Table 1.

Summary of the effects of UVA and UVB on human body and the selective mechanisms involved in the evolution of pigmentation. The estimated strength of natural selection operating to darken and lighten pigmentation is indicated by numbers of “+” and “−” signs, respectively. See text for references for proposed mechanisms.

Agent	Strength and direction of selection	Proposed selective mechanism(s)
UVA	+++	Photolysis of folate (as 5-methyltetrahydrofolate [5MTHF] in serum) directly and by ROS in the presence of flavins and porphyrins, resulting in reduction of folate available for cell division
UVA	++	Competition for folate: increased folate needs for DNA damage repair and as 1-carbon donor in methylation of DNA competing with folate needed for melanogenesis
UVA	++	Disruption of melanin production because of sensitivity of tyrosinase to high levels of ROS
UVA	+	Malignant melanoma (as the only skin cancer that causes death to individuals of reproductive age)
UVA	+	Photoconversion of excess vitamin D3 to inactive metabolites
UVB	+++	Production of cyblobutane pyrimidine dimers and damaged nucleotides requiring repair resulting from DNA absorption of photons; activation of folate-dependent DNA repair processes
UVB	+	Direct photolysis of folate (as 5MTHF in serum), reducing the amount of folate available for cell division and regulation of tyrosinase activity in melanogenesis
UVB	+	Competition for folate: increased folate needs for DNA damage repair and as 1-carbon donor in methylation of DNA competing with folate needed for melanogenesis
UVB	No effect	Sunburn
UVB	No effect	Damage to DNA and its repair system and alterations of the immune system lead to progressive genetic alterations and the formation of nonmelanoma skin cancers
UVB	−	Cutaneous photosynthesis of vitamin D3
UVB	−	Greater need for vitamin D in females probably causing increasing sexual dimorphism in pigmentation; exaggerated by sexual selection in some populations