Both mercury and cadmium directly influence calcium homeostasis resulting from the suppression of scale bone cells: the scale is a good model for the evaluation of heavy metals in bone metabolism.
To examine the effects of heavy metals such as cadmium and mercury on calcium homeostasis, plasma calcium and calcitonin were measured in goldfish. Cadmium induced hypocalcemia both at 4 and at 8 days. In methylmercury-treated goldfish, the plasma calcium level increased at 2 days and then decreased at 8 days. The plasma calcitonin level increased in correspondence with the increased plasma calcium by methylmercury treatment, although cadmium did not cause a significant change. To elucidate the mechanism in detail, fish scales, which have both osteoclasts and osteoblasts and are similar to mammalian membrane bone, were used in the present study. We measured tartrate-resistant acid phosphatase (TRAP) and alkaline phosphatase (ALP) activity as respective indicators of activity in both types of cells. TRAP activity in the scales decreased by treatment of cadmium and methylmercury at 6 h incubation. Particularly, cadmium (even at 10(-13) M) significantly suppressed TRAP activity, suggesting that this system is utilized as an acute biosensor for cadmium. ALP activity decreased after exposures of 64 and 96 h, although the activity did not change after 6, 18, and 36 h. In addition, mRNA expression of the estrogen receptor and insulin-like growth factor 1, which participate in osteoblastic growth and differentiation, was less than the control values by treatment with both metals. This study demonstrates that mercury directly acts on the bone cells and influences calcium homeostasis and indicates that, in a short-term exposure, mercury has a different action from that of cadmium and induces hypercalcemia.
Noto Marine Laboratory, Institute of Nature and Environmental Technology, Kanazawa University, 927-0553, Ishikawa, Uchiura, Japan. nobuo@kenroku.kanazawa-u.ac.jp
Nobuo
N
Suzuki
Megumi
M
Yamamoto
Kazuo
K
Watanabe
Akira
A
Kambegawa
Atsuhiko
A
Hattori
D000135:Acid Phosphatase / Q000187:drug effects; D000469:Alkaline Phosphatase / Q000187:drug effects; D000818:Animals; D001842:Bone and Bones / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D002104:Cadmium / Q000494:pharmacology*; D002116:Calcitonin / Q000097:blood / Q000187:drug effects; D002118:Calcium / Q000097:blood / Q000378:metabolism*; D002478:Cells, Cultured; D005260:Female; D006054:Goldfish / Q000033:anatomy & histology / Q000378:metabolism; D006706:Homeostasis / Q000187:drug effects*; D006996:Hypocalcemia / Q000139:chemically induced; D007334:Insulin-Like Growth Factor I / Q000187:drug effects / Q000235:genetics; D007527:Isoenzymes / Q000187:drug effects; D008297:Male; D008628:Mercury / Q000494:pharmacology*; D008668:Metallothionein / Q000187:drug effects / Q000235:genetics; D019216:Metals, Heavy / Q000378:metabolism; D008767:Methylmercury Compounds / Q000494:pharmacology; D011960:Receptors, Estrogen / Q000187:drug effects / Q000235:genetics; D000071681:Tartrate-Resistant Acid Phosphatase
D007527:Isoenzymes; D019216:Metals, Heavy; D008767:Methylmercury Compounds; D011960:Receptors, Estrogen; D002104:Cadmium; D007334:Insulin-Like Growth Factor I; D002116:Calcitonin; D008668:Metallothionein; D000469:Alkaline Phosphatase; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase; D008628:Mercury; D002118:Calcium