REEVALUATION OF TRACE ELEMENTS-DEFICIENCY

为了研究锌缺乏症引起的生理变化，建立了大鼠锌缺乏症模型。虽然出现了严重的症状，但模型存活了很长时间。结果表明，该模型适用于研究缺锌的影响。摄入缺锌饮食抑制了体重的增加。此外，饲粮的口服摄入降低了碱性磷酸盐的活性和血清锌的价值。在缺锌模型中，皮肤和食管出现肥大伴角化不全。胸腺和睾丸也有萎缩。在接下来的研究中，为了研究组织病理学变化与细胞凋亡的关系，我们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变化。细胞凋亡加速主要通过TdT介导的dUTP-生物素颈部末端标记法（TUNEL）检测。当给予缺锌饮食时，睾丸和胸腺细胞凋亡增加，并出现萎缩等形态学改变。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的受损直接相关。另一方面，用免疫组化的方法检测了锌缺乏的睾丸中iNOS的表达。凋亡增加前iNOS表达增加。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.