REEVALUATION OF TRACE ELEMENTS-DEFICIENCY

建立大鼠缺锌模型，研究缺锌引起的生物学变化。虽然出现了严重的症状，但该模型仍存活了很长时间。这一结果表明，该模型适用于缺锌效应的研究。摄入缺锌饮食抑制了体重的增加。此外，口服饲料还降低了碱性磷酸酶的活性和血清锌的值。缺锌模型大鼠皮肤和食道角化不全，皮肤肥大。在下一项研究中，为了研究组织病理学变化与细胞凋亡的关系，对睾丸和胸腺进行了检查。苏木精-伊红染色观察组织病理学改变。TdT介导的dUTP-生物素颈端标记法(TUNEL)主要检测细胞的促凋亡作用。当给予缺锌饮食时，在出现萎缩等形态变化的迹象之前，睾丸和胸腺中的细胞凋亡就增加了。这些结果表明，细胞凋亡率的增加导致胸腺和睾丸萎缩，细胞凋亡率的增加与免疫和生殖系统受损直接相关。另一方面，用免疫组织化学方法检测了缺锌饲料喂养的大鼠睾丸中iNOS的表达。诱导型一氧化氮合酶的表达在细胞凋亡率增加之前即可见。这些结果表明，NO也与锌缺乏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.