Tanaka M, Yanagi M, Shirota K, Une Y, Nomura Y, Masaoka T, Akahori F
Department of Veterinary Pathology, School of Veterinary Medicine, Azabu University, Kanagawa, Japan.
Vet Hum Toxicol. 1995 Jun;37(3):203-8.
Three-w-old male Sprague-Dawley rats were given a zinc (Zn)-deficient (0 ppm Zn) or a Zn-adequate diet (30 ppm Zn) supplemented with 0, 0.5 or 100 ppm cadmium (Cd) for up to 5 mo. The proximal convoluted tubules of the kidneys had degenerative changes in the rats fed the Zn-deficient diet containing 100 ppm Cd [Zn 0, Cd 100], but there were no lesions in other groups. Electron microscopy showed cytoplasmic vacuolation of the proximal tubules, mitochondrial swelling and coagulative necrosis in Zn 0:Cd 100 rats. The present study revealed diminished bone growth and cortical thinning of the femur, but there was no osteomalacia seen in Itai-Itai disease patients. The results indicate that Zn deficiency may enhance the renal toxicity of Cd, but that dietary Cd did not cause osteomalacia even under severe Zn-deficient conditions.
将三周龄雄性斯普拉格-道利大鼠分别给予锌(Zn)缺乏(0 ppm锌)或锌充足饮食(30 ppm锌),并补充0、0.5或100 ppm镉(Cd),持续5个月。在喂食含100 ppm镉的锌缺乏饮食的大鼠[锌0,镉100]中,肾脏近曲小管出现退行性变化,但其他组未见病变。电子显微镜显示,锌0:镉100组大鼠近端小管出现细胞质空泡化、线粒体肿胀和凝固性坏死。本研究显示股骨生长减缓且皮质变薄,但痛痛病患者未见骨软化症。结果表明,锌缺乏可能增强镉的肾毒性,但即使在严重锌缺乏条件下,饮食中的镉也不会导致骨软化症。