Protective effects of thymoquinone and melatonin on intestinal ischemia-reperfusion injury.

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.

Beneficial effects of melatonin and BQ-123 on the rat testis damage caused by cigarette smoke.

BACKGROUND/AIM: Several studies have demonstrated that cigarette smoke has detrimental effects on testicular function. However, it is unknown whether melatonin or BQ-123 has beneficial effects on the rat testis damage caused by cigarette smoke. The aim of the present study was to investigate the beneficial effects of melatonin or BQ-123 on the testicular damage caused by cigarette smoke. MATERIALS AND METHODS: Twenty Wistar rats were randomly divided into 4 equal groups: control group (n = 5), cigarette smoke group (n = 5), melatonin group (n = 5), and BQ-123 group (n = 5). At the end of 4 weeks, all the rats were sacrificed for histopathological evaluation and subsequent stereological analysis. The optical fractionator counting method, the most efficient and unbiased method, was used to estimate the total number of spermatogonia and spermatocytes. RESULTS: All the control testes demonstrated complete spermatogenesis. There was a significant decrease in the germ cells of rats exposed to cigarette smoke for 4 weeks. After the application of melatonin or BQ-123, the total number of spermatogonia and spermatocytes in the testes was significantly higher. CONCLUSION: Based on these findings, melatonin and BQ-123 are able to minimize the degenerative effects of cigarette smoke by increasing the germ cell count.

Acute cardiotoxic effects of high dose toluene: an experimental study.

OBJECTIVE: This study aimed to investigate the acute cardiotoxic effects of high dose toluene and its damage mechanisms on heart tissue in the acute period. METHODS: 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. RESULTS: 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. CONCLUSION: The present study demonstrated that high doses of toluene cause apoptosis and may lead to impairment of cardiac function in the acute period.

Aquaporin-1 and aquaporin-3 expressions in the intervertebral disc of rats with aging.

OBJECTIVE: The intervertebral disc (IVD) undergoes biochemical and morphologic degenerative changes during the process of aging. Aquaporins (AQPs) are a family of water channel proteins that facilitate water and small solute movement in tissues and may have a potential role in the aging degeneration of IVDs. One of the important problems in understanding disc degeneration is to find cellular molecules which contribute to the pathogenesis of IVDs. XThe aim of this study was to demonstrate the expression of aquaporin 1 and 3 in nucleus pulposus (NP), annulus fibrosus (AF) cells of rat lumbar intervertebral discs from both young and aged animals using immunohistochemistry. MATERIAL AND METHODS: Twenty Wistar-albino rats were included in the study. The rats were separated into two groups: 2-month-old rats (n=10) as the young group, 18-month-old rats (n=10) as the old group. The intervertebral disc tissues obtained from the lumbar spine (L1-L4, 4 discs) were used for immunohistochemical staining of AQP-1 and 3. RESULTS: This study demonstrated that AQP-1 and AQP-3 immunoreactivity significantly decreased in NP and AF of aged rats compared to the young rats. CONCLUSION: We suggest that AQP-1 and 3 may contribute to the age related degeneration of the intervertebral disc.

Prenatal exposure to diclofenac sodium changes the morphology of the male rat cervical spinal cord: a stereological and histopathological study.

Diclofenac sodium is one of the most commonly used non-steroidal anti-inflammatory drugs. It may cause alteration in the nervous system during neuronal development. However, there is no investigation concerning its role in the cervical spinal cord. Pregnant rats were divided into two groups, namely drug-treated and control (saline-injected) groups. To obtain the offspring of the drug-treated group, a dose of 1mg/kg daily diclofenac sodium (Voltaren, 75 mg/3 ml ampoule, Novartis) was injected into the pregnant rats beginning from the 5th day after mating to the 20th day of the pregnancy. To obtain the control group of offspring, serum physiological at a 1 ml/kg daily dose was injected into the pregnant control rats during the same period. Male offspring were obtained after delivery and each group was divided into two subgroups: 4-week-old and 20-week-old. The total neuron number in diclofenac sodium-treated rats was significantly lower than in the control group animals. The total volume of the cervical spinal cord segments (C1-C4) was also estimated. There was a significant difference between the volumes of the two groups, especially in the 20-week-old subgroup. This may suggest that development of neurons and volume of cervical spinal cord are affected in prenatal animals after administration of diclofenac sodium.

Stereologic analysis of bone produced by distraction osteogenesis or autogenous bone grafting in mandible.

