The effect of allopurinol on focal cerebral ischaemia: an experimental study in rabbits.

In this experimental study, the neuroprotective effect of the xanthine oxidase inhibitor allopurinol on focal cerebral ischaemia created by permanent middle cerebral artery occlusion (MCAO) was investigated. Using high performance liquid chromatography (HPLC), we measured hypoxanthine, xanthine, and uric acid (UA) levels in rabbit brains following focal cerebral ischaemia. Rabbits were randomly and blindly assigned into four groups of eight animals each. The control groups received 2% carboxymethylcellulose solution, while 10% allopurinol 150 mg/kg was given to the treatment group 1 h before ischaemia. Each group was subdivided into two groups which were sacrificed 4 h or 24 h after ischaemia, respectively. UA and xanthine values of the rabbits in the control groups were quite high at both times and highest after 24 h, particularly in the centre of the ischaemia. A significant decrease in UA and xanthine values was observed in rabbits that were given allopurinol (P<0.05). According to our results, it was concluded that allopurinol pretreatment protects neural tissue in the early period after arterial occlusion and prevents cerebral injury in the late period, especially in the perifocal area, possibly by preventing the formation of free radicals with xanthine oxidase inhibition.

Tear nitrite and nitrate levels as nitric oxide end products in patients with Behçet's disease and non-Behçet's uveitis.

To evaluate the role of nitric oxide (NO) in ocular inflammation, tear nitrite and nitrates (NN) as NO end products were determined in 11 patients with Behçet's disease (BD) and in 11 with non-Behçet's uveitis (NBU) during the active and remission stages and in 12 healthy controls. Median (with the range) NN levels were 82.29 (59. 60-98.25) micromol/l in the active and 98.25 (52.88-246.92) micromol/l in the remission stage of BD; 88.17 (25.99-116.73) micromol/l in the active and 83.00 (31.04-250.28) micromol/l in the remission stage of NBU and 109.17 (88.17-158.74) micromol/l in the controls. The NN levels in the active stage of BD and NBU were significantly decreased when compared to the controls (p < 0.05; Kruskal-Wallis test). Decreased NN levels at the activation stage may be caused by the rapid transformation of the NO to peroxynitrites, which are highly oxidizing and cytotoxic substances.

Selenium concentrations in serum, lens and aqueous humour of patients with senile cataract.

Selenium (Sc) is a trace element which incorporates into the selenoenzyme glutathion peroxidase. Cataractogenesis may be caused either by the excess or deficiency of this trace element. More recently, its potential of becoming a possible environmental pollutant has been emphasized. In an attempt to reveal the relationship of this element with cataractogenesis, we detected its level in 48 serum, 36 lens and 9 aqueous humour samples of 48 patients with senile cataract, comparing the results with appropriate controls. Selenium levels (mean +/- SD) of cataractous patients were found to be 0.28 +/- 0.04 microgram/ml (CI: 0.27 to 0.29 microgram/ml) in sera (controls: 0.32 +/- 0.04 microgram/ml; CI: 0.30 to 0.34 microgram/ml, p < 0.0001), 5.43 +/- 3.07 microgram/g dry weight (CI: 4.43 to 6.43 microgram/g dry weight) in lens (controls: 4.43 +/-2.53 microgram/g dry weight; CI: 2.78 to 6.08 microgram/g dry weight; p=0.374) and 0.19 +/- 0.06 microgram/ml (CI:0.15 to 0.23 microgram/ml) in aqueous humour samples (controls: 0.31 +/-0.12 microgram/ml; CI: 0.24 to 0.38 microgram/ml, p = 0.02). When patient subgroups were analyzed, serum Se levels were found to be 0.28 +/- 0.05 microgram/ml (CI: 0.26 to 0.30 microgram/ml in the nuclear cataract and 0.28 +/- 0.02 microgram/ml (CI: 0.27 to 0.30 microgram/ml) in the cortical cataract. Lens Se levels, on the other hand, were detected as 5.91 +/- 3.56 microgram/g dry weight (CI:4.49 to 7.33 microgram/g dry weight) in the nuclear cataract and 4.47 +/- 1.40 microgram/g dry weight (CI: 3.68 to 5.26 microgram/g dry weight) in the cortical cataract. It is anticipated that decreased Se in aqueous humour and sera of patients with senile cataract may reflect defective antioxidative defense systems which may lead to the formation of cataract.

Lipid peroxidation in experimental spinal cord injury. Comparison of treatment with Ginkgo biloba, TRH and methylprednisolone.

Ischaemia-induced lipid peroxidation is one of the most important factors producing tissue damage in spinal cord injury. In our study, the protective effects of Ginkgo biloba, thyroid releasing hormone (TRH) and methylprednisolone (MP) on compression injury of the rat spinal cord were investigated. For this study 45 rats in four groups, including control, MP, TRH and Gingko biloba, were used to determine the formation of malondialdehyde (MDA). All the animals were made paraplegic by the application clip method of Rivlin and Tator. Rats were divided randomly and blindly to one of four treatment groups (ten animals in each). MP and Ginkgo biloba treatments significantly decreased MDA levels (F = 54.138, P < 0.01). These results suggest that MP and Ginkgo biloba may have a protective effect against ischaemic spinal cord injury by the antioxidant effect.

Portal tract macrophages are increased in alcoholic liver disease.

Previous studies indicated decreased numbers and depressed clearance function of hepatic macrophages in alcoholic liver disease (ALD). We examined hepatic macrophages by immunohistochemical techniques in 45 liver biopsies from patients with a spectrum of ALD and compared them with 20 histologically normal biopsies from non-alcoholic patients. Antisera against lysozyme, alpha 1-antitrypsin (alpha 1AT) and a cytoplasmic molecule on macrophages (MAC-387) were used and the number of positively staining hepatic sinusoidal macrophages and portal tract macrophages assessed separately. Portal tract macrophage numbers were increased with all three markers in biopsies exhibiting only fatty change (P less than 0.05) and with MAC-387 in all ALD groups. In agreement with previous studies, lysozyme positive hepatic sinusoidal macrophages were decreased in all ALD groups. However, the other markers did not show any significant decrease and MAC-387 positive macrophages were increased in livers with cirrhosis plus hepatitis (P less than 0.01). The use of three markers revealed phenotypic heterogeneity of hepatic macrophages with antibodies to lysozyme and alpha 1 AT staining more hepatic sinusoidal macrophages than MAC-387, but MAC-387 and anti-lysozyme staining more portal tract macrophages than anti-alpha 1AT. Since hepatic macrophages appear to be heterogeneous and capable of diverse functions including the release of cytotoxic mediators, the finding of increased numbers, even in early ALD, suggests they may contribute to the increased numbers, even in early ALD, suggests they may contribute to the tissue damage.