Comparative analysis of the protective effects of caffeic acid phenethyl ester (CAPE) on pulmonary contusion lung oxidative stress and serum copper and zinc levels in experimental rat model.

The aim of this study was to investigate the effects of caffeic acid phenethyl ester (CAPE) in the lungs by biochemical and histopathological analyses in an experimental isolated lung contusion model. Eighty-one male Sprague-Dawley rats were used. The animals were divided randomly into four groups: group 1 (n = 9) was defined as without contusion and without CAPE injection. Group 2 (n = 9) was defined as CAPE 10 µmol/kg injection without lung contusion. Group 3 (n = 36) was defined as contusion without CAPE-administrated group which consisted of four subgroups that were created according to analysis between days 0, 1, 2, and 3. Group 4 (n = 27) was defined as CAPE 10 µmol/kg administrated after contusion group divided into three subgroups according to analysis on days 1, 2, and 3. CAPE 10 µmol/kg was injected intraperitoneally 30 min after trauma and on days 1 and 2. Blood samples were obtained to measure catalase (CAT) and superoxide dismutase (SOD) activities and level of malondialdehyde (MDA) and for blood gas analysis. Trace elements such as zinc and copper were measured in serum. The lung tissue was also removed for histopathological examination. Isolated lung contusion increased serum and tissue SOD and CAT activities and MDA levels (p < 0.05). Both serum and tissue SOD, MDA, and CAT levels on day 3 were lower in group 4 compared to group 3 (p < 0.05). Further, the levels of SOD, MDA, and CAT in group 4 were similar compared to group 1 (p > 0.05). CAPE also had a significant beneficial effect on blood gases (p < 0.05). Both serum zinc and copper levels were (p < 0.05) influenced by the administration of CAPE. Histopathological examination revealed lower scores in group 4 compared to group 3 (p < 0.05) and no significant differences compared to group 1 (p > 0.05). CAPE appears to be effective in protecting against severe oxidative stress and tissue damage caused by pulmonary contusion in an experimental setting. Therefore, we conclude that administration of CAPE may be used for a variety of conditions associated with pulmonary contusion. Clinical use of CAPE may have the advantage of prevention of pulmonary contusion.

Effects of short-term exposure to powerline-frequency electromagnetic field on the electrical activity of the heart.

ABSTRACT The heart is a contractile organ that can generate its own rhythm. The contraction, or the rhythm, of the heart may be influenced by electromagnetic field (EMF) exposure, because of the heart's excitability characteristic. In previous studies, different methods have been used to study the possible effects of an extremely low frequency electromagnetic field (ELF-EMF) on the heart. But the studies' designs were not similar, and the results were also different. Recent studies have shown some evidence that short-term EMF exposure can influence the heart more than long-term exposure. This study investigated how the heart is affected in the first EMF exposure. In a simulation of the daily exposure of humans to a power frequency, Wistar albino rats were used. By utilizing the Helmholtz-coil set, we obtained a 50-Hz, 1-µT EMF and examined rat heart activity during short-term EMF exposure. No effect was observed under this exposure condition. The results obtained do not confirm a possible mechanism in the electrical activity of the rat heart model.

Vitamin C and E combination modulates oxidative stress induced by X-ray in blood of smoker and nonsmoker radiology technicians.

X-ray radiation is detrimental to human cells and may lead to development of life-threatening diseases. Cigarette smoke contains about 500 chemicals that include organic and oxidant compounds whereas vitamin C and E (VCE) have scavenger effects on the compounds. We investigated effects of VCE administration on X-ray-induced oxidative toxicity in blood of smoker and nonsmoker X-ray technicians. Twenty technicians and 30 healthy age-matched subjects control were used in the study. Ten of the X-ray technicians and 15 of the control were smokers. Blood samples were taken from the control. Oral vitamin C (500 mg) and vitamin E (150 mg) were daily supplemented to the smoker and nonsmoker X-ray technicians for 5 weeks. Blood samples were taken from the X-ray technicians after and before 5 weeks. Plasma and erythrocytes lipid peroxidation (LP), reduced glutathione (GSH) levels, erythrocytes glutathione peroxidase (GSH-Px), and plasma antioxidant vitamin concentrations were investigated in control and X-ray technicians with smoker and nonsmoker. Plasma and erythrocytes LP levels were higher in the total X-ray group and smoker X-ray group than in control and nonsmoker X-ray group, respectively although the LP level was decreased by the VCE treatment. The plasma vitamin C, vitamin A, vitamin E, and beta-carotene concentrations were lower in the X-ray group than in control although their concentrations were increased by the treatment. The erythrocytes GSH level and GSH-Px activity were found to be higher in the treatment group than in the X-ray group. Plasma GSH level was not found to be different in all group. Reactive oxygen species may play role in the mechanism that has been proposed to explain the biological side effect of X-ray radiation and smoke. VCE prevents the smoke and X-ray-induced oxidative stress to strengthen antioxidant vitamin concentrations in the blood of the technicians.

