Methotrexate (MTX), a folic acid antagonist, is widely used as a cytotoxic chemotherapeutic agent. MTX-associated neurotoxicity is an important clinical problem. The aim of this study was to investigate the role of caffeic acid phenethyl ester (CAPE) on cerebellar oxidative stress induced by MTX in rats. A total of 19 adult male rats were divided into three experimental groups as follows: MTX group (MTX treated), MTX+CAPE group (MTX+CAPE treated), and control group. MTX was administered intraperitoneally (i.p.) with a single dose of 20 mg kg(-1) on the second day of experiment. CAPE was administered i.p. with a dose of 10 micromol kg(-1) day(-1) for 7 days. Malondialdehyde (MDA) levels and activities of superoxide dismutase (SOD) and catalase (CAT) were determined in cerebellar tissue of rats. MTX caused to significant increase in MDA levels (an important marker of lipid peroxidation) in the MTX group compared with the controls (p = 0.006). CAPE significantly reduced the MTX induced lipid peroxidation in the MTX+CAPE group compared to the MTX (p = 0.007). The activities of SOD and CAT were significantly increased in the MTX group when compared with the control group (p = 0.0001, p = 0.004, respectively). The increased activities of these enzymes were significantly reduced by CAPE treatment (p = 0.004, p = 0.034, respectively). As a result, CAPE may protect from oxidative damage caused by MTX treatment in rat cerebellum.
A 31-year-old patient with multiple sclerosis (MS), treated with interferon beta-1b (IFNB-1b) for two years, presented with fatigue and dizziness. Coombs' positive autoimmune hemolytic anemia (AIHA) was found. Other potential etiologies of AIHA were ruled out. An association with IFNB-1b was highly suspected. Interferon therapy was discontinued and prednisone therapy instituted. There was resolution of the hemolytic anemia, and prednisone therapy was tapered gradually. To the best of our knowledge, there is no reported case of the development of AIHA associated with IFNB-1b use in MS patients. We conclude that if an unexplained drop in hematocrit occurs with a MS patient receiving IFNB-1b, autoimmune mediated hemolysis should also be considered.
N(G)-Nitro-L-arginine methyl ester hydrochloride (L-NAME) is a non-specific nitric oxide (NO) inhibitor and it has been used to eliminate the role of NO in many studies like animal models for hypertension. In this study, we aimed to investigate whether lisinopril treatment has any biochemical and/or histopathological effect on rat liver tissue in a L-NAME-induced hypertension model. Forty-eight 6-weeks-old male Spraque-Dawley rats were used in the study. The animals used in the study were randomly divided into four equal groups. To induce hypertension, L-NAME was added to drinking water at a concentration of 600 mg/l and each rat was given 75 mg/kg/day of L-NAME for 6 weeks. Tail cuff systolic blood pressure (SBP) was measured at first, third, and sixth weeks. There was a significant difference between the experiment groups and controls. In only lisinopril given and L-NAME plus lisinopril administered groups, each rat was given 10 mg/kg of lisinopril for 6 weeks. At the end of the study, the animals were sacrificed. Blood and tissue samples were collected for biochemical and histopathological analysis. It has been observed that mean NO level was significantly decreased in L-NAME given group (p<0.05). Mean ALT levels were significantly increased in lisinopril and L-NAME plus lisinopril given groups, when compared with the control group (p<0.05). AST levels were in normal range in all groups (p>0.05). Hepatocyte degeneration was prominent in lisinopril given group, whereas mononuclear cell infiltration was significant in L-NAME given groups. Although the beneficial effects in L-NAME-induced hypertension treatment, lisinopril can lead to some unexpected results like hepatocyte degeneration, serum enzyme level elevation, and slight mononuclear cell infiltration.
<P>The authors describe a case of pheochromocytoma presenting with bithalamic infarction, dementia, and elevated intraocular pressure. The patient received glaucoma treatment to suppress high intraocular pressure in addition to antihypertensive and antidiabetic medication for his complaints. Bilateral fundus examination and visual field defects revealed glaucoma-like changes. Adrenelectomy improved all complaints and all medications were stopped. Intraocular pressure and visual field changes improved. Pheochromocytoma presenting with bithalamic infarction, dementia, and increased IOP in the same patient is unusual. Adrenelectomy can improve dementia, increased IOP, and glaucoma-like changes in such cases. [<CITE>Ophthalmic Surg Lasers Imaging</CITE> 2007;38:245-247.]</P> <H4>AUTHORS</H4> <P>From the Department of Neurology (S. Kutluhan, S. Kilbas, SD, GA); and the Department of Ophthalmology (OÇ, YB), Süleyman Demirel University Medical School, Isparta, Turkey.</P> <P>Accepted for publication January 20, 2007.</P> <P>Address correspondence to Yavuz Bardak, MD, Department of Ophthalmology, Süleyman Demirel University Medical School, Çünür, Isparta, 32260 Turkey.</P>
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