| Project/Area Number |
09557032
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
Hygiene
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| Research Institution | Saitama Medical School |
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Principal Investigator |
WADA Osamu Saitama Medical School, Medicine, Professor, 医学部, 教授 (60009933)
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| Co-Investigator(Kenkyū-buntansha) |
NODERA Makoto Saitama Medical School, Assistant, 医学部, 助手 (70189413)
YANAGISAWA Hiroyuki Saitama Medical School, Associate Professor, 医学部, 助教授 (10200536)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥12,600,000 (Direct Cost: ¥12,600,000)
Fiscal Year 1999: ¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 1998: ¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 1997: ¥7,000,000 (Direct Cost: ¥7,000,000)
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| Keywords | rat / zinc deficiency / testis / thymus / atrophy / apoptosis / 脱毛 / TUNEL法 / 亜鉛 / 動物モデル / 欠乏 / 血清亜鉛 / ALP活性 / 錯角化 |
|---|
| Research Abstract |
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.
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