The formation of fatty acyl esters of retinol, the major form of vitamin A in epidermis, is catalysed by microsomal enzymes. To study the regulation of retinol esterification, we exposed hairless mice to ultraviolet (UV) irradiation which destroys vitamin A and to topical retinol treatment. Vitamin A (retinol and retinyl esters) in serum and epidermis was analysed by high-performance liquid chromatography at 0-12 days after a single irradiation with UVB (280-320 nm; 0.34 J/cm2) or UVA (320-400 nm; 1.0 J/cm2). The immediate vitamin A reducing effects of UVB and UVA were similar, but UVB elicited a more rapid replenishment of epidermal vitamin A with a corresponding transient depletion of serum retinol after 2-3 days. The activity of retinyl ester synthetase, measured by an in vitro radiochemical assay, was unaffected by the irradiations. By contrast, the acyl-CoA:retinol acyltransferase (ARAT; EC 2.3.1.76) activity increased to 167% on the 2nd day after UVB-irradiation and to 124% after topical retinol, but was otherwise quite constant. The UVB- and retinol-induced ARAT activity was less dependent on exogenous palmitoyl-CoA than that of control microsomes and experiments indicated that this might be due to an increased endogenous concentration of long-chain acyl-CoA in the microsomes. We conclude that extreme variations in the vitamin A supply to epidermis, such as a rapid influx of unesterified retinol, may modulate the epidermal ARAT activity.