Aluminum toxicity perturbs long bone calcification in the embryonic chick

• Published in: Archives of toxicology Vol. 73; no. 7; pp. 359 - 366
• Main Authors: FIRLING, C. E, HILL, T. A, SEVERSON, A. R
• Format: Journal Article
• Language: English
• Published: Berlin Springer 01.09.1999
• Subjects: Alkaline Phosphatase - metabolism; Aluminum Compounds - toxicity; Animals; Biological and medical sciences; Calcification, Physiologic - drug effects; Calcium - metabolism; Chemical and industrial products toxicology. Toxic occupational diseases; Chick Embryo; Citrates - toxicity; Collagen - metabolism; Embryonic and Fetal Development - drug effects; Femur - chemistry; Femur - diagnostic imaging; Femur - drug effects; Femur - embryology; Hindlimb - chemistry; Hindlimb - diagnostic imaging; Hindlimb - drug effects; Hindlimb - embryology; Medical sciences; Metals and various inorganic compounds; Osteocalcin - blood; Parathyroid Hormone - blood; Peptide Fragments - blood; Procollagen - blood; Radiography; Sodium Citrate; Tibia - chemistry; Tibia - diagnostic imaging; Tibia - drug effects; Tibia - embryology; Toxicology; Embryonic development; Embryo; Toxicity; Acute; Diseases of the osteoarticular system; Aluminium; Vertebrata; Chronic; Malformation; Mineralization; Tibia; Animal; Calcification; Light metal; Chicken; Bone; Teratogen; Aves
• ISSN: 0340-5761; 1432-0738
• DOI: 10.1007/s002040050674

Long bone calcification in chick embryos acutely- or chronically-treated with aluminum (Al) citrate was investigated. Acutely treated embryos received 100 microl of 60 mM Al citrate, 60 mM sodium (Na) citrate, or 0.7% sodium chloride on day 8 of incubation. Chronically treated embryos received a daily 25 microl dose of the above solutions beginning on day 8. Following 2-8 days of additional incubation, blood was collected, embryos killed, hind limbs radiographed, and tibias collected. Radiography indicated that Al administration resulted in a persistent angulation in the mid-diaphysis of tibias and femurs and a transient mineralization defect during the 10- to 12-day period of incubation. Tibias from 10- to 12-day embryos which were administered Al contained significantly less (P < 0.005) bone calcium (Ca) compared with tibias from NaCl-treated embryos. By day 14 there were no significant differences among the Ca content of tibias from embryos acutely treated with Al citrate, Na citrate or NaCl. Similarly, the rate of (45)Ca uptake by tibias of embryos treated with Al was significantly lower on days 10 (acute) and 12 (chronic) with no significant differences in Ca uptake rate among the three treatment groups by day 16. In each treatment group bone alkaline phosphatase (ALPase) activity increased approximately tenfold between days 10 and 16. At all stages, bone ALPase activity was consistently higher and significantly different (chronic) compared with levels in NaCl-treated embryos. In contrast, Al had no significant effect on the rate of tibia collagen and noncollagenous protein synthesis or serum levels of procollagen carboxy-terminal propeptide (PICP), osteocalcin, and parathyroid hormone (PTH).