caa a22 4500 469093749 CHVBK 20180323133025.0 cr unu---uuuuu 170328e19921201xx s 000 0 eng 10.1007/BF02576288 doi (NATIONALLICENCE)springer-10.1007/BF02576288 β-Alanyl- L -histidinato zinc prevents hydrocortisone-induced disorder of bone metabolism in rats [Elektronische Daten] [Y. Segawa, N. Tsuzuike, Y. Itokazu, E. Tagashira, M. Yamaguchi] Summary: The preventive effect of β-alanyl-L-histidinato zinc (AHZ) on osteopenia was investigated in rats treated with hydrocortisone. Rats received hydrocortisone (75 mg/kg body weight per day) s.c. for 30 days. The steroid treatment caused a significant increase in serum alkaline phosphatase activity and parathyroid hormone (PTH-c) level, while serum calcium inorganic phosphorus, and zinc concentrations were not significantly altered. The femoral-diaphyseal alkaline phosphatase activity, deoxyribonucleic acid (DNA), and calcium contents were significantly decreased by the treatment of steroid, although the bone zinc content was not appreciably altered. When AHZ (10, 30, and 100 mg/kg per day) was administered p. o. for 30 days to rats giving the steroid, the dose of AHZ (30 and 100 mg/kg) completely prevented the increases in serum alkaline phosphatase activity and PTH-c level and the decreases in femoral-diaphyseal alkaline phosphatase activity, DNA, and calcium contents caused by the steroid treatment. The dose of AHZ (10, 30, and 100 mg/kg) significantly increased zinc content in the femoral diaphysis. Present results indicate that the dose of AHZ can prevent the disorder of bone metabolism caused by hydrocortisone treatment AHZ may have a therapeutic role in the steroid-induced osteopenia. Springer-Verlag, 1992 β-Alanyl- L -histidinato zinc nationallicence Zinc nationallicence Hydrocortisone nationallicence Bone metabolism nationallicence Osteopenia nationallicence Rat femur nationallicence Segawa Y. Department of Pharmacology, Central Research Laboratories, Zeria Pharmaceutical Co., Saitama, Japan aut Tsuzuike N. Department of Pharmacology, Central Research Laboratories, Zeria Pharmaceutical Co., Saitama, Japan aut Itokazu Y. Department of Pharmacology, Central Research Laboratories, Zeria Pharmaceutical Co., Saitama, Japan aut Tagashira E. Department of Pharmacology, Central Research Laboratories, Zeria Pharmaceutical Co., Saitama, Japan aut Yamaguchi M. Laboratory of Metabolism and Endocrinology, Graduate School of Nutritional Sciences, University of Shizuoka, 52-1 Yada, 422, Shizuoka, Japan aut Research in Experimental Medicine Springer-Verlag 192/1(1992-12-01), 317-322 0300-9130 192:1<317 1992 192 433 https://doi.org/10.1007/BF02576288 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF02576288 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Segawa Y. Department of Pharmacology, Central Research Laboratories, Zeria Pharmaceutical Co., Saitama, Japan aut NATIONALLICENCE 700 1- Tsuzuike N. Department of Pharmacology, Central Research Laboratories, Zeria Pharmaceutical Co., Saitama, Japan aut NATIONALLICENCE 700 1- Itokazu Y. Department of Pharmacology, Central Research Laboratories, Zeria Pharmaceutical Co., Saitama, Japan aut NATIONALLICENCE 700 1- Tagashira E. Department of Pharmacology, Central Research Laboratories, Zeria Pharmaceutical Co., Saitama, Japan aut NATIONALLICENCE 700 1- Yamaguchi M. Laboratory of Metabolism and Endocrinology, Graduate School of Nutritional Sciences, University of Shizuoka, 52-1 Yada, 422, Shizuoka, Japan aut NATIONALLICENCE 773 0- Research in Experimental Medicine Springer-Verlag 192/1(1992-12-01), 317-322 0300-9130 192:1<317 1992 192 433 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer