Petrolatum: interference with the oxidation of arachidonic acid

Authors

  • NEAL S. PENNEYS,

    Corresponding author
    1. Department of Dermatology, University of Miami School of Medicine, Miami, U. S. A.
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      Supported in part by Grant AM19O79 and AM14941 from the National Institutes of Health and by the Dermatology Foundation of Miami. Dr Penneys is the recipient of the Research Career Development Award, AM 00203, from the National Institutes of Health. Presented in part at the Society for Investigative Dermatology, May 1979.

  • WILLIAM EAGLSTEIN,

    1. Department of Dermatology, University of Miami School of Medicine, Miami, U. S. A.
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  • VINCENT ZIBOH

    1. Department of Dermatology, University of Miami School of Medicine, Miami, U. S. A.
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Dr Neal S. Penneys, Department of Dermatology, R-11, University of Miami School of Medicine, Box 016940, Miami, F1, 33101, U. S. A.

SUMMARY

Microsomal preparations from petrolatum-treated wound skin contained significantly less arachidonic acid-dependent oxidative capacity when compared to activities in untreated wounded skin (t = 6.06, P < 0.001). Microsomes from both untreated and petrolatum-treated wounded skin produced similar quantities of PGE2 and PGF; however, microsomal lipoxygenase activity in petrolatum-treated wounded skin was depressed when compared to that in untreated wounded skin. Microsomal preparations from normal pig skin treated with petrolatum oxidized arachidonic acid at a similar rate to those from untreated control skin.

Increasing quantities of petrolatum progressively inhibited the synthesis of PGE2 and PGF by fetal calf skin microsomes in vitro as determined by both the oxidation of arachidonic acid and the quantification of radioactive product.

Topical application of banal compounds that contain lipid substances may therefore alter the cutaneous inflammatory response by local suppression of pathways that generate hydroxy-fatty acids, substances that are known to be chemotactic and pro-inflammatory.

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