Selenium and vitamin E modulates cigarette smoke exposure-induced oxidative stress in blood of rats.

Cigarette smoke contains about 5,000 chemicals that include organic and metallic compounds. The current study was undertaken to investigate the effects of selenium and vitamin E on oxidative stress-induced damage in rats exposed to cigarette smoke. Forty male rats were equally divided into four groups. The first and second groups were used as control and cigarette smoke groups, respectively. Selenium was administered to rats constituting the third group for 27 days. The Se and vitamin E combination was given to animals in fourth group for 27 days. All groups except the control, were exposed to cigarette smoke starting at the third day of the experiment and continuing for 27 days. The blood samples from all groups were taken at the end of 27 days. Plasma lipid peroxidation, triacylglycerol, and total cholesterol levels were higher in the cigarette smoke group than in the control, although erythrocytic superoxide dismutase and glutathione peroxidase activities were lower in the cigarette smoke group than in the control. The plasma lipid peroxidation, triacylglycerol, and total cholesterol levels were lower in cigarette smoke+Se+VE group than in the cigarette smoke group, although erythrocytic superoxide dismutase activity and glutathione peroxidase activity in selenium and vitamin E-administered groups were higher than in the exposed to cigarette smoke group. High-density lipoprotein-cholesterol level was not affect by selenium and vitamin E administrations. In conclusion, selenium and vitamin E seem to have protective effects on the cigarette smoke-induced blood toxicity by supporting the enzymatic antioxidant redox systems.

The effects of diazinon on lipid peroxidation and antioxidant enzymes in rat erythrocytes: role of vitamins E and C.

Reactive oxygen species caused by organophosphates may be involved in the toxicity of various pesticides. Therefore, in this study, we aimed to investigate the effects of acute exposure to organophosphate insecticide diazinon (DI) and possible ameliorating role of vitamins E and C, with the following parameters: lipid peroxidation (LPO) and the activity of the glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) in rat erythrocytes. The experimental groups were arranged as control group, DI-treated group (DI) and DI + vitamin E + vitamin C-treated group (DI + Vit). DI + Vit groups were treated orally with a single dose of 335 mg/kg DI body weight. Vitamins E and C were injected at doses of 150 mg/kg body weight intramuscular (in) and 200 mg/kg body weight intraperitoneal (ip), respectively, 30 min after the treatment of DI in DI + Vit group. Blood samples were taken 24 h after the DI. The results showed that DI administration caused to increase in LPO and the activities of SOD and GSH-Px enzymes in erythrocytes. Also, the combination of vitamins E and C decreased LPO and the activities of GSH-Px and SOD compared with the DI group. In conclusion, although treating rats with single dose DI increases LPO and antioxidant enzyme activities in erythrocytes, vitamins C and E combination can reduce LPO caused by DI.

Melatonin modulates 900 Mhz microwave-induced lipid peroxidation changes in rat brain.

