Die Verteilung von Nicotinsaeure und Nicotinamid im Panseninhalt von Schafen

Beschreibung einer Nachweismethode fuer Nicotinsaeure (NIA) und Nicotinamid (NAM) aus biologischen Proben mittels HPLC. In groben Futterpartikeln des Pansens wurde 9.2 mcg freie NIA, 3.9 mcg gebundeneNIA und 0 mcg NAM/g TS gefunden, in der partikelfreien Fluessigkeit lag die NIA-Konzentration immer unter 0.5 mcg/ml, in den gazefiltrierbaren Partikeln betrug die NIA-Konzentration bei Fuetterung von Kraftfutter/Heu 128 mcg und bei Mais/Haferstroh 103 mcg/g TS. Bei intraruminaler Gabe wurde NAM im Pansen innerhalb von 2 Std. zu NIA umgesetzt, letztere wurde von der Pansenschleimhaut nicht absorbiertAvailable from: Zentralstelle fuer Agrardokumentation und -information (ZADI), Villichgasse 17, D-53177 Bonn / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekSIGLEDEGerman

The Effects of a Vitamin D–deficient Diet on Chronic Cadmium Exposure in Rats

Itai-itai disease (IID) of humans is one of the most severe forms of chronic Cadmium (Cd) intoxication occurring mainly in post-menopausal women and is characterized by osteoporosis with osteomalacia, renal tubular disorder, and renal anemia. Some researchers insist the major cause of IID is not Cd but malnutrition, especially hypovitaminosis D. We administrated a low concentration of Cd chloride intravenously to OX female rats that were fed a vitamin D deficient diet or a normal diet for 50 weeks. The vitamin D deficient diet decreased serum concentration of vitamin D, but did not affect the metabolism of the kidney or bone. Cd treatment alone induced a decrease in serum concentration of vitamin D as well as renal dysfunction, renal anemia and abnormal bone metabolism. Osteoporosis with osteomalacia, tubular nephropathy, fibrous osteodystrophy and bone marrow hyperplasia occurred following Cd treatment. In rats treated with Cd and administered a vitamin D deficient diet, the toxic effects of Cd on kidney, bone and hematopoiesis were enhanced in comparison to rats treated with the Cd and a normal diet. The present experiment demonstrated that hypovitaminosis D did not evoke morphologic features of IID in humans but did enhance the Cd-induced toxicity in the rat model of this disease