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In the current study, we examined the effects of Cd on Cd, Cu, Zn and Fe levels in placenta and maternal and fetal plasma and tissues, the placental weight,, total fetal and maternal body weights, and fetal and maternal tissue weights during pregnancy. A total of 21 adult female rats were treated during gestation with drinking water containing one of the following: 70 mg/L of CdCl2, a combination of 70 mg/L of CdCl2 and 70 mg/L Of CuSO4, or no addition (control). Placenta Cu and Fe levels, fetal liver and kidney Cu levels, and fetal liver tissue weights were lower in the group administered Cd than in the control group. Also, Cd levels in the placenta, maternal and fetal liver, and maternal kidney were higher in the group treated with Cd than in controls. In the group administered both Cd and Cu, fetal body and tissue weights did not change, but Cd levels in the placenta, maternal and fetal liver, and maternal kidneys were higher than in controls. Zn and Fe levels in the maternal kidney and fetal liver were also lower in this group. Cd exposure during pregnancy resulted in Cd accumulation in maternal and fetal tissues during pregnancy and a decrease in the total weight of fetuses, and the combination of Cd and Cu caused some changes in the both maternal and fetal levels of Cu, Zn, and Fe, but it did not cause changes in the total fetal body weight or the weights of individual tissues. (C) Versita Warsaw and Springer-Verlag Berlin Heidelberg. All rights reserved. C1 [Turgut, Sebahat; Emmungil, Guelten; Turgut, Guenfer; Genc, Osman] Pamukkale Univ, Fac Med, Dept Physiol, TR-20070 Denizli, Turkey. [Enli, Yasar; Demir, Sueleyman; Kaptanoglu, Buenyamin] Pamukkale Univ, Fac Med, Dept Biochem, TR-20070 Denizli, Turkey.

Cisplatin (CDDP) is one of the most commonly used antineoplastic agents in current clinical practice. The major toxicities of CDDP are nonhaematological as nephrotoxicity and ototoxicity. Free oxygen radicals are known to play major role in CDDP-induced acute renal failure in rats. α-Tocopherol is one of the well-known antioxidant agents. This study was designed to investigate the role of α-tocopherol pretreatment against CDDP-induced lipid peroxidation in rat kidney. Male Wistar rats were divided into three groups and treated as follows: control (saline intraperitoneally), CDDP (10 mg/kg, intraperitoneally), α-tocopherol (200 mg/kg, plus CDDP, intraperitoneally). Rats were sacrificed on third day of the treatment, and kidney tissues were obtained and analyzed. CDDP-treated rats showed high malondialdehyde (MDA) levels (p< 0.05). In the CDDP plus α-tocopherol group, renal MDA levels were not significantly different from the controls. These data suggest that α-tocopherol may be used to prevent CDDP-induced lipid peroxidation.

Cisplatin (CDDP) is one of the most commonly used antineoplastic agents in current clinical practice. The major toxicities of CDDP are nonhaematological as nephrotoxicity and ototoxicity. Free oxygen radicals are known to play major role in CDDP-induced acute renal failure in rats. ?-Tocopherol is one of the well-known antioxidant agents. This study was designed to investigate the role of ?-tocopherol pretreatment against CDDP-induced lipid peroxidation in rat kidney. Male Wistar rats were divided into three groups and treated as follows: control (saline intraperitoneally), CDDP (10 mg/kg, intraperitoneally), ?-tocopherol (200 mg/kg, plus CDDP, intraperitoneally). Rats were sacrificed on third day of the treatment, and kidney tissues were obtained and analyzed. CDDP-treated rats showed high malondialdehyde (MDA) levels (p< 0.05). In the CDDP plus ?-tocopherol group, renal MDA levels were not significantly different from the controls. These data suggest that ?-tocopherol may be used to prevent CDDP-induced lipid peroxidation.