Microwaves (MW) from cellular phones may affect biological systems by increasing free radicals, which may enhance lipid peroxidation levels of the brain, thus leading to oxidative damage. Melatonin is synthesized in and secreted by the pineal gland at night and exhibits anti-oxidant properties. Several studies suggest that supplementation with anti-oxidant can influence MW-induced brain damage. The present study was designed to determine the effects of MW on the brain lipid peroxidation system, and the possible protective effects of melatonin on brain degeneration induced by MW. Twenty-eight Sprague-Dawley male rats were randomly divided into three groups as follows: (1) sham-operated control group (N = 8); (2) study 900-MHz MW-exposed group (N = 8); and (3) 900-MHz MW-exposed+melatonin (100 microg/kg sc before daily MW exposure treated group) (N = 10). Cortex brain and hippocampus tissues were removed to study the levels of lipid peroxidation as malonyl dialdehyde. The levels of lipid peroxidation in the brain cortex and hippocampus increased in the MW group compared with the control group, although the levels in the hippocampus were decreased by MW+melatonin administration. The brain cortex lipid peroxidation levels were unaffected by melatonin treatment. We conclude that melatonin may prevent MW-induced oxidative changes in the hippocampus by strengthening the anti-oxidant defense system, by reducing oxidative stress products.

A novel antioxidant agent caffeic acid phenethyl ester prevents shock wave-induced renal tubular oxidative stress.

The aim of this study was to evaluate the effects of the novel free radical scavenger caffeic acid phenethyl ester (CAPE) on extracorporeal shock wave lithotripsy (ESWL) induced renal impairment. The study was performed using 30 rabbits which were divided into two groups, each exposed to 3,000 shock waves at 18 kV: (1) control group, (2) ESWL+CAPE treated group. Malodialdehyde (MDA), urine N-acetyl-beta-glucosaminidase (NAG) activity, uric acid and white cell counts were used as markers of oxidative stress. Following shock wave exposure there was a significant rise in MDA, NAG and uric acid and white cell counts. CAPE reduced the rise in MDA, NAG, uric acid and white cell counts. Thus CAPE treatment to a great extent prevented the induction of these renal changes. Our results suggest that the antioxidant capacity of the kidney tissue was reduced after ESWL treatment and that the tissue was exposed to oxidant stress. We conclude that CAPE treatment provided significant protection against ESWL induced free radical damage.

Effects of dietary long chain PUFAs on hippocampal lipid peroxidation and NMDA receptor subunits A and B concentration in streptozotocin-diabetic rats.

This study examined the effects of streptozotocin (STZ)-diabetes and dietary long chain polyunsaturated fatty acids (LC-PUFAs) on hippocampal N-methyl-D-aspartate (NMDA) receptor subunit expression and lipid peroxidation. MDA level was significantly increased after 8 weeks of STZ-diabetes. LC-PUFAs administration significantly reduced MDA levels in diabetic rats. NR2A and NR2B protein concentrations were significantly decreased by about 30% in diabetic rats. Dietary LC-PUFAs partially restored NR2A and NR2B in diabetic rats whereas the most significant increase was seen in nondiabetic rats. Consequently, dietary LC-PUFAs can partially restore hippocampal NMDA receptors and decrease lipid peroxidation in diabetes. LC-PUFAs are thus a possible prophylactic means for preventing the cognitive deficiencies of diabetes.

The effects of diazinon on lipid peroxidation and antioxidant enzymes in erythrocytes in vitro.

Diazinon is one of the most widely used organophosphate insecticides (OPI) in agriculture and public health programs. The aim of this study was to investigate how an OPI, diazinon, affects lipid peroxidation (LPO) and the antioxidant defense system in vitro. For this purpose, two experiments were carried out. In experiment 1, the effects of various concentrations of diazinon on LPO and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) in erythrocytes were studied. Each diazinon concentration was incubated with a previously prepared erythrocyte samples at +4 degrees C for 0, 60 and 180 min. After incubation, the malondialdehyde (MDA) levels and the activities of SOD, GSH-Px and CAT were determined. In experiment 2, in order to determine the direct effect of diazinon on the activities of SOD, GSH-Px and CAT, the erythrocytes were haemolysed and incubated with the various concentrations of diazinon at +4 degrees C for 0, 60 and 180 min. In experiment 1, MDA levels and the activities of SOD and GSH-Px increased with increasing diazinon concentration and incubation period, but CAT activity remained unchanged. In experiment 2, SOD activity was significantly decreased, and GSH-Px activity was significantly increased. From these results, it can be concluded that in vitro administration of diazinon results in the induction