Bone modeling in gallium nitrate-treated rats

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Abstract
Gallium nitrate (GaN) reduces cancer-related hypercalcemia and inhibits bone resorptionin vitro. This study investigated the effects of chronic GaN administration on bone, kidney, and parathyroid gland activity of growing rats. Experimental animals received GaN (1.75 mg elemental gallium i.p. QOD×8, Ga+), and controls received the solvent (Ga−). In the bone of Ga+ rats the number of osteoclasts was increased (Ga+: 70.4±2.31 osteoclasts/mm2; Ga−: 46.5±1.61 osteoclasts/mm2,P+ than in Ga− calvaria (Ga+: Alp 223±23.4 U/mg prot, Ga−: Alp 145±13.3 U/mg prot,P+: Acp 69.5±4.7 U/mg prot, Ga−: 57.5±2.8 U/mg prot,P+: 112.9±17.6 pg/ml, Ga−: 41.4±7.4 pg/ml,P+: 2.4±0.02 mmol/l, Ga−: 2.6±0.03 mmol/l,P+: 0.11±0.04 mmol/l, Ga−: 0.33 ±0.03 mmol/lP<0.01). In conclusion, Ga, at the dosage used, does not inhibit the activity of osteoblasts in rats and does not interfere with mineralization but increases the number of osteoclasts through stimulation of parathyroid gland activity, induced by a fall in serum calcium. The hypocalcemia seems to be related to skeletal resistance to PTH and to increased renal calcium loss.