PubMed · 14360757
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N G SMITH, J SCHULZ. 1955. Partial albinism.. https://doi.org/10.1001/archderm.1955.01540280044009
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The thyroid hormone plays an essential role in the metamorphosis in flatfish, during which external asymmetry (for example, eye relocation and pigmentation) is established. However, no information is available on the expression mechanisms of metamorphic asymmetry. Since the presence of malformed juveniles (having either ocular or blind side characteristics on both sides) was known in spotted halibut (Verasper variegatus), the effect of the timing of thyroid hormone treatment was investigated. When thyroxine (T4, 10 or 30 ng/ml) was administered to the hypothyroid larvae (continuously receiving 30 microg/ml thiourea) from 25 days after hatching (DAH), the occurrence of one type of symmetrical juvenile (symmetrical pseudoalbino having blind side characteristics on both sides) increased to more than three times, and the occurrence was significantly greater than that observed in the control group. In the fish in which T4 treatment was initiated prior to 15 DAH or after 60 DAH, the occurrence of another type of symmetrical juvenile (symmetrical ambicolorate having ocular side characteristics on both sides) became more than two times, and its occurrence was significantly greater than that observed in the control group. These results suggest that both sides of the larval body independently possess the potential to become either the ocular or the blind side of the juvenile body and that the timing of thyroid hormone increase is the determining factor of "which side to become." Based on previous studies, since thyroid hormone is expected to induce blind side characteristics, the differential responsiveness to thyroid hormone-longer in the left side (blind side in normal juvenile) than the right-is strongly suggested as the central mechanism for metamorphic asymmetry in spotted halibut.
Our knowledge about the radioprotective effects of melatonin against X-ray-induced skin damage is still lacking. To examine these effects, an animal model of 60 Albino rats was used. The animals were divided into five groups: Group 1, nonirradiated; Group 2, X-ray irradiated (XRI, 8 Gy); Group 3, XRI pretreated with solvent (ethanol and phosphate-buffered saline); Group 4, nonirradiated group treated with melatonin; and Group 5, XRI pretreated with melatonin. The skin was evaluated for ultrastructural changes using transmission electron microscopy (TEM). When compared to the nonirradiated skin (Groups 1 and 4), XRI skin (Groups 2 and 3) showed features of both cell injury and increased metabolic activity. The former included changes such as condensation of the nuclei, vacuolization of the cytoplasm, dilatation of the rough endoplasmic reticulum, swelling of the mitochondria with cristolysis, destruction of the ribosomes and intermediate filaments, fragmentation of the keratohyaline granules and loss of the irregularity of the basal cell borders. The central cells of the sebaceous gland alveoli had larger irregular nuclei and few lipid droplets in their cytoplasm. The hair follicle cells had heterochromatic nuclei and less electron dense cytoplasm containing few complements of the organelles. The features of increased metabolic activity included increased euchromatin, irregularity of the nuclear membrane and increased branching of the melanocytes. Also, an increased number of the Birbeck granules were seen in the Langerhans cells. When compared to the irradiated skin (Groups 2 and 3), these changes were mild or absent in the skin of XRI animals pretreated with melatonin (Group 5). The ability of melatonin to minimize the injurious effects of XRI suggests a radioprotective role. The clinical ramifications of these observations warrant further studies.
The monomeric small GTPase Rab27a is specifically localized on both secretory granules and lysosome-related organelles. Although natural mutations of the Rab27a gene in human Griscelli syndrome and in ashen mice cause partial albinism and immunodeficiency reflecting the dysfunction of lysosome-related organelles, phenotypes resulting from the defective exocytosis of secretory granules have not been reported. To explore the roles of Rab27a in secretory granules, we analyzed insulin secretion profiles in ashen mice. Ashen mice showed glucose intolerance after a glucose load without signs of insulin resistance in peripheral tissues or insulin deficiency in the pancreas. Insulin secretion from isolated islets was decreased specifically in response to high glucose concentrations but not other nonphysiological secretagogues such as high K+ concentrations, forskolin, or phorbol ester. Neither the intracellular Ca2+ concentration nor the dynamics of fusion pore opening after glucose stimulation were altered. There were, however, marked reductions in the exocytosis from insulin granules predocked on the plasma membrane and in the replenishment of docked granules during glucose stimulation. These results provide the first genetic evidence to our knowledge for the role of Rab27a in the exocytosis of secretory granules and suggest that the Rab27a/effector system mediates glucose-specific signals for the exocytosis of insulin granules in pancreatic beta cells.