product but also lipoxygen enzyme product(s) are involved in the mechanism of ODC induction.