Vitamin D and the metabolism of epidermis.
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Animals↗
Biomedical subjects
J H Pavlovitch
Publications and source records attributed to J H Pavlovitch.
Skin calcium-binding protein: distribution in other tissues.
The distribution of epidermal calcium-binding protein was examined in rat tissues using immunodiffusion and immunofluorescence techniques to investigate its possible physiological role. Epidermal calcium-binding protein was demonstrated in the basal proliferative cell layer of all Malpighian epithelia and related tissues (epidermis, sebaceous glands, cornea, esophagus, and vagina) as well as in ependyma of brain and in the epithelia of the lens. No immunoreactivity for epidermal calcium-binding protein was found in other tissues including dermis, muscle, cartilage, blood vessels, nerve tissue, liver, endocrine glands, urogenital tract, and intestinal and respiratory epithelium. The presence of a protein immunologically indistinguishable from epidermal calcium-binding protein in proliferative cells suggests that it may be involved in the control of calcium-dependent processes perhaps related to mechanical damage and continued proliferation.
Animals↗
Vitamin D nutrition increases skin tyrosinase response to exposure to ultraviolet radiation.
The influence of vitamin D nutrition on melanogenesis in skin induced by UV radiation was studied in pigmented adult rats. Melanogenesis, assessed by the activity of skin tyrosinase (radiometric assay), was studied in vitamin-D-deficient and vitamin-D-fed rats exposed to UV (0.1 J/cm2, 290-320 nm). The tyrosinase activity in skin was not significantly changed by vitamin D treatment alone. In contrast, the induction of tyrosinase activity provoked by UV radiation was greater in vitamin-D-fed than in vitamin-D-deficient rats. The increase in skin tyrosinase activity in response to UV was preceded by an increase in skin cAMP levels. This rise in cAMP was greater in vitamin-D-treated rats than in vitamin-D-deficient rats. The pretreatment of rats with phosphodiesterase inhibitor potentiated the effect of vitamin D on skin tyrosinase activity. The low serum calcium levels in the vitamin-D-deficient group were evidently not responsible for the lower UV induction of skin tyrosinase activity because the vitamin-D-deficient rats with normal serum calcium levels (supplemented with 20% lactose and 2% calcium in the diet) were also unable to show maximal induction of skin tyrosinase activity in response to UV radiation requires the presence of adequate vitamin D. cAMP may be involved in the mediation of this effect. The relationship observed between the vitamin D status of animals and tyrosinase activity of skin could provide an effective feed-back control for protection against UV and vitamin D intoxication.
1-Methyl-3-isobutylxanthine↗
Skin calcium binding protein is localized in the cytoplasm of the basal layer of the epidermis.
Using a serum raised in rabbits against a calcium binding protein extracted from rat skin, the cutaneous localization of this protein was studied by indirect immunofluorescence. The skin calcium binding immunoreactivity was found in the epidermis but not in the dermis; it was localized in the cytoplasm of the basal cell layer of both skin and malpighian mucosa. There was not species specificity; this allowed the tracing of the protein in human epidermis as well where it was also expressed only in the basal cells. This is the first demonstration of the unique localization of a specific protein within the cytoplasm of the basal cell layer of the epidermis. This localization may help to elucidate the physiological role of this protein.
Animals↗
Suppressive effects of 24,25-dihydroxycholecalciferol on bone resorption induced by acute bilateral nephrectomy in rats.
The possible suppressive effects of 24,25-dihydroxycholecalciferol on secondary hyperparathyroidism and increased bone resorption were investigated in adult rats raised on a diet normal in calcium, phosphorus, and vitamin D, and subjected to acute bilateral nephrectomy. The animals had received subcutaneous radiocalcium 4 wk before the experiment. 5 h after nephrectomy an increase in serum total calcium, (45)Ca-specific activity, citrate, phosphorus, and magnesium concentrations were observed. Serum immunoreactive parathyroid hormone increased, while serum calcitonin decreased. The osteoclast count in the tibial metaphyses was augmented. The biochemical and histological changes observed were partly parathyroid hormone and calcitonin independent, as they also occurred in parathyroidectomized hypocalcemic rats. Pretreatment with 650 pmol of 24,25-dihydroxycholecalciferol 16 h before nephrectomy prevented bone calcium mobilization and diminished the rise in serum total calcium and citrate both in parathyroid-intact and in parathyroidectomized animals. In parathyroid-intact rats, serum immunoreactive parathyroid hormone and calcitonin remained normal in spite of the fall in serum-ionized calcium, and the number of osteoclasts did not increase. In parathyroidectomized rats, 24,25-dihydroxycholecalciferol did not prevent the postnephrectomy rise in the osteoclast count. This latter observation suggests that this metabolite exerts its effect on bone either by acting on cells other than osteoclasts, i.e., the osteocytes, or by inhibiting cell activity. At equimolar dosage 1,25-dihydroxycholecalciferol had a potent stimulatory effect on bone resorption. This effect of 1,25-dihydroxycholecalciferol was partly blocked by the simultaneous administration of 24,25-dihydroxycholecalciferol. The potential clinical significance of these observations remains to be determined.
24,25-Dihydroxyvitamin D 3↗
[Effect of vitamin D on skin metabolism (author's transl)].
To examine for a possible local action of vitamin D on skin, its histology DNA content, melanogenetic response to UV and proliferative activity (incorporation of 3H thymidine into DNA) were studied on vitamin D deficient and vitamin D fed rats. The skin thickness DNA content and melanogenetic response to UV (assessed as the activity of skin tyrosinase) were greater in vitamin D fed than in vitamin deficient rats. In keratinocyte cell cultures vitamin D (10-9 M-10-12 M) increased DNA synthesis in suprabasal cells whereas it had no effect on DNA synthesis in basal cells. The influence of vitamin D on skin thickness and melanogenetic response to UV could provide an effective feed-back control for protection against UV penetration and vitamin D intoxication.
Animals↗