To our knowledge, in the literature, any other investigation that numerically compared osteoblasts retrieved from transport distraction osteogenesis and bone grafting procedures using stereological methods is not reported. The purpose of this study was to compare the total number of osteoblast cells at 3 months in bone produced by distraction osteogenesis and that in autogenous bone graft. A total of 19 growing sheep (male aged 7 or 8 mo; weighing between 21 and 28 kg) were used in this study. Mandibular discontinuity defects created in mandibles of sheep were reconstructed by transport distraction osteogenesis and iliac crest bone graft and allowed to heal for 3 months. The animals were then killed, and the jaws were resected and prepared to be decalcified. Stereological and histologic examinations were performed. Intramembranous ossification and osteoid and trabecular formations were observed in both groups. In the distraction group, the mean +/- standard deviation (SD) numerical density of the osteoblasts was found to be higher (0.0004866 +/- [0.000044])when compared with those of both the graft (0.0003458 +/- [0.000030]) and control groups (0.0002714 +/- [0.000022]). Statistically significant differences were found among the groups (P < 0.05). Stereologic evaluation of bone in the sheep model demonstrated significantly greater osteoblast density in bone formed through transport distraction osteogenesis when compared with bone grafting and the control. Therefore, further studies should be conducted to evaluate the differences in both osteoblastic and osteoclastic cellular activities at different time points in distraction osteogenesis and autogenous bone grafting to assess the healing process of bone for clinical applications.

The combination of vitamin D3 and dehydroascorbic acid administration attenuates brain damage in focal ischemia.

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.

Increased frequency of familial Mediterranean fever in northern Turkey: a population-based study.

Familial Mediterranean fever (FMF) is a systemic relapsing autoinflammatory disorder occurring in populations originating from the Mediterranean basin, mainly Turks, Levantine Arabs, Sephardic Jews, Druze, and Armenians. The prevalence of FMF shows considerable geographical variation. In Turkey, the prevalence rates were reported as 0.0027-0.25%. This field survey was conducted in different regions to investigate the frequency of FMF in a northern province of Turkey. This study was conducted in 70 areas (12 urban and 58 rural) in the province of Tokat, which is in northern Turkey. The population of Tokat was reported to be 828,000 at the last census in Turkey in 2000, about 530,000 for individuals aged >18 years ( http://www.die.gov.tr ). Mean age of 1,095 (541 male and 554 female; urban 555 and rural 540) subjects was 41 +/- 17 (range 18-95 years). FMF frequency in this study was 1/123 (0.82%, 95 CI: 0.40-1.61). Mean age of patients were 27 years (20-41) and mean age of symptoms were 16.3 years (11-23). In conclusion, the frequency of FMF in this study was 1/123 (0.82%) which was higher than expected. This rate is the highest frequency of FMF reported from Turkey. Further large sample studies are needed to define to true prevalence of FMF in Turkey.

The intra-articularly located ligament variation of the first metatarsophalangeal joint.

An intra-articularly located ligament in the first metatarsophalangeal joint of the left foot has been detected in a patient. The intra-articular ligament was dorsomedially attached to the head of the first metatarsal and to the inferior part of the articular face of the base of the proximal phalanx of the big toe. In a literature search we could not find any report of a ligament located intra-articularly in this particular joint. Such a variation may have a role in the etiology of hallux valgus.

Levels of oxidative stress parameters and the protective effects of melatonin in psychosis model rat testis.

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.

Effect of prenatal exposure to diclofenac sodium on Purkinje cell numbers in rat cerebellum: a stereological study.

Diclofenac sodium (DS) is commonly used as a non-steroidal anti-inflammatory drug. Although several adverse effects are clearly established, it is still unknown whether prenatal exposure to DS has an effect on the development of the cerebellum. In this study, we investigated the total number of Purkinje cells of the cerebellum in a control group and in a DS-treated group of male rats using a stereological method. The DS in a dose of 1 mg/kg daily was intraperitoneally injected to the drug-treated group of pregnant rats beginning from the 5th day after mating for a period of 15 days during pregnancy. Physiological serum at 1 ml dose was intraperitoneally injected to the control group of pregnant rats at the same period. After delivery, male offspring were obtained and each main group was divided into two subgroups that were 4-week-old (4W-old) and 20-week-old (20W-old). Our results showed that the total number of Purkinje cells in offspring of drug-treated rats was significantly lower than in the offspring of control animals. These results suggest that the Purkinje cells of a developing cerebellum may be affected by administration of DS during the prenatal period.

