Background-Familial Mediterranean fever (FMF) is a genetically linked disorder common amongst races ofthe Eastern Mediterranean region. Typical symptoms include episodic pain syndrome extending throughout the chest or abdomen associated with histopathological signs of amyloidosis of the kidney. Aim-To investigate possible connections between the aseptic inflammation that occurs during pain crises and cell membrane structural and functional integrity in patients with FMF. Methods-Oxidative stress parameters in 42 patients in remission and during a pain crisis were compared with 21 normal subjects. Results-The patient group had significantly greater concentrations of chemiluminescent and thiobarbituric acidreactive substances in the blood plasma and lower concentrations of a-tocopherol than the control group while in remission; these changes were exacerbated during pain crises. Analyses of the phospholipid composition of erythrocyte membranes showed significant increases in amounts of acidic phospholipids (phosphatidic acid, monophosphatidylinositol and cardiolipin) and lysophosphatidylcholine compared with healthy subjects. Conclusions-The pattern of differences in membrane phospholipid composition was consistent with increased oxidative stress in patients with FMF. (7 Clin Pathol 1996;49:453-455)

The phospholipid and ganglioside composition in bone marrow progenitors of lymphocytes, thymocytes and mature lymphocytes of intact rats and rats with sarcoma 45 were studied. The lymphocytes and their progenitors were isolated by Ficoll-Paque density centrifugation. The phospholipids and gangliosides were separated by thin-layer chromatography following standard chloroform:methanol extraction from the cells. Alterations in the lipid spectrum (both phospholipids and gangliosides) were shown to take place during lymphocyte differentiation. The rate of ganglioside sialylation diminished, which was expressed as an increase in mono- and di-, and a decrease in tri- and tetrasialoganglioside levels. Tumor-induced alterations in lymphocyte lipid composition involve all stages of lymphocyte differentiation. These shifts are believed to be connected with a disturbance of the antineoplastic function of lymphocytes and, consequently, the immune response of the tumor-bearing organism.

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Alflatoxin B1 (AFB1) is the most hepatotoxic and : Background hepatocarcinogenic of the aflatoxins and occurs as a contaminant in a variety of foods. The toxicity of AFB1 has been shown to be associated with a wide range of pathological events, such as enhanced apoptosis and oxidative events. Currently there is no treatment for mycotoxin exposure. The aim of this study was to evaluate the potential ability of picolinyl-L-phenylalaninate (PLP), picolinyl-L-tryptophanate (PLT), and nicotinyl-L-tryptophanate (NLT) Schiff base amino acid derivatives to act against damaging effects of AFB1 using a rat model of mycotoxicosis. For this purpose, a range of markers of immune and antioxidant systems in liver and blood plasma samples, as well as the apoptotic rate in neutrophils and monocytes was assessed.Mongrel : Methods white pubescent rats (with 180-200g b/w) were used in all experiments. Concentration of the markers of immune and antioxidant systems was measured in plasma by ELISA, using commercially available kits according to manufacturers' instructions. The rate of apoptosis in neutrophils and monocytes was analyzed by flow cytometry.AFB1 induced : Results mycotoxicosis caused significant elevation of malonic dialdehyde contents (plasma and liver: p = 0.0001 compared with untreated rats), the levels of superoxide dismutase (p=0.005), total non-enzymatic water-soluble antioxidants (p = 0.0001), and terminal complement complex (p = 0.021). Moreover, the increased rates of early and late apoptosis in neutrophils and monocytes were observed as well. Treatment with PLP, PLT and NLT were shown to mitigate these effects, though to a different extent.The : Conclusions results obtained in this study clearly demonstrated that chronic AFB1 exposure induced oxidative cell damage, immunosuppression and apoptosis of circulating immune cells. The oral administration of Schiff base cyclic amino acid derivatives was capable of minimizing the detrimental effects of mycotoxicosis by possessing multi-mechanistic effects that target AFB1-induced pathological events.