Abstract
Summary
A single dose of thallium acetate, which in itself produces no detectable organ lesions in the rat, causes severe nephrocalcinosis strictly limited to the corticomedullary junction line if an otherwise non-nephrotoxic dose of dihydrotachysterol (DHT) is administered simultaneously. The DHT-induced calcification in aorta and in traumatized skin regions is greatly aggravated by concurrent treatment with thallium acetate. This sensitizing effect of thallium acetate cannot be ascribed to its stressor action, since under comparable circumstances, exposure to stress (restraint) actually prevents the manifestations of DHT-intoxication.
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