Caffeic acid phenethyl ester (CAPE) protects rat skeletal muscle against ischemia-reperfusion-induced oxidative stress.

Oxygen-derived free radicals have been implicated in the pathogenesis of skeletal muscle injury after ischemia-reperfusion. Caffeic acid phenethyl ester, an active component of propolis extract, exhibits antioxidant properties. The aim of this study was to assess the effects of caffeic acid phenethyl ester (CAPE) and alpha-tocopherol (vit E) on ischemia/reperfusion (I/R) injury in a rat hind limb ischemia/reperfusion model. For this purpose, ischemia was induced in anesthetized rats by unilateral (right) femoral artery clipping for 2 h followed by 2 h of reperfusion. Four groups were studied: sham, I/R, I/R+CAPE and I/R+vit E. Drugs were administered intraperitoneally after 1 h of ischemia and I/R rats received saline vehicle. After 2 h of reperfusion, venous blood was sampled and the right gastrocnemius muscle was harvested. Plasma and tissue were assayed for malondialdehyde (MDA), superoxide dismutase (SOD) and nitric oxide (NO) metabolites. Tissue was also assayed for catalase (CAT) activity. Both tissue and plasma NO levels, MDA levels, SOD activities was significantly increased in I/R groups compared to control groups. The two treated groups showed decreased MDA and NO in both muscle and plasma compared to the I/R group. No differences were noted in muscle tissue SOD in three I/R groups, but SOD activity were increased in the plasma of I/R+CAPE and I/R+vit E groups compared with I/R group. Whereas tissue CAT activity was not changed among groups. Our results indicate that CAPE has antioxidant properties similar to those of vit E in this model and may attenuate the harmful effects of hind limb I/R in skeletal muscle.

Oxidative stress in prefrontal cortex of rat exposed to MK-801 and protective effects of CAPE.

MK-801 was shown to be one of the most neurotoxic non-competitive NMDA receptor antagonists. It is known that repeated injection of MK-801 was proposed in an animal model in psychosis. The aims of this study are to investigate the contributing effect of oxidative stress in MK-801-induced experimental psychosis model, and to show that prevention of oxidative stress may improve prognosis. Furthermore, there is evidence that oxygen free radicals play an important role in the pathophysiology of schizophrenia. In this study, Wistar Albino rats were divided into three groups: 1st group: Control, 2nd group: MK-801, 3rd group: MK-801+CAPE (Caffeic acid phenethyl ester) group. MK-801 was given intraperitoneally at the dose of 0.5 mg/kg/day for 5 days. CAPE was given to the treatment group while exposed to MK-801. In control group, saline was given intraperitoneally at the same time. After 7 days, rats were killed by decapitation. Prefrontal cortex (PFC) of rats was removed for biochemical and histological analyses. As a result, malondialdehyde (MDA), protein carbonyl (PC), nitric oxide (NO) levels and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and xanthine oxidase (XO) and adenosine deaminase (AD) enzyme activities were found to be increased significantly in prefrontal cortex (PFC) of MK-801 group (p<0.0001) compared to control group. In CAPE treated rats, prefrontal tissue MDA, PC, NO levels and, GSH-Px, XO, AD enzyme activities were significantly decreased when compared to MK-801 groups (p<0.0001) whereas catalase (CAT) enzyme activity was not changed. Moreover, in the light of microscopic examination of MK-801 groups, a great number of apoptotic cells were observed. CAPE treatment decreased the apoptotic cell count in PFC. The results of this study showed that MK-801-induced neurotoxicity caused oxidative stress in PFC of rats. This experimental study may also provide some evidences for the new treatment strategies with antioxidants in schizophrenia.

The protective effects of omega-3 fatty acids against MK-801-induced neurotoxicity in prefrontal cortex of rat.

