Disease relevance of Ethylphenylpropiolate

• Since the proliferative agent ethylphenylpropiolate had no effect on protein kinase C in epidermis from SENCAR mice, the ability of benzoyl peroxide to influence protein kinase C activity in mouse skin may reflect its tumor promoting capabilities rather than its ability to induce hyperplasia [1].
• Verbascosaponin A and scropolioside A were active after a long latency period against ethyl phenylpropiolate edema, as are glucocorticoids [2].

High impact information on Ethylphenylpropiolate

• The nonpromoting but hyperplasiogenic agents ethyl phenylpropiolate and acetic acid significantly elevated XO activity within 48 h of topical application [3].
• On the other hand, pretreatment with TPA caused a refractory effect on ODC induction by mezerein but potentiated ODC induction by ethylphenylpropiolate [4].
• Ethylphenylpropiolate, a nonpromoting hyperplastic agent in mouse skin, had no effect on yolk sac morphology or function at its maximum solubility (1.85 mM) [5].
• Single applications of 12-O-tetradecanoylphorbol-13-acetate (TPA), mezerein or ethyl phenylpropriolate (EPP) to mouse skin at appropriate doses cause similar degrees of hyperplasia and comparable levels of induction of epidermal ornithine decarboxylase (ODC) activity [6].
• In agreement with previous findings, TPA induced a persistent epidermal hyperplasia and an increase in dark keratinocytes, although a similar finding was made for EPP and n-dodecane [7].

Chemical compound and disease context of Ethylphenylpropiolate

• Dehydrotumulosic acid significantly diminished the mouse ear edema induced by ethyl phenylpropiolate, while pachymic acid was ineffective [8].
• On topical application, sinapaldehyde and scopoletin dose-dependently inhibited ethyl phenylpropiolate-induced edema of the rat ear [9].
• The topical anti-inflammatory activity of three non-phenolic linear 1,7-diarylheptanoids, previously isolated from a Thai medicinal plant, Curcuma xanthorrhiza (Zingiberaceae) and four new semi-synthetic derivatives of the naturally occurring compounds were assessed in the murine model of ethyl phenylpropiolate-induced ear edema [10].
• It was found that all extracts possessed strong inhibitory effects on the acute phase of inflammation as seen in ethyl phenylpropiolate (EPP)- and arachidonic acid (AA)-induced ear edema as well as in carrageenin-induced paw edema in rats [11].

Biological context of Ethylphenylpropiolate

• A lesser active tumor promoter, phorbol dibenzoate; and ethyl phenylpropiolate, a purely hyperplastic agent, also lowered lipid peroxidation; while phorbol, a non-promoter, did not show any significant effect [12].

Anatomical context of Ethylphenylpropiolate

• Hyperplasiogenic agents such as mezerein and ethylphenylpropiolate were also effective in causing a reduction in the level of epidermal cytosol GC receptor level, but weak tumor promoters such as phorbol dibenzoate and 4-O-methyl TPA were less effective than TPA [13].

Gene context of Ethylphenylpropiolate

• Multiple treatments with TPA or ethyl phenylpropiolate resulted in a sustained elevation of XO activity which peaked at five treatments and then declined [3].

Analytical, diagnostic and therapeutic context of Ethylphenylpropiolate

• Two-dimensional gel electrophoresis was used to compare the changes in mouse epidermal proteins induced by the potent tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA), by the moderate promoter mechanical abrasion, and by the weakly promoting hyperplasiogenic agents mezerein and ethylphenylpropiolate [14].

References