Department of Chemistry and Biochemistry, Medical Faculty, University of Rijeka, B Branchetta 22, 51 000 Rijeka, Croatia.
Biol Trace Elem Res. 2011 Oct;143(1):332-43. doi: 10.1007/s12011-010-8841-8. Epub 2010 Sep 16.
To elucidate the role of iron in the pathomechanisms of autoimmune CNS disorders, we estimated the tissue concentrations of Fe(2+) in the brain, spinal cord, and liver in the chronic relapsing form of experimental autoimmune encephalomyelitis (EAE). The disease was induced in Dark Agouti (DA) strain of rats, by subcutaneous injection of bovine brain homogenate in complete Freund's adjuvant (CFA). Control rats consisted of unsensitized rats and of rats treated with CFA or saline. The data obtained by clinical assessment and by inductively coupled plasma spectrometry have shown that the attacks of disease (on the 12th and 22nd post-immunization day) were followed by high accumulation of iron in the liver. Additionally, during the second attack of disease, the decreased concentration of Fe(2+) was found in cervical spinal cord. The data point to regulatory effects of iron and hepatic trace elements regulating mechanisms in the pathogenesis of EAE.
为了阐明铁在自身免疫性中枢神经系统疾病发病机制中的作用，我们测定了慢性复发型实验性自身免疫性脑脊髓炎（EAE）大鼠脑、脊髓和肝脏组织中 Fe(2+)的浓度。该疾病通过牛脑匀浆在完全弗氏佐剂（CFA）中的皮下注射，在 Dark Agouti（DA）大鼠中诱导。对照组由未致敏大鼠和用 CFA 或生理盐水处理的大鼠组成。通过临床评估和电感耦合等离子体光谱法获得的数据表明，疾病发作（免疫后第 12 天和第 22 天）后，肝脏中铁的蓄积量增加。此外，在第二次疾病发作期间，发现颈脊髓中的 Fe(2+)浓度降低。这些数据表明，铁和肝脏微量元素调节机制在 EAE 的发病机制中具有调节作用。