To investigate the effect of amifostine (AMI, WR-2721) against lipid peroxidation caused by adriamycin in rat heart tissue, male Wistar rats, weighing 190-220 g, were divided into three groups and treated as follows: 1) vehicle (saline) control (n = 6); 2) Adriamycin (10 mg/kg, intraperitoneally) (n = 6); 3) Adriamycin plus amifostine (200 mg/kg) (n = 6). Amifostine was applicated to rats 30 minutes previously from Adriamycin application. Rats were sacrificed on third day after drug application and hearts were removed. The hearts were washed with cold saline solution and were stored at -20°C until analysed. The tissues were thawed and homogenised with an Ultra Turrax. Lipid peroxidation was assayed as the malondialdehyde (MDA) levels reacting with thiobarbituric acid, according to the method of Ohkawa. Tissue MDA levels were significantly increased by adriamycin (p

We intended to study the effect of swimming exercise on the brain, liver and heart malondialdehyde (MDA) levels which are the last product of oxidation, and to compare them with the brain, liver and heart MDA levels of controls. The experiments were carried out on 20 Wistar rats which were fed with a standard laboratory chow diet ad libitum. Rats were distributed in two groups, control group (n = 10) and exercise group (n = 10). The exercise group rats were exposed to swimming exercise for 30 minutes. After this animals in each group were sacrificed by decapitation, their brain, liver and heart tissues were quickly removed. MDA levels of the brain, liver and heart were determined according to the method in which MDA reacts with thiobarbituric acid. Results were evaluated by the Mann-Whitney U test. The liver and heart MDA levels in the exercise group were (29.59+/-6.73 and 10.49+/-1.90 nmol/g tissue, respectively) significantly higher than in the control group (21.78+/-3.46 and 8.86+/-1.25 nmol/g tissue, p

Kaplan, Suleyman/0000-0003-1477-5002; AYYILDIZ, Mustafa/0000-0002-6594-3080 WOS: 000185127200005 There are many studies on zinc as a possible cause of neuronal hyperactivity and cell death. The present study was designed to investigate the changes in total pyramidal cell number of rat hippocampus after intracortical zinc sulphate (ZnSO4, 200 mug/kg, i.e.) and a nitric oxide synthase (NOS) inhibitor aminoguanidine (AG) administration. Animals were divided into three groups as control, zinc and the treatment (zinc+AG) groups. Each group was divided into two subgroups, as 7-day group and 15-day group. Zinc sulphate was injected intracortically into 2 mm lateral of Bregma. The same volume of saline (2 mul) was given to the rats belonging to the control group. Rats in the third group were given ZnSO4 + AG in the same injection point. Animals in the third group only received 100 mg/kg AG intraperitoneally twice a day for periods of 7 or 15 days. Total pyramidal neuron number was estimated using the optical fractionator method. The total number of pyramidal cells found in the left hippocampus was 653,468 +/- 3,452 and 601,860 +/- 3,348 in the control groups; 257,968 +/- 1,277 and 250,555 +/- 1,443 in the zinc groups; 382,519 +/- 1,973 and 365,880 +/- 2,658 in the treatment groups in 7-day post treatment and 15-day post treatment rats, respectively. These results suggest that zinc has a neurotoxic effect on pyramidal neurons in rat hippocampus (p < 0.05) and an inhibitor of nitric oxide synthase, AG, decreases cell loss (p < 0.05). This shows that nitric oxide (NO) contributes to this type of neurotoxicity in the rat hippocampus and also suggests a possible therapeutic role for NOS inhibitor in neurodegenerative diseases.

The aim of this study was to evaluate the effects of sevoflurane anaesthesia on renal functions by conducting with or without soda lime comparatively. Eighteen male Wistar rats were divided into three equal groups randomly. Sevoflurane in 1.5 % concentration were administered directly to first group in 4 L/min fresh gas flow (50 % O2 + 50 % N2O), while the second group were applied the same gas mixture through soda lime, that is exposed to 150 mL/min carbon dioxide. Third group were control group, breathing room air. Glucose in blood specimens at the begining and end of application and glucose, gamma glutamyl transferase and protein levels were measured in urine samples collected during application period. Renal tissue specimens were evaluated histopathologically. Groups were similar with respect to blood glucose levels. Although urine glucose levels were higher in both of two study groups compared to control (p