The aims of this study are to investigate the contribution effect of oxidative stress in MK-801-induced experimental psychosis model, and to show that prevention of oxidative stress may improve prognosis. Because oxidative damage has been suggested in the neuropathophysiology of schizophrenia, the possible protecting agents against lipid peroxidation are potential target for the studies in this field. For this purpose, Wistar Albino rats were divided into three groups: the first group was used as control, MK-801 was given to the rats in the second group and MK-801+omega-3 essential fatty acids (EFA) was given to the third group. MK-801 was given intraperitoneally at the dose of 0.5mg/(kgday) once a day for 5 days in experimental psychosis group. In the second group, 0.8g/(kgday), omega-3 FA (eicosapentaenoic acid, 18%, docosahexaenoic acid, 12%) was given to the rats while exposed MK-801. In control group, saline was given intraperitoneally at the same time. After 7 days, rats were killed by decapitation. Prefrontal brain area was removed for histological and biochemical analyses. As a result, malondialdehyde (MDA), as an indicator of lipid peroxidation, protein carbonyl (PC), as an indicator of protein oxidation, nitric oxide (NO) levels and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities as antioxidant enzymes, and xanthine oxidase (XO) and adenosine deaminase (AD) activities as an indicator of DNA oxidation was found to be increased significantly in prefrontal cortex (PFC) of MK-801 group (P<0.0001) compared to control group. In omega-3 FA treated rats, prefrontal tissue MDA, PC and NO levels as well as SOD, GSH-Px, XO, and AD enzyme activities were significantly decreased when compared to MK-801 groups (P<0.0001) whereas catalase (CAT) enzyme activity was not changed. Moreover, in the light of microscopic examination of MK-801 groups, a great number of apoptotic cells were observed. omega-3 FA supplementation decreased the apoptotic cell count in PFC. The results of this study revealed that oxidative stress and apoptotic changes in PFC may play an important role in the pathogenesis of MK-801-induced neuronal toxicity. This experimental study also provides some evidences for the protective effects of omega-3 FA on MK-801-induced changes in PFC of rats.

A preliminary study of the levels of testis oxidative stress parameters after MK-801-induced experimental psychosis model: protective effects of CAPE.

We evaluated the effects of caffeic acid phenethyl ester (CAPE) on antioxidant enzyme levels and histopathologic changes in dizocilpine (MK-801) induced schizophrenic rat testis. A total of 30 adult male Wistar-Albino rats were divided into three groups. Group-I was used as control. Rats in the Group-II were intraperitoneally injected with MK-801, whereas those in Group-III were intraperitoneally injected with CAPE in addition to MK-801. The testes were collected for biochemical and histopathological examinations. Antioxidant enzyme activities, malondialdehyde, protein carbonyl and nitric oxide levels in testicular tissues were analyzed with spectrophotometric methods. Induction of schizophrenia resulted in a significant oxidative stress by increasing the levels of antioxidant enzymes. Tissue malondialdehyde and protein carbonyl levels were also increased. Treatment with CAPE led to significant decrease in oxidative injury. Administration of CAPE reduced the detrimental histopathologic changes caused by MK-801. The results showed that experimentally induced schizophrenia caused oxidative stress in testes of rats and treatment with CAPE reduced these harmful effects.

Protective effects of caffeic acid phenethyl ester on skeletal muscle ischemia-reperfusion injury in rats.

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 honeybee propolis. 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) on an in vivo model of skeletal muscle I/R injury. Rats were divided into three equal groups each consisting of six rats: Sham operation, I/R, and I/R plus CAPE (I/R+CAPE) groups. CAPE was administered intraperitoneally 60 min before the beginning of the reperfusion. At the end of experimental procedure, blood and gastrocnemius muscle tissues were used for biochemical analyses. Tissue protein carbonyl (PC) levels and the activities of XO, myeloperoxidase (MPO) and AD in I/R group were significantly higher than that of control (p < 0.01, p < 0.05, p < 0.01, p < 0.005, respectively). Administration of CAPE significantly decreased tissue PC levels, MPO and XO activities in skeletal muscle compared to I/R group (p < 0.01, p < 0.05, p < 0.05, respectively). In addition, plasma creatine phosphokinase (CPK), XO and AD activities were decreased in I/R+CAPE group compared to I/R group (p < 0.05, p < 0.05, p < 0.001). The results of this study revealed that free radical attacks may play an important role in the pathogenesis of skeletal muscle I/R injury. Also, the potent free radical scavenger compound, CAPE, may have protective potential in this process. Therefore, it can be speculated that CAPE or other antioxidant agents may be useful in the treatment of I/R injury as well as diffused traumatic injury of skeletal muscle.

Oxidative stress in testicular tissues of rats exposed to cigarette smoke and protective effects of caffeic acid phenethyl ester.

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 x 30 min/d) and rats in Group III were exposed to cigarette smoke and received daily intraperitoneal injections of CAPE (10 micromol/kg x 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.

