Trace minerals in experimental subarachnoid haemorrhage: zinc, copper and manganese levels in rat brain tissue, blood and urine


Cosan T. E., Demir T., Yayla E., Cosan D., Berber A., Kaynak Z.

ACTA NEUROCHIRURGICA, sa.4, ss.443-448, 2006 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Basım Tarihi: 2006
  • Doi Numarası: 10.1007/s00701-006-0745-1
  • Dergi Adı: ACTA NEUROCHIRURGICA
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.443-448
  • Eskişehir Osmangazi Üniversitesi Adresli: Evet

Özet

Background. Zinc (Zn), copper (Cu) and manganese (Mn) are involved in regulatory systems in the cell. Their role in neuromodulator activities and redox reactions has been implicated in the pathogenesis of neurological disorders. The aim of this study was to determine changes of Zn, Cu and Mn levels in brain tissue, blood and urine after experimental subarachnoid haemorrhage (SAH). The possible importance of these trace minerals on the pathogenesis of SAH was also discussed. Method. Rats were divided into three groups; namely a SAH group, a control group and a normal group. Blood samples in the SAH group and normal saline in the control group were injected into the cisterna magna. No surgical procedures were performed on the normal group. Brain tissue, blood and urine samples were measured for trace minerals by atomic absorption spectrophotometry. Measurements were taken on days 3, 7 and 10 after the onset in the control and SAH groups, and on the first day in the normal group. Findings. The reduced blood Zn levels and increased Zn urine loss observed in the SAH group were conspicuously significant. Furthermore, significant changes in Mn levels were also seen at different stages of the trial in the SAH group. However, differences found in the Cu levels between the groups were not significant enough to explain the results. Interpretation. These results suggest that the low blood Zn levels seen throughout the stages, the low brain tissue Mn levels seen during the latter part of the trial, and the low blood Mn levels observed during the early stages, may all be related to an increased risk in experimental SAH in rats. These differences may have possible role in the pathogenesis of SAH, and further investigations into the reduced blood Mn levels observed during the study may lead to new insight into the treatment of SAH.