Photoinduced Cutaneous Inflammatory Responses by Erythrosine

Abstract

Erythrosine- (ERY) induced photosensitized immediate toxic reactions in rabbit skin were studied. Increase in vascular permeability (VP) and accumulation of polymorphonuclear leukocytes (PMNs) were quantitated using radiolabeled human serum albumin ([¹²⁵I]HSA) and [⁵¹Cr] PMNs, respectively. ERY (10–400 nmol) injected intradermally and subsequently exposed to ultraviolet-visible radiation (320–700 nm) (UVA-VIS) for 2 hr produced skin edema in situ due to increase of VP with a dose-response relationship. This increase in VP was approximately 3.5 times when either 100 nmol of ERY or 10 nmol of rose bengal (RB) was injected separately, compared to the respective control sites (protected from UVA-VIS irradiation). The accumulation of PMNs at the sites injected with ERY and exposed to light also showed a dose-response relationship. β-Carotene (100 nmol), when injected intradermally in conjunction with ERY and exposed to light, reduced the leakage of plasma approximately 50% relative to sites without β-carotene. Chlorpheniramine maleate (40 μg) or indomethacin (INDO) (5–20 nmol), injected intradermally 15 min before ERY (100 nmol) and exposed subsequently to light, reduced leakage of plasma into extra vascular spaces by approximately 60%. Vitamin E (2 mlU) slightly inhibited the ERY plus light-induced leakage of plasma. These results suggest that UVA-VIS irradiation of ERY generates highly reactive species that are cytotoxic to local tissue target cells, presumably mast cells, causing the release of mediators such as histamine, neutrophil chemotactic factor, and others. These mediators are responsible for the immediate responses such as exudation of plasma and the emigration of inflammatory cells at sites partially inhibited by chlorpheniramine maleate, an H₁-blocker. The reactive species includes singlet oxygen since β-carotene, a known singlet oxygen scavenger, partially inhibited this response. Prostanoids also seem to play a role in plasma exudation when ERY-injected dermal sites are irradiated to UVA-VIS light, since indomethacin inhibited the reaction.