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Background/Aim: In the present study, we aimed to compare the potential protective effects of thymoquinone and melatonin by using equivalent dose, on oxidative stress-induced ischemia-reperfusion (IR) injury in the intestinal tissue of rats. Materials and Methods: The study was performed using 32 male Wistar-Albino rats (weighing 180-200 g) randomly divided into four groups: Group I, sham group; Group II, IR group; Group III, IR with melatonin group; and Group IV, IR with thymoquinone group. After laparotomy, ischemia and reperfusion were performed for 60 and 120 min, respectively, on all the groups. Intestinal tissue sections were stained using routine histological methods and examined under the light microscope. In addition, the sections were immunohistochemically stained using the TUNEL method for determination of apoptosis. Superoxide dismutase (SOD) activity, glutathione peroxidase (GSH-Px) activity, and malondialdehyde (MDA) levels in the intestinal tissue were also measured. Results: The IR group had significantly elevated tissue SOD activity, GSH-Px activity, and MDA levels compared with the sham group. Administration of thymoquinone and melatonin efficiently reduced these increases. Statistically significant number of apoptotic cells was observed in the intestinal tissue of IR group rats compared with the sham group. Treatment with thymoquinone and melatonin markedly reduced the number of apoptotic cells. Conclusion The effects of melatonin and thymoquinone on IR-induced oxidative stress in rat intestines were similar. Our findings suggest that melatonin and thymoquinone protect against IR-induced injury to intestinal tissues.

Aim： To show the oxidative stress after cigarette smoke exposure in rat testis and to evaluate the effects of caffeic acid phenethyl ester （CAPE）. Methods： Twenty-one rats were divided into three groups of seven. Animals in Group Ⅰ were used as control. Rats in Group Ⅱ were exposed to cigarette smoke only （4 × 30 min/d） and rats in Group Ⅲ were exposed to cigarette smoke and received daily intraperitoneal injections of CAPE （10 μmol/kg.d）. After 60 days all the rats were killed and the levels of nitric oxide （NO） and anti-oxidant enzymes such as superoxide-dismutase, catalase and glutathione peroxidase （GSH-Px） and the level of malondialdehyde were studied in the testicular tissues of rats with spectrophotometric analysis. Results： There was a significant increase in catalase and superoxide-dismutase activities in Group Ⅱ when compared to the controls, but the levels of both decreased after CAPE administration in Group Ⅲ. GSH-Px activity was decreased in Group Ⅱ but CAPE caused an elevation in GSH-Px activity in Group Ⅲ. The difference between the levels of GSH-Px in Group Ⅰ and Group Ⅱ was significant, but the difference between groups Ⅱ and Ⅲ was not significant. Elevation of malondialdehyde after smoke exposure was significant and CAPE caused a decrease to a level which was not statistically different to the control group. A significantly increased level of NO after exposure to smoke was reversed by CAPE administration and the difference between NO levels in groups Ⅰ and Ⅲ was statistically insignificant. Conclusion： Exposure to cigarette smoke causes changes in the oxidative enzyme levels in rat testis, but CAPE can reverse these harmful effects. （Asian J Andro12006 Mar; 8： 189-193）

This study aimed to investigate the acute cardiotoxic effects of high dose toluene and its damage mechanisms on heart tissue in the acute period. Twenty adult male Wistar Albino rats (200-220 g) were used in this controlled experimental animal study. Animals were divided into two equal groups: a control group (Group 1) and a high dose (6 mL/kg/gavage) toluene-administered group (Group 2). Arterial blood pressure (BP) and heart rate (HR) values were measured at 30th, 60th and 90th minutes after toluene was administered. At the end of the experimental period, blood samples and heart tissues were taken from the rats. Serum troponin T levels were assayed. Heart tissue sections were stained using routine histological methods and examined under a light microscope. In addition, the sections were immunohistochemically stained using the avidin-biotin-peroxidase method to determine caspase-3 immunoreactivity and TUNEL to detect apoptosis. To compare the apoptotic index, the Mann-Whitney U test was used. For comparisons between the two groups, the independent t- test was used. In addition, time-based changes of intra-group parameters were evaluated using paired t tests. BP and HR values were low in toluene-treated rats compared to the control group. Troponin T levels were increased in toluene-administered animals as compared with controls [Toluene group: 0.140 (0.010-2.000) ng/mL vs control group: 0.010 (0.010-0.010) ng/mL, p=0.01]. Histopathologic examination of heart tissue sections showed congestion and edema in toluene administrated rats. Higher TUNEL positivity and (+++) immunoreactivity for caspase-3 protein were observed in the toluene group compared to the control group. The present study demonstrated that high doses of toluene cause apoptosis and may lead to impairment of cardiac function in the acute period.

