Skin β-Endorphin Mediates Addiction to UV Light

Abstract

SUMMARY Ultraviolet light is an established carcinogen yet evidence suggests that UV-seeking behavior has addictive features. Following UV exposure, epidermal keratinocytes synthesize Proopiomelanocortin that is processed to Melanocyte Stimulating Hormone, inducing tanning. We show that in rodents another POMC-derived peptide, β-endorphin, is coordinately synthesized in skin, elevating plasma levels after low-dose UV. Increases in pain-related thresholds are observed, and reversed by pharmacologic opioid antagonism. Opioid blockade also elicits withdrawal signs after chronic UV exposure. This effect was sufficient to guide operant behavioral choices to avoidance of opioid withdrawal (conditioned place aversion). These UV-induced nociceptive and behavioral effects were absent in β-endorphin knockout mice and in mice lacking p53-mediated POMC induction in epidermal keratinocytes. While primordial UV addiction, mediated by the hedonic action of β-endorphin and anhedonic effects of withdrawal, may theoretically have enhanced evolutionary vitamin D biosynthesis, it now may contribute to the relentless rise in skin cancer incidence in man.

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“…However, the criteria to assess the prevalence of tanning dependency have been challenged (Schneider et al, 2015). From an animal model, there is evidence supporting a role of enhanced synthesis of beta-endorphin by low dose UV (Fell et al, 2014). Increased expression of beta-endorphin has been shown in epidermal cells taken from human subjects that were exposed to irradiation with UVB (Jussila et al, 2016).…”

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