REEVALUATION OF TRACE ELEMENTS-DEFICIENCY

本研究通过建立大鼠锌缺乏模型，探讨金属缺乏引起的生物学变化。虽然出现了严重的症状，但模型存活时间较长。这一结果表明，该模型适用于研究锌缺乏的影响。摄入锌缺乏的饮食抑制体重的增加。此外，口服摄入的饮食降低碱性磷酸酶的活性和血清锌的值。在缺锌模型中，在皮肤和食管中观察到肥大伴角化不全。本研究还对小鼠睾丸和胸腺进行了组织病理学观察，以探讨其与细胞凋亡的关系。苏木精-伊红染色观察组织病理学变化。用TUNEL法检测细胞凋亡的促进作用.当给予缺锌饮食时，在睾丸和胸腺中检测到细胞凋亡的增加，然后出现萎缩等形态学变化的迹象。这些结果表明，细胞凋亡的增加导致胸腺和睾丸萎缩，细胞凋亡的增加与免疫和生殖系统受损直接相关。另一方面，通过免疫组织化学方法检测了缺锌饲料下睾丸中iNOS的表达。iNOS表达的增加先于凋亡的增加。这些结果表明，NO也与缺锌引起的睾丸损伤有关。

A rat model of zinc (Zn) deficiency was made in order to investigate the biological changes induced by metal deficiencies. Although sever symptoms developed, the model alive for long time. This result indicates that this model is suitable for investigating the effects of Zn deficiency. Ingestion of the Zn-deficiency diet suppressed the increase in body weight. Also, oral intake of the diet reduced the activities of alkaline phosphates and the value of serum Zn. In the Zn deficiency models, hypertrophy with parakeratosis was seen in the skin and esophagus. Atrophy of the thymus and testis was also found in them.In the next study, to investigate the relationship between histopathological changes and apoptosis, the testis and thymus were examined. Histophathological changes ware examine by Hematoxylin-Eosin stain. And acceleration of apoptosis was mainly tested by the TdT - mediated dUTP- biotin neck end labeling (TUNEL) method. When the Zn-deficiency diet was given, increases in apoptosis were detected in the testis and thymus before signs of morphological changes such as atrophy. These results suggest that increase in apoptosis cause atrophy of thymus and testis and that the increase in apoptosis directly correlates to compromised immune and reproductive systems.On the other hand, expression of iNOS was examined in the testis fed on Zn-deficient diet by immunohistochemistry. An increase of iNOS expression was seen before the increase of apoptosis. These findings indicate that NO is also related to testicular damages caused by Zn deficiency.