The activities of liver adenosine deaminase, xanthine oxidase, catalase, superoxide dismutase enzymes and the levels of malondialdehyde and nitric oxide after cisplatin toxicity in rats: protective effect of caffeic acid phenethyl ester.

The aim of this experimental study was to investigate the effects of caffeic acid phenethyl ester (CAPE), an antioxidant agent, on cisplatin-induced hepatotoxicity through adenosine deaminase (AD), xanthine oxidase (XO), catalase (CAT), superoxide dismutase (SOD) activities and malondialdehyde (MDA) and nitric oxide (NO) levels in liver tissue of rats. Wistar albino rats were divided into three groups: control group (n = 6), cisplatin group (n = 9) and CAPE + cisplatin group (n = 8). All the chemicals used were applied intraperitoneally. Spectrophotometric methods were used to determine the activities of the above-mentioned enzymes in the liver tissue. NO level and XO activity were found to be increased in the cisplatin group compared to the control group. NO level was found to be decreased in the cisplatin + CAPE group in comparison with the cisplatin group. There was no significant change in the activity of XO between the cisplatin and cisplatin + CAPE groups. The activity of SOD was lower in the cisplatin group than both the control and cisplatin + CAPE groups. There was no significant change in the activity of CAT between the control and cisplatin groups. CAT activity was increased in the cisplatin + CAPE group compared to the cisplatin group. The AD activity and MDA level remained unchanged in all groups. The results obtained suggested that CAPE significantly attenuated the hepatotoxicity as an indirect target of cisplatin in an animal model of cisplatin-induced nephrotoxicity.

Brief communication: omega-3 essential fatty acid supplementation and erythrocyte oxidant/antioxidant status in rats.

Fish oil contains large amounts of essential omega-3 fatty acids, such as eicosapentaenoic and docosahexaneoic acids, which are building structures of cell membranes. The goal of this study was to elucidate the effects of dietary omega-3 fatty acid supplementation on the oxidant/antioxidant status of erythrocytes in rats. The malondialdehyde (MDA) and nitric oxide (NO) levels and the catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX) activities were assayed in erythrocytes of male Wistar albino rats after 30 days of dietary supplementation with fish oil (0.4 g/kg/day). Erythrocyte CAT activity in the treated group was increased in comparison with the control group. Erythrocyte MDA and NO levels were lower in the treated group than the controls. Erythrocyte GSH-Px and SOD activities did not differ significantly in the 2 groups. Negative correlations were found between SOD and CAT activities, and between SOD and GSH-Px activities in the treated group. In conclusion, omega-3 fatty acid supplementation helps to prevent lipid peroxidation and to safeguard erythrocytes from oxidative injury. Dietary supplementation with omega-3 fatty acids might possibly protect tissues from oxygen free radical injury in the various diseases in which the oxidant/antioxidant defense mechanisms are disturbed.

Hypothalamic superoxide dismutase, xanthine oxidase, nitric oxide, and malondialdehyde in rats fed with fish omega-3 fatty acids.

Phospholipids located in the cellular membrane play a critical role in the fluid-mosaic model of membrane structure and membrane function. Evidence is mounting for the role of abnormal phospholipid metabolism in some neuropsychiatric disorders including schizophrenia. As an important essential fatty acid (EFA), omega-3 (omega-3) fatty acid series are found in large amounts in fish oil. The aim of this experimental study was to assess the changes of some of the oxidant and antioxidant parameters in the hypothalamus of rats fed with omega-3 EFA diet (0.4 g/kg/day) for 30 days. Eight control rats and nine rats fed with omega-3 were decapitated under ether anesthesia, and hypothalamus was removed immediately. Malondialdehyde (MDA) and nitric oxide (NO) levels as well as superoxide dismutase (SOD) and xanthine oxidase (XO) enzyme activities in the hypothalamus were measured. SOD activity was significantly decreased in omega-3 EFA treated group compared to control group (p < 0.014). Tissue MDA and NO levels were also decreased in omega-3 EFA treated group compared to control rats (p < 0.0001). Xanthine oxidase activity was found to be increased in omega-3 EFA treated rats when compared to the control group (p < 0.0001). Taken together, this preliminary animal study provides strong support for a therapeutic effect of omega-3 EFA in some neuropsychiatric disorders in which reactive oxygen species (ROS) are recently accused to be an important physiopathogenetic factor.