The effect of fugu parathyroid hormone 1 (fugu PTH1) on osteoblasts and osteoclasts in teleosts was examined with an assay system using teleost scale and the following markers: alkaline phosphatase (ALP) for osteoblasts and tartrate-resistant acid phosphatase (TRAP) for osteoclasts. Synthetic fugu PTH1 (1-34) (100 pg/ml to 10 ng/ml) significantly increased ALP activity at 6 h of incubation. High-dose (10 ng/ml) fugu PTH1 significantly increased ALP activity even after 18 h of incubation. In the case of TRAP activity, fugu PTH1 did not change at 6 h of incubation, but fugu PTH1 (100 pg/ml to 10 ng/ml) significantly increased TRAP activity at 18 h. Similar results were obtained for human PTH (1-34), but there was an even greater response with fugu PTH1 than with human PTH. In vitro, we demonstrated that both the receptor activator of the NF-B ligand in osteoblasts and the receptor activator NF-B mRNA expression in osteoclasts increased significantly by fugu PTH1 treatment. In an in vivo experiment, fugu PTH1 induced hypercalcemia resulted from the increase of both osteoblastic and osteoclastic activities in the scale as well as the decrease of scale calcium contents after fugu PTH1 injection. In addition, an in vitro experiment with intramuscular autotransplanted scale indicated that the ratio of multinucleated osteoclasts/mononucleated osteoclasts in PTH-treated scales was significantly higher than that in the control scales. Thus, we concluded that PTH acts on osteoblasts and osteoclasts in the scales and regulates calcium metabolism in goldfish.3

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Wistar rats (male) were divided into 3 groups - group A (GA) served as control, group B (GB) were daily administered chlorpyrifos (Anu Products Ltd., India) orally at a dose of 5 mg/kg b wt. and animals in group C (GC) received daily an oral administration of chlorpyrifos at a dose of 10 mg/kg b wt. Rats were sacrificed on 1st, 2nd, 4th, 6th and 8th week after initiation of the experiment. Kidneys were extirpated and fixed in aqueous Bouin's solution. The tissues thus fixed were routinely processed for histological studies. The present study showed that the histopathological changes were caused in kidney of rats by chlorpyrifos administration. The changes noticed were mainly the shrinkage of glomerulus at initial stage of treatment, the tubular dilation, the glomerular hypercellularity, hypertrophy of tubular epithelium, degeneration of glomerulus and renal tubules, deposition of eosin-positive substances in the glomerulus and renal tubules and infiltration of leucocytes. A decrease in the body weight gain was observed in chlorpyrifos-treated rats. However, variable intensities of these changes were noticed depending upon the doses and duration of the treatment.

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