Disease relevance of Tanning

• Aplastic anemia associated with canthaxanthin ingested for 'tanning' purposes [1].
• Most exposures to ultraviolet A tanning devices began after 1980; therefore, epidemiologic studies have difficulty in revealing any increase in risk of CMM starting after 1980 because of the latent period between exposure and occurrence of melanoma [2].
• Human MC1R gene loss-of-function mutations are associated with fair skin, poor tanning and increased skin cancer risk [3].
• OBJECTIVE: To assess the efficacy of acitretin and commercial tanning bed therapy for the treatment of moderate to severe chronic plaque-type psoriasis [4].
• These observations appear to have relevance to the O2-requiring immediate tanning reaction of the skin stimulated by solar radiation and in the induction of skin photosensitization [5].

Psychiatry related information on Tanning

• Two of these analogs, a linear peptide, melanotan I, and a cyclic truncated peptide, melanotan II (MTI and MTII, respectively) have been patented and tested clinically for studies on tanning of the skin (MTI) and for diagnosis and treatment of male erectile dysfunction (MTII) [6].

High impact information on Tanning

• Our findings suggest that in humans, as in other mammals, the MC1R is a control point in the regulation of pigmentation phenotype and, more importantly, that variations in this protein are associated with a poor tanning response [7].
• The latter was obtained from human cords and was made available as an onshelf graft for surgery following glutaraldehyde tanning [8].
• Individuals with a low tanning ability and a low DRC had a higher risk for CMM (OR = 8.6; 95% CI = 2.7 to 27.5) than individuals with a higher tanning ability and a high DRC [9].
• Overall, any use of tanning devices was associated with odds ratios of 2.5 (95% confidence interval [CI] = 1.7 to 3.8) for SCC and 1.5 (95% CI = 1.1 to 2.1) for BCC [10].
• Forty-three years after its initial description, the elucidation of the molecular identity of bursicon and the verification of its receptor allow for studies of bursicon actions in regulating cuticle tanning, wing expansion, and as yet unknown functions [11].

Chemical compound and disease context of Tanning

• The clinical trials included 18 subjects with hyperpigmentation who used 5% niacinamide moisturizer and vehicle moisturizer in a paired design, and 120 subjects with facial tanning who were assigned to two of three treatments: vehicle, sunscreen and 2% niacinamide + sunscreen [12].
• Thus excessive solar exposure produces, besides erythema and tanning, the resetting of the vitamin D3 synthetic mechanism with blunting of the response to UVB [13].
• Refractile crystalline deposits may also be a manifestation of drug toxicity like the antineoplastic agent tamoxifen, the anesthetic methoxyflurane and the oral tanning agent canthaxanthine [14].
• Pyruvate oxidase from Pediococcus species was immobilized with gelatin and insolubilized in film form by tanning with glutaraldehyde [15].

Biological context of Tanning

• Transcriptional activation of tyrosinase and TRP-1 by p53 links UV irradiation to the protective tanning response [16].
• The data further suggest that tanning is part of a p53-mediated adaptive response of mammalian skin to DNA damage from ultraviolet irradiation [17].
• The formol tanning gives a good rigidity and elasticity in adapting to different blood volumes without aneurysmal dilatation [18].

Anatomical context of Tanning

• Human umbilical veins were prepared as vascular grafts by tanning with dialdehyde starch or gluteraldehyde and by structural re-inforcement with an outer polyester fiber mesh [19].
• Lead may decrease the osmotic and peroxidative fragility of erythrocytes from vitamin E-deficient rats by "tanning" the red cell membrane [20].
• As the concentration of glutaraldehyde used in tanning is increased, the initial specific activity of collagen-asparaginase membranes decreased asymptotically to a limiting value [21].
• Dopa decarboxylase (DDC) functions in insect catecholamine biochemistry to produce materials essential for cross-linking reactions that result in tanning and/or melanization, include tanning of the mosquito egg chorion and encapsulation of parasites [22].
• METHODS: We have attempted to destroy melanocytes by using the QS ruby laser after tanning in a patient with extensive vitiligo [23].

Associations of Tanning with chemical compounds

• It is readily available through commercial tanning salons and mail advertisements, but despite advertising claims that it is harmless, investigation regarding the safety of oral doses of canthaxanthin in humans has not been conducted [1].
• Involvement of tyrosine residues in the tanning of proteins by 3-hydroxyanthranilic acid [24].
• Laccase 2 is the phenoloxidase gene required for beetle cuticle tanning [25].
• We previously reported a direct relation between aldehyde tanning and bioprosthesis calcification and the absence of calcification in the absence of aldehyde [26].
• Theophylline enhanced the effect of small doses of cAMP or of blood, diluted 1:8, active in the puparium tanning factor [27].

Gene context of Tanning

• In ultraviolet-induced tanning, the protein levels of various gene products critical for pigmentation (including tyrosinase and tyrosinase-related protein-1) are increased in response to ultraviolet B irradiation, but changes in mRNA levels of these factors have not been investigated in vivo [28].
• Two kinds of phenoloxidases, laccase and tyrosinase, have been proposed to participate in tanning, but proof of the true identity of the enzyme(s) responsible for this process has been elusive [25].
• The sas gene was cloned, and both the cuticular tanning and the larval lethal phenotypes were complemented by P-element-mediated transformation with a genomic DNA-cDNA construct [29].
• Our results suggest that the mechanism of the tanning response of human skin may involve the transcriptional regulation of certain pigmentary genes, and that pro-opiomelanocortin-derived melanocortins such as alpha-melanocyte-stimulating hormone and adrenocorticotropic hormone may play a part in regulating these genes in vivo [28].
• This superpotent analog is now entering a Phase I clinical trial with possible therapeutic applications for the treatment of hypomelanotic disorders such as vitiligo and for pharmacologic tanning without the need for sunlight exposure [30].

Analytical, diagnostic and therapeutic context of Tanning

• An MSH analogue ([Nle4,D-Phe7]alpha-MSH) that exhibits superpotency and prolonged biological activity has been synthesized, biologically characterized, and is presently in clinical trials to determine its possible clinical use in tanning of the skin [31].
• A high-performance liquid chromatographic (HPLC) procedure has been developed for the quantification of Melanotan-II (MT-II), a cyclic heptapeptide which promotes rapid tanning of the skin, in rat plasma [32].
• Inhibition of UVR-induced tanning and immunosuppression by topical applications of vitamins C and E to the skin of hairless (hr/hr) mice [33].
• Primary prevention behaviors include applying SPF 15+ sunscreen 30 minutes before exposure, reapplying SPF 15+ sunscreen every 1 1/2 to 2 hours or after swimming or sweating, dressing in protective clothing, using shade, limiting exposure during peak sun hours, and avoiding artificial sources of ultraviolet radiation such as tanning beds [34].
• These results demonstrate that MT-II has tanning activity in humans given only 5 low doses every other day by subcutaneous injection [35].

References