Elias Peter M, Williams Mary L
Department of Veterans Affairs Medical Center, Dermatology Service, University of California San Francisco, California.
Department of Dermatology, Dermatology Service, University of California San Francisco, California.
Am J Phys Anthropol. 2016 Oct;161(2):189-207. doi: 10.1002/ajpa.23030. Epub 2016 Jun 21.
The evolution of human skin pigmentation must address both the initial evolution of intense epidermal pigmentation in hominins, and its subsequent dilution in modern humans. While many authorities believe that epidermal pigmentation evolved to protect against either ultraviolet B (UV-B) irradiation-induced mutagenesis or folic acid photolysis, we hypothesize that pigmentation augmented the epidermal barriers by shifting the UV-B dose-response curve from toxic to beneficial. Whereas erythemogenic UV-B doses produce apoptosis and cell death, suberythemogenic doses benefit permeability and antimicrobial function. Heavily melanized melanocytes acidify the outer epidermis and emit paracrine signals that augment barrier competence. Modern humans, residing in the cooler, wetter climes of south-central Europe and Asia, initially retained substantial pigmentation. While their outdoor lifestyles still permitted sufficient cutaneous vitamin D3 (VD3) synthesis, their marginal nutritional status, coupled with cold-induced caloric needs, selected for moderate pigment reductions that diverted limited nutritional resources towards more urgent priorities (=metabolic conservation). The further pigment-dilution that evolved as humans reached north-central Europe (i.e., northern France, Germany), likely facilitated cutaneous VD3 synthesis, while also supporting ongoing, nutritional requirements. But at still higher European latitudes where little UV-B breaches the atmosphere (i.e., present-day UK, Scandinavia, Baltic States), pigment dilution alone could not suffice. There, other nonpigment-related mutations evolved to facilitate VD3 production; for example, in the epidermal protein, filaggrin, resulting in reduced levels of its distal metabolite, trans-urocanic acid, a potent UV-B chromophore. Thus, changes in human pigmentation reflect a complex interplay between latitude, climate, diet, lifestyle, and shifting metabolic priorities.
人类皮肤色素沉着的演变必须兼顾人类强烈的表皮色素沉着的最初演变以及其在现代人类中的后续淡化。虽然许多权威人士认为表皮色素沉着的进化是为了抵御紫外线B（UV-B）辐射诱导的诱变或叶酸光解，但我们推测色素沉着通过将UV-B剂量反应曲线从有毒转变为有益，增强了表皮屏障。虽然致红斑的UV-B剂量会导致细胞凋亡和死亡，但亚红斑剂量对通透性和抗菌功能有益。高度黑素化的黑素细胞会使表皮外层酸化，并发出旁分泌信号，增强屏障能力。现代人类居住在欧洲中南部和亚洲较凉爽、湿润的地区，最初保留了大量色素沉着。虽然他们的户外生活方式仍能使皮肤合成足够的维生素D3（VD3），但他们有限的营养状况，加上寒冷引起的热量需求，促使色素适度减少，从而将有限的营养资源转向更紧迫的需求（即代谢节约）。随着人类到达欧洲中北部（即法国北部、德国），进一步的色素淡化可能促进了皮肤VD3的合成，同时也满足了持续的营养需求。但在欧洲更高的纬度地区，很少有UV-B能穿透大气层（即当今的英国、斯堪的纳维亚半岛、波罗的海国家），仅靠色素淡化是不够的。在那里，其他与色素无关的突变进化出来以促进VD3的产生；例如，在表皮蛋白丝聚合蛋白中发生突变，导致其远端代谢物反式尿刊酸（一种有效的UV-B发色团）水平降低。因此，人类色素沉着的变化反映了纬度、气候、饮食、生活方式和不断变化的代谢优先级之间的复杂相互作用。