WOS: 000168217600007 The effects of the calcium channel blocker flunarizine on cadmium-induced Purkinje cell loss in the cerebellum of rats were investigated. Rats were divided into three groups: control, cadmium, and cadmium+flunarizine. Saline was administered intracortically to the first group, cadmium sulphate (0.0021 mg/kg) to the second group, and cadmium sulphate (0.0021 mg/kg) and flunarizine (1 mg/kg) to the third group. All rats were observed for 1 week, but only the rats in the third group were injected with flunarizine (10 mg/kg/day, i.p.) during this period. One week later, all rats were perfused intracardially. Series of frontal sections from the cerebellum were stained with thionin. Purkinje cells were counted at x 400 magnification under a light microscope. Purkinje cell density was 20.62 +/- 0.68/mm (average +/- SD) in the right hemisphere and 20.56 +/- 0.79/mm in the left hemisphere of the control group; 14.23 +/- 0.34/mm in the right hemisphere and 14.17 +/- 0.44/mm in the left hemisphere of the cadmium group; and 18.46 +/- 0.59/mm in right hemisphere and 17.76 +/- 0.84/mm in left hemisphere of the cadmium+flunarizine group. The results suggest that flunarizine may attenuate Purkinje cell death caused by cadmium (P < 0.05).

WOS: 000171790300004 The present study was designed to investigate the effects of nicardipine on cadmium-induced Purkinje cell loss in cerebellum of rats. Animals were divided into three groups as control, cadmium and cadmium + nicardipine groups. Saline, cadmium sulphate (0,0021 mg/kg) and cadmium sulphate (0,0021 mg/kg) + nicardipine (1 mg/kg) were intracortically administered respectively. All rats were observed for one week, but only the rats in the third group were injected nicardipine (10 mg/kg/day, i.p.) during this period. One week later, all rats were perfused intracardially. Series of frontal sections from cerebella were stained with Thionin staining. Purkinje cells were counted under x400 magnification via a light microscope. Cadmium administration caused 25-35 % decrease in Purkinje cell density in Crus I, Crus II and Lobulus Simplex areas of cerebellum in cadmium group (p

WOS: 000168217600008 Epilepsy is a neurological disorder that affects approximately 1% of the world population. It is accepted that calcium influx into the cell is the first step of epileptic neuronal events. In the present study, the effects of flunarizine on epileptiform activity were investigated in an experimental epilepsy model induced by intracortical (i.c.) penicillin administration. The left cerebral cortex was exposed by craniotomy in anaesthetised rats. The epileptic focus was produced by injection of penicillin G potassium (500 units) into the somatomotor cortex. After epileptiform activity reached maximum frequency and amplitude, flunarizine was injected into the same area with a Hamilton microinjector. Before flunarizine administration, the average frequency of spikes was 18.7 +/- 2.1 /min and the average amplitude of the spikes was 1123 +/- 85 muV. Microinjection of flunarizine (10, 100 muM) into the same area inhibited electrocorticogram epileptiform activity for 4-5 minutes (p

A lot of substance have been known to cause neuronal hyperactivity and cell death. Effects of cadmium on cerebral and cerebellar neurons are subject to interest for a long time which is present in cigarette smoke and filthy air. In present study, it was aimed to investigate the effects of cadmium sulphate (CdSO4) on purkinje cells in Lobulus Simplex area in cerebellum of rats. CdSO4 (0.0021 mg/kg) is administered intracortically in 1.5 mm laterally of left Bregma with 1-2 mm depth. The same ratio of saline is administered to rats in control group. Seven-day group was treated for 7 days and animals in 30-day group received a 30 days treatment. Then, rats were perfused by neutral formaline intracardially. Cerebellum was separated from other structures of the brain and cut into sections with a distance 75-100 (m and with a thickness 6 ?m. Sections were stained with thionin staining. Purkinje cells were counted under a light microscope with a magnification of 400x. Density of purkinje cells was found to be 18.79 ± 0.16 neuron/mm in right cerebellum and 19.22 ± 0.15 neuron/mm in left cerebellum of control group. In 7-day group, neuronal density was found to be 13.08 ± 2.64 neuron/mm and 13.57 ± 2.73 neuron/mm for right and left hemispheres, respectively. In 30-day treatment group, neuronal density was found to be 11.57 ± 2.02 and 11.98 ± 2.41 neuron/mm for right and left cerebellum, respectively. The difference between groups was statistically significant (p < 0.05). Results obtained from present study suggest that cadmium has neurotoxic effect and causes a decrease in cell number.

