Effects of ethanol on chicksin vivo and on chick embryo tibiae in organ culture
Autor: | W. K. Ramp, W. C. Murdock, W. A. Gonnerman, Tai-Chan Peng |
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Rok vydání: | 1975 |
Předmět: |
medicine.medical_specialty
Endocrinology Diabetes and Metabolism chemistry.chemical_element Iodoacetates Chick Embryo Calcium Carbohydrate metabolism Organ culture Bone and Bones Phosphates chemistry.chemical_compound Calcification Physiologic Organ Culture Techniques Endocrinology In vivo Internal medicine Bone cell medicine Animals Magnesium Orthopedics and Sports Medicine Bone mineral Bone Development Ethanol Hypocalcemia Tibia Sodium Proteins Phosphorus General Medicine medicine.disease Culture Media Hematocrit chemistry Lactates Stress Mechanical Hypermagnesemia Chickens |
Zdroj: | Calcified Tissue Research. 17:195-203 |
ISSN: | 1432-0827 0008-0594 |
Popis: | Hypocalcemia previously reported in rats and dogs following oral administration of ethanol may have been caused by a movement of calcium from blood to bone. This present study was undertaken to determine whether ethanol also causes hypocalcemia in chicks and to investigate the direct effects of ethanol on mineral accretion, glucose metabolism and growth of embryonic chick tibiae in an organ culture system. A high dose of ethanol (6 g/kg body wt) produced hypocalcemia, hypermagnesemia and an elevated hematocrit in chicks. Results in vitro were as follows: 1) 5 to 30 mul ethanol/ml medium produced dose-related increases in bone mineral from 58-440%; 2) lactate production was inhibited at all ethanol levels; 3) increased mineral accretion did not occur in ethanol-treated tibiae when iodoacetate was in the medium, but did occur in mechanically disrupted bones exposed to ethanol; and 4) the ethanol response in bone was directly related to the medium phosphate concentration. The results lead to the following conclusions: 1) ethanol has a direct stimulatory effect on bone mineral accretion and an inhibitory effect on bone glucose metabolism in vitro; 2) viable bone cells and an adequate phosphate supply are necessary for the ethanol response, but tissue integrity is not; and 3) the hypocalcemic effect of ethanol in vivo may at least partially result from ethanol-stimulated bone mineral deposition. |
Databáze: | OpenAIRE |
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