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Öğe The Effects of Cisplatin on the Kidney Metabolism: Role of Ginkgo Biloba Extract(2004) Yilmaz H.R.; Işik B.; Güleç M.; Sö?üt S.; Akyol Ö.In this study, we aimed to examine whether antitumour drug cisplatin affect the metabolism of the kidney and consequently causes kidney damage and, Ginkgo biloba extract prevents this damage in rats. The experimental groups were as follows: Control group, Cisplatin-treated group (Cisplatin), and a group treated with Cisplatin plus Ginkgo biloba extract (GBE). The Cisplatin and Cisplatin+GBE groups were treated intraperitoneally with a single dose of 7 mg/kg body weight sisplatin at 4th day of the treatment. GBE was administrated at a dose of 100 mg/kg body weight orally, three days before and seven days after the treatment with cisplatin in the cisplatin+GBE group. Kidney tissues were taken 7 day after the cisplatin administration. The activities of kidney hexokinase (HK), glucose-6-phosphate dehydrogenase (G6PD), lactate dehydrogenase (LDH) and malate dehydrogenase (MDH) serum enzymes were determined in each sample. The results of the experiment demonstrated that HK, G6PD, LDH, and MDH activities were increased significantly in the cisplatin group compared with control group. HK and G6PD activities were increased significantly in the cisplatin group compared with control group. G6PD activity was increased significantly in the cisplatin+GBE group compared with cisplatin group, and LDH activity was decreased significantly in the cisplatin+GBE group compared with cisplatin group. From these results, it can be concluded that cisplatin may cause kidney damage through metabolic enzymes and, GBE may prevent damage caused by cisplatin.Öğe Nonsynaptic neurotransmission(2003) Akyol Ö.; Ünal S.Information in the brain is transmits by both synaptic and nonsynaptic neurotransmission (NSN). NSN includes the diffusion through the extracellular fluid of neurotransmitters released from nonsynaptic varicosities and high-affinity transmitter receptors and transporters. This high-affinity uptake system is the target of many neurotransmitters such as noradrenaline, dopamine, serotonin, acetylcholine and nitric oxide (NO) and also many drugs such as tricyclic antidepressants, psychostimulants serotonin reuptake blockers, and anticonvulsants. NSN also includes the diffusion of substances such as NO and carbon monoxide (CO) through both extracellular fluid and cellular membranes. It has been shown that NO can influence the function of uptake carrier systems. In this paper, the possible roles of NSN in the brain activity and drug actions are reviewed.Öğe The relationships between plasma and erythrocyte antioxidant enzymes and lipid peroxidation in patients with rheumatoid arthritis(Elsevier Masson SAS, 2001) Akyol Ö.; Işçi N.; Temel I.; Özgöçmen S.; Uz E.; Murat M.; Büyükberber S.Objective. The present study was undertaken to evaluate the activities of some key erythrocyte and plasma enzymes participating in free radical metabolism and the end product of lipid peroxidation in rheumatoid arthritis, and whether there are any differences for these parameters between newly diagnosed untreated patients and rheumatoid arthritis patients on drug therapy. Patients and methods. Superoxide dismutase and catalase activities, and malondialdehyde levels were determined in erythrocytes and plasma samples from 54 patients with rheumatoid arthritis (21 of whom without any treatment and 33 on classical therapy regimens) and from 33 healthy controls. Results. There were no statistically significant differences in mean values of activities of the erythrocyte enzymes between the patients and controls. Malondialdehyde levels were significantly increased in both newly diagnosed untreated patients and patients on drug therapy compared to control subjects. Malondialdehyde levels were lower in the treated group than the newly diagnosed untreated group (0.214 ± 0.111 ?mol/L and 0.388 ± 0.075 ?mol/L, respectively) (P < 0.0001). Mean plasma superoxide dismutase activity was lower in the group of newly diagnosed untreated patients compared to those of the treated and control groups (1.31 ± 0.069 U/mL, 1.79 ± 0.94 U/mL and 2.48 ± 0.94 U/mL, respectively) (P < 0.0001, untreated vs control groups). Conclusions. These results suggest sufficient antioxidant enzyme activities in erythrocytes in patients with rheumatoid arthritis and also increased lipid peroxidation end products in newly diagnosed untreated patients compared to control group and patients on drug therapy. © 2001 Éditions scientifiques et médicales Elsevier SAS.
