INFLUENCE OF ULTRAVIOLET-B RADIATION ON VITAMIN-D3 METABOLISM IN VITAMIN-D3-RESISTANT NEW-WORLD PRIMATES

We investigated the occurrence of rickets in adolescent tamarins (Saguinus imperator) residing at the Los Angeles Zoo. Compared to tamarins in the same colony without clinical evidence of bone disease (N = 6), rachitic platyrrhines (N = 3) had a decrease in their serum calcium concentration (P < .05). The affected tamarins also had lower serum 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) levels than did nonaffected colony mates, but 2-10-fold higher concentrations than in Old World primates of a comparable developmental stage. New World primates in many different genera are known to exhibit target organ resistance to the active vitamin D3 metabolite, 1,25-(OH)2D3, compensated by maintenance of high circulating concentrations of 1,25-(OH)2D3. The relatively low serum 1,25-(OH)2D3 concentration in rachitic tamarins and ultraviolet B radiation-deficient environment of these primates suggested that bone disease may be linked to a deficiency in the substrate for 1,25-(OH)2D3, 25-hydroxyvitamin D3 (25-OHD3). Chronic exposure of platyrrhines in three different vitamin D resistant genera to an artificial UVB source resulted in 1) a significant increase in the mean serum 25-OHD3 (P < .001) and 1,25-(OH)2D3 (P < .02) level over that encountered in platyrrhines not exposed to UVB; and 2) prevention of rachitic bone disease in irradiated individuals. These data further show that the serum 25-OHD3 and 1,25-OH2D3 levels are positively correlated in vitamin D-resistant platyrrhines (r = 0.64; P = .0014) and suggest that a compromise in cutaneous vitamin D3 production by means of UVB deprivation may limit necessary 1,25-(OH)2D3 production.