Aim： To evaluate the effects of melatonin on antioxidant enzyme levels and histopathologic changes in dizocilpine （MK-801）-induced psychosis model rat testis. Methods： A total of 24 adult male Wistar-Albino rats were divided into three groups with 8 in each. Group I was used as control. Rats in Group II were injected with MK-801 （0.5 mg/kg body weight i.p. for 5 days）. In addition to MK-801, melatonin （50 mg/kg body weight i.p. once a day for 5 days） was injected into the rats in Group Ⅲ. The testes were harvested bilaterally for biochemical and histopathological examinations. Antioxidant enzyme activities, malondialdehyde, protein carbonyl and nitric oxide （NO） levels in testicular tissues were analyzed using spectrophotometric analysis methods. Histopathological examinations of the testes were also performed. Results： MK-801 induced testicular damage, which resulted in significant oxidative stress （OS） by increasing the levels of antioxidant enzymes. The malondialdehyde, protein carbonyl and NO levels were increased in testicular tissues of rats. Treatment with melatonin led to significant decrease in oxidative injury. Administration of melatonin also reduced the detrimental histopathologic effects caused by MK-801. Conclusion： The results of the present study showed that MK-801 cause OS in testicular tissues of rats and treatment with melatonin can reduce the harmful effects＇of MK-801. （Asian JAndro12008 Mar; 10： 259-265）

Aim: Neurotoxicity is the next common side effect of cisplatin (CDDP)-based chemotherapeutics following nephrotoxicity. We investigated the effect of CDDP on some brain metabolic enzyme activities such as hexokinase (HK), glucose-6-phosphate dehydrogenase (G6PD), lactate dehydrogenase (LDH), and malate dehydrogenase (MDH) in an experimental model of CDDP toxicity, and examined the protective role of Caffeic acid phenethyl ester (CAPE), a phenolic antioxidant derived from the honeybee propolis, on the enzyme activities mentioned above. Methods: Female Wistar albino rats were divided into three groups: sham operation group (n:6), CDDP group (n:9), and CAPE + CDDP group (n:8). All the chemicals used were applied intraperitoneally. HK, G6PD, LDH, and MDH activities were determined spectrophotometrically in the brain supernatant at the end of the surgical procedures. Results: There were decreased G6PD activities and increased MDH activities in CDDP group compared to control group (p<0.05, p<0.05). LDH activities were increased in CAPE+CDDP group compared to CDDP group (p<0.001). Conclusion: These results provide a new point of view on the glucose metabolizing enzymes of brain tissue affected from CDDP and the protective effects of CAPE on these enzymes.

The aim of this study is to determine the protective effects of vitamin D 3 and dehydroascorbic acid (DHA), a blood-brain barrier transportable form of vitamin C, against ischemia/reperfusion (I/R) injury on a middle cerebral artery occlusion/reperfusion model of brain since reactive oxygen species play an important role in the pathophysiology of I/R injury in brain. In order to examine antioxidant status and lipid peroxidation, we assayed malondialdehyde (MDA) levels as a marker of lipid peroxidation, and reduced glutathione (GSH) and superoxide dismutase (SOD) enzyme activities as free radical scavenging enzymes in cortex and corpus striatum (CS). Wistar albino rats were divided into five equal groups of each consisting of seven rats: control, I/R, I/R + DHA, I/R + vitamin D 3 , and I/R + vitamin D 3  + dehydroascorbic acid groups. MDA levels were found to be increased in the I/R group, I/R + DHA, and I/R + vitamin D 3 groups compared with the control group in both cortex and corpus striatum. However, MDA level were found to be significantly decreased in only I/R + vitamin D 3  + DHA group compared with the I/R group in cortex ( P  < 0.0001). MDA levels were not significantly different in I/R + DHA, and I/R + vitamin D 3 groups compared with the I/R group. GSH and SOD enzyme activities were significantly decreased in I/R, I/R + DHA, and I/R + vitamin D 3 groups compared with the control group in both cortex and corpus striatum (CS) ( P  < 0.0001). Whereas, both GSH and SOD activity were increased in I/R + vitamin D 3  + DHA group compared with the I/R group in both cortex and CS ( P  < 0.001 in cortex, P  < 0.001 in CS for SOD P  < 0.002 in cortex P  < 0.03 in CS for GSH). Our results demonstrate that the combination of vitamin D 3 and DHA treatment prevent free radical production and dietary supplementation of vitamin D 3 and DHA which may be useful in the ischemic cerebral vascular diseases.

There is a great evidence that reactive oxygen species (ROS) play an important role in the pathophysiology of ischemia -reperfusion(I/R)injury in skeletal muscle.Caffeic acid phenethyl ester(CAPE)is a component of honeybeep ropolis.It has antioxidant, anti-inflammatory and free radical scavenger properties.The aim of this study is to determine the protective effects of CAPE against I/R injury in respect of protein oxidation, neutrophil in filtration, and the activities of xanthine oxidase(XO)and adenosine deaminase(AD)onan

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