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以超微结构形态计量学及硫胺素焦磷酸酶（ＴＰＰａｓｅ）细胞化学和血清睾酮放射免疫测定等，探讨镉对大鼠精囊腺的影响及其作用机理。结果表明，大鼠腹腔内注射氯化镉（２ｍｇ／ｋｇ体重）后１ｈ，主细胞超微结构出现改变，ＴＰＰａｓｅ反应产物开始减少，１５～３０ｄ退变最明显，６０ｄ呈恢复趋势。主要改变为线粒体肿胀，高尔基复合体囊泡扩大，髓样结构及脂滴增多。注射后１５ｄ，主细胞大分泌颗粒体密度、面数密度明显减少，３０ｄ消失，６０ｄ有所恢复。大分泌颗粒直径于３ｄ开始减小，１５ｄ降至正常直径１／２，６０ｄ仍未恢复。注射镉后７ｄ血清睾酮含量显著降低，６０ｄ仍未恢复正常。提示镉对精囊腺有早期直接损伤作用，睾酮下降及毛细血管内皮损伤则又加速精囊腺退变。
The effects of cadmium on seminal vesicle in rats and its mechanism were investigated by ultrastructural morphometry, cytochemistry of thiamine pyrophosphatase (TPPase) and radioimmunoassay of serum testosterone. The results showed that the ultrastructure of the main cells changed at 1h after intraperitoneal injection of cadmium chloride (2mg / kg body weight), and the reaction products of TPPase began to decrease. The degeneration was most obvious at 15 ~ 30d and recovered at 60d. The main changes to mitochondria swelling, Golgi complex vesicle expansion, medullary structure and lipid droplets increased. Fifteen days after injection, the density of major cell secretory granules and the number density decreased significantly, disappearing on the 30th day and recovering on the 60th day. The diameter of the cells secreted in the beginning of 3d decreased, 15d reduced to normal diameter 1/2, 60d still did not recover. Serum testosterone levels were significantly reduced 7 days after injection of cadmium, 60d still not returned to normal. Tip cadmium on the seminal vesicle early direct damage, decreased testosterone and capillary endothelial injury and accelerate seminal vesicle degeneration.