In the present study, changes in Purkinje cell density of rat cerebellum after intracortical cadmium sulphate (CdSO4) and nicardipine, a calcium antagonist administration have been investigated. Animals were divided into three groups. First group received saline while the second group received CdSO4 (0.0021 mg/kg) and the third group received CdSO4 (0.0021 mg/kg) and nicardipine (1 mg/kg). Rats were than survived for seven days under physical observation. Only the third group received daily nicardipine injection (10 mg/kg/day, i.p.) during this period. After one week all animals were perfused intracardially. Serial sections obtained from cerebellum were stained by Thionin staining method. Purkinje cells were counted under 400x magnification of a light microscope. Purkinje cell density is found to be 20.53 ± 0.69/mm in right and 20.46 ± 0.47/mm in left hemisphere of control group; 13.36 ± 0.58/mm in right and 13.23 ± 0.44/mm in left hemisphere of cadmium group; 16.36 ± 0.69/mm in right and 16.00 ± 0.84/mm in left hemisphere of cadmium + nicardipine group. These results suggest that cadmium has neurotoxic effects and nicardipine may protect neurons from cadmium-induced toxicity (p < 0.05).

There are lots of reports about zinc causes cell death due to neuronal hyperactivity. In this study, effect of nicardipine (a calcium antagonist) on cell death caused by zinc was investigated. Zinc sulphate (500 ?g/kg) was injected intracortically into 2 mm lateral of bregma. The same of volume of saline (2 ?l) was given to the rats of control group. In the third group, zinc + nicardipine were injected into same place of the brain. Animal groups were observed for a week. The zinc + nicardipine group received daily nicardipine (10 mg/kg) for seven days. After a week, the rats were perfused intracardially with neutral formaline. The hippocampal sections were stained with hematoxylen-eosine. Pyramidal cells were counted under light microscope (with 400x magnification). The density of pyramidal cell was found in the control, zinc and zinc + nicardipine as 126.48 ± 1.8 neuron/mm, 38.3 ± 0.52 neuron/mm, 88.4 ± 1.4 neuron/mm respectively. The differences between the groups were found to be statistically significant (p < 0.001). The results show that nicardipine considerably decreases cell death caused by zinc in the hippocampus of rat. Nicardipine an exert this effect by preventing the influx of calcium.

The neurotoxic and convulsant effects of zinc have been shown in several reports. In this study the density of pyramidal neurons was investigated in hippocampus after intracortical injections of zinc sulfate. Rats were divided into three groups. Zinc sulfate (500 ?g/kg) was injected into the left hippocampus (near the Bregma) in first group. Zinc sulfate (500 ?g/kg) and verapamil (1 mg/kg) were injected to the same region into the left hippocampus in the second group and an identical volume of saline (2 ?l, %0.9) was given to the same region in third group as control group. After one-week observation, animals were perfused intracardially with neutral formalin (%10) under deep anaesthesia. The serial hippocampal sections were stained with the hematoxylen-eosine. The pyramidal neurons in the dorsal hippocampus were counted under light microscope (with 400 x magnification). The density of pyramidal cell was found in control, zinc and zinc + verapamil 112.48 ± 4.58/mm, 35.12 ± 1.35/mm, 93.90 ± 2.06/mm as respectively. The present results provide direct evidence that zinc might be a relatively potent neurotoxic in the central nervous system. Therefore it can be concluded that verapamil as a calcium antagonist decreased the central neural loss which is caused by zinc sulfate, by preventing calcium into the cell.