Cartwright L E, Walter J F
J Am Acad Dermatol. 1983 Jun;8(6):830-6. doi: 10.1016/s0190-9622(83)80012-7.
Sunscreens containing 5-methoxypsoralen (5-MOP) are currently being marketed to promote tanning by inducing psoralen-mediated ultraviolet (UV) A (320-400 nm) melanogenesis. The rationale is that this may prevent UVB (290-320 nm) radiation-induced skin damage. However, mouse studies have shown that 5-MOP has the same cutaneous photocarcinogenic potential as 8-methoxypsoralen. In addition, the 5-MOP--containing sunscreen Sun System III (SS III), when combined with UVA, induces epidermal ornithine decarboxylase activity, an enzyme associated with tumor promotion. Therefore, we investigated whether SS III had sufficient psoralen concentration to be tumorigenic in hairless mice exposed to chronic, intermittent UVA radiation. SS III was applied to hairless mice 5 days per week for 20 weeks. After each application the mice were exposed to 2.5 to 10 joules/cm2 UVA radiation. All test groups developed atypical squamous papillomas in direct proportion to the dosage of UVA radiation received. A shorter latency period for tumor development was seen with larger UVA doses. Test animals followed up to 1 year developed invasive squamous cell tumors. Control groups (SS III without UVA and UVA without SS III) remained free of tumors. Animals receiving SS III plus UVA developed persistent skin thickening and increased dermal cyst formation similar to that reported with chronic exposure to UVB, a known carcinogenic wavelength. Over-the-counter sunscreens containing 5-MOP do contain sufficient psoralen concentrations to cause cutaneous phototoxicity and photocarcinogenicity in mice, and their use in humans should be discouraged in the interest of preventing further UV-induced skin damage and skin cancer.
目前市场上销售的含5-甲氧基补骨脂素(5-MOP)的防晒霜,可通过诱导补骨脂素介导的紫外线(UV)A(320 - 400纳米)黑色素生成来促进晒黑。其原理是这可能预防UVB(290 - 320纳米)辐射引起的皮肤损伤。然而,小鼠研究表明,5-MOP与8-甲氧基补骨脂素具有相同的皮肤光致癌潜力。此外,含5-MOP的防晒霜Sun System III(SS III)与UVA联合使用时,会诱导表皮鸟氨酸脱羧酶活性,该酶与肿瘤促进有关。因此,我们研究了SS III在暴露于慢性、间歇性UVA辐射的无毛小鼠中是否具有足以致癌的补骨脂素浓度。SS III每周5天应用于无毛小鼠,持续20周。每次涂抹后,小鼠接受2.5至10焦耳/平方厘米的UVA辐射。所有测试组均出现非典型鳞状乳头状瘤,与接受的UVA辐射剂量成正比。UVA剂量越大,肿瘤发生的潜伏期越短。随访1年的实验动物出现了侵袭性鳞状细胞肿瘤。对照组(不含UVA的SS III和不含SS III的UVA)未出现肿瘤。接受SS III加UVA的动物出现持续的皮肤增厚和真皮囊肿形成增加,类似于长期暴露于已知致癌波长UVB时所报道的情况。含5-MOP的非处方防晒霜确实含有足以在小鼠中引起皮肤光毒性和光致癌性的补骨脂素浓度,为防止进一步的紫外线诱导的皮肤损伤和皮肤癌,应不鼓励在人类中使用此类防晒霜。