期刊名称:Journal of Nutritional Science and Vitaminology
印刷版ISSN:0301-4800
电子版ISSN:1881-7742
出版年度:1977
卷号:23
期号:4
页码:349-360
DOI:10.3177/jnsv.23.349
出版社:Center for Academic Publications Japan
摘要:This study was conducted to examine the effects of certain nutritional variables on the onset of renal damage due to oral admini-stration of Cd, and to investigate its reversibility by dietary switch-over in female rats during an observation period of 7 months. Four dietary regimens were adopted: Two basal diets, including a multi-nutritionally deficient diet (10% protein, 0.05% Ca, 0.14% P and no fiber) (designated L) and a normal balanced stock diet (designated N); each diet was fed with and without the addition of Cd 200ppm, and then the 4 diets were designated L (-), N (-), L (+) and N (+). (+) indicates the addition of Cd, while (-) is without addition of Cd. In comparison with the N (+) group, rats fed the L (+) diet for 7 months revealed the following distinct characteristics: 1) Marked growth re-tardation due mainly to decreases in food intake and food efficiency (Cd-induced protein-calorie malnutrition). 2) Marked depilation, general or localized, due to abnormal behavior of biting and eating each other's hair. 3) Progressive increase in Cd output in urine, particularly five months after starting the dietary treatment, and an increased output of uri-nary protein. 4) Significant elevation of accumulated Cd in the kidney (and also in the liver). These observations were further supported by “switch-over” experiments, showing that the above-mentioned changes were reversed to normal when the L (+) diet was replaced by either the L (-) or even the N (+) diet, whereas the abnormal changes became evident when the diet was switched to the L (+) diet three months after the experiment. Moreover, renal ac-cumulation of Cd was remarkably increased in the L (+) group, in spite of much less Cd intake than in the N (+) group. These findings strongly suggest that nutritional factor(s) play an impor-Cant role in the early development of Cd poisoning, in particular in the development of renal damage, presumably due to enhanced input of Cd in the body.