Reactive oxygen species (ROS) and serum ferritin levels are both considered to be important biological factors in the pathogenesis of myelodysplastic syndrome (MDS). This study evaluated the levels of ROS in 40 patients with MDS (19 males and 21 females) using the Free Radical Analytical System, FRAS4, and derivatives of reactive oxygen metabolite kits. The patients' mean age was 67.3 years (range 58 - 86 years). The sera of 34 (85%) patients exhibited higher levels of oxidative stress than the reference range. There was a positive correlation between ROS levels and serum ferritin levels, and a negative correlation between ROS levels and haemoglobin levels. There was a negative relationship between serum haemoglobin and ferritin levels. The results indicated that iron accumulation or severe anaemia could contribute to oxidative stress in MDS patients. Iron chelation and antioxidant therapy may be suitable for the management of MDS.

Nonspecific cross‐reacting antigen (NCA) immunoreactivity was localized in normal and neoplastic human tissues using a monoclonal antibody to 55, 90 and 95 kDa molecules of NCA. This was compared to the localization of immunoreactive carcinoembryonic antigen (CEA) as demonstrated by polyclonal and monoclonal antibodies. In frozen sections, CEA was localized in normal surface epithelium of the stomach and colon where NCA was only weakly detected. Type 1 and type 2 like pneumocytes were positive for NCA, while CEA was localized only in type 2‐like pneumocytes. CEA and NCA were both demonstrated in ductal cells of frozen pancreatobiliary and mammary tissues. The antigenicity of CEA and NCA in normal tissues was significantly lost after paraffin embedding as compared to frozen sections. NCA was consistently demonstrated in eccrine sweat glands embedded in paraffin. In various tumor tissues, CEA and NCA were colocalized and expression increased sufficiently to be detected in paraffin sections. Adenocarcinomas of the stomach and colon and cystadenocarcinoma of the pancreas, as well as neuroendocrine carcinomas of the lung and thyroid, showed a CEA predominance over NCA. In ductal adenocarcinomas of the pancreas and breast and in cholangiocarcinoma, NCA reactivity was greater than CEA. Keratiniring foci of most squamous cell carcinomas of mucosal origin and some adenocarcinomas equally expressed both. Hepatocellular carcinoma, lobular mammary carcinoma and papillary thyroid carcinoma were positive only with unabsorbed polyclonal antibody which widely recognizes CEA‐related substances. Renal cell carcinoma, prostatic adenocarcinoma, transitional cell carcinoma, anaplastic carcinomas, choriocarcinoma and basal cell carcinomas showed little or no immunoreactivity. Hence the relative ratio of CEA/NCA expression in tumors was dependent on the tissue of origin and histologic type. The cytoplasmic granular staining of NCA in cancer cells was a noteworthy difference from the plasma membrane‐associated localization of CEA. Acta Pathol Jpn 40: 85–97, 1990.

Summary4-Aminopyrazolopyrimidine (4-APP)-induced fatty livers were analyzed biochemically and immunohistochemically. Biochemically, lipid peroxide levels measured by thiobarbituric acid method in the rat liver homogenates were markedly increased following 4-APP administration. However, glutathione peroxidase (GSH-PO) activity in the same homogenates was decreased. In addition, immunohistochemical localization of GSH-PO in 4-APP-treated rat liver was also decreased. Based on our data, we strongly suggested that pathogenesis of 4-APP induced-fatty liver may be due to uncontrolled free radical formation, peroxidation of lipids, and an associated lipid accumulation in the liver.Key Words : 4-aminopyrazolopyrimidine (4-APP), fatty liver, pathogenesis, lipid peroxidation, glutathione peroxidase (GSH-PO) Pathogenesis of the fatty livers induced by certain kinds of chemical agents such as carbon tetrachloride [1] and ethanol [2] has been well identified as due to free radical production in the cellular components and followed by the lipid peroxidation. Concomitantly with triglyceride accumulation in the livers of rats receiving carbon tetrachloride or ethanol, liver peroxide values are also increased. On the other hand, glutathione peroxidase (GSH-PO) has been well recognized to effectively reduce the organic hydroperoxides induced by liver injury [3].In the present study, in order to confirm the relationship between fatty changes and lipid peroxidation in the liver, we made biochemical and immunohistochemical analyses of the livers of rats administered with 4-aminopyrazolopyrimidine (4-APP) as agent, which inhibits the secretion of triglycerides from liver [4][5][6].