Effects of hyperthyroidism induced by L-thyroxin administration on lipid peroxidation in various rat tissues.

Thyroid dysfunctions are associated with many pathological signs in the body. One of these is lipid peroxidation that develops due to over- or under-secretion of thyroid hormones. The present study was conducted to determine lipid peroxidation that develops in different tissues including the brain, liver and heart of rats in experimental hyperthyroidism induced by L-thyroxin. The study was carried out on 30 male Sprague-Dawley rats. They were divided into three groups as control, sham hyperthyroidism and hyperthyroidism. Malondialdehyde (MDA) and glutathione (GSH) levels in rat tissues were determined at the end of a 3-weeks period of L-thyroxin administration. It was observed that MDA levels in the hyperthyroidism group were significantly higher in the cerebral cortex, liver and ventriculer tissue of heart (p < 0.001) than in the control and in sham hyperthyroidism groups. GSH levels were higher in the hyperthyroidism group than in control and sham hyperthyroidism groups in all tissues (p < 0.001). Results demonstrate that hyperthyroidism induced by L-thyroxin activates both oxidant and antioxidant systems in cerebral, hepatic and cardiac tissues. However, the increase in antioxidant activity cannot adequately prevent oxidative damage.

The effect of leptin on penicillin-induced epileptiform activity in rats.

Leptin is an adipose tissue-derived peptide hormone, which acts as a satiety factor to reduce appetite by interactions with hypothalamic neurons. The other possible physiological functions of leptin are still unclear. In this study, we have evaluated dose-dependent effect of leptin on penicillin-induced epileptiform activity, analyzed by electrocorticogram (ECoG). The epileptiform activity was induced by microinjection of penicillin into the left sensorymotor cortex. Thirty minutes after penicillin injection, 1, 2 or 10 microg of leptin was administrated intracerebroventricularly (i.c.v.). Leptin (1, 2 or 10 microg) alone did not significantly change the spike amplitudes in non-penicillin pretreated control animals. One or two micrograms of leptin significantly increased the frequency of epileptiform activity in the penicillin-pretreated animals. The high dose of leptin (10 microg) did not significantly change either amplitude or frequency of epileptiform activity. One microgram i.c.v. leptin was the most effective dose in changing of frequency on penicillin-induced epileptiform activity. The proconvulsant effects of leptin appeared 90 min after leptin (1 and 2 microg) injection. These data indicate that leptin increases the frequency of penicillin-induced epileptic activity. We speculate that this action of leptin might suggest that leptin may be a proconvulsant substance.

Effects of trace element levels on platelet aggregation.

Platelet aggregation was measured by an optical method in 32 patients with iron-deficiency anemia at the time of diagnosis and after a period of supplementation with iron. Epinephrine- and adenosine diphosphate-induced platelet aggregation were lower in anemic patients than in the controls (p<0.05). After iron-supplementation therapy, these values showed no significant differences. If induced by collagen or ristocetin, platelet aggregation was the same for patients and controls, but increased after treatment of patients (p<0.05). The plasma zinc values did not show significant differences among the subjects included in this study. These results show that iron is involved in the enzymatic systems that regulate platelet aggregation. The exact nature of this interaction is still to be determined.

Characterization of T lymphocyte subtypes in endotoxin-induced uveitis and effect of pentoxifylline treatment.

PURPOSE: The aims of the study were twofold: 1) to investigate the role of T lymphocyte subtypes in the pathogenesis of endotoxin-induced uveitis (EIU) and 2) to study the possible beneficial effect of pentoxifylline, an inhibitor of neutrophil motility, and Tumor Necrosis Factor-alpha on this disease. METHODS: Forty-two inbred male Lewis rats were divided into seven equal groups. 200 microg of Escherichia coli 055: B55 lipopolysaccharide (LPS) was injected in one hind footpad of the Group 2, 3, 4, 5, 6, and 7 rats. Group 5, 6, and 7 rats also received concomitant intraperitoneal pentoxifylline (PTX) during food pad injection of LPS. Group 1 rats were used as controls with intra-peritoneal normal saline injection. Eight, 24, and 48 hours after treatment, the rats were euthanized. Neutrophil leukocyte, mononuclear cells, and CD4+, CD8+, and CD45RA+ cell infiltration in the anterior uveal tissue were determined either by hematoxylin-eosin or monoclonal antibody staining. Tumor Necrosis Factor-alpha (TNF-alpha) levels were also measured in the aqueous and blood samples. We compared the numbers of infiltrating cells in the different groups. RESULTS: We found that peak infiltration of lymphocyte, neutrophils, and CD4+ cells occurred at 24 hours. However, CD8+ and CD45RA+ cell number reached their highest levels at 48 hours. There was no inflammatory cell infiltration in the control rats. Concomitant pentoxifylline treatment did not affect any of these parameters, although it effectively reduced TNF-alpha concentrations in the anterior chamber and the serum. CONCLUSION: We conclude that, 1) T lymphocytes might be involved in the pathogenesis of endotoxin-induced uveitis. 2) The potential role of pentoxifylline in the treatment of human uveitis is questionable. However, these are initial findings and need confirmation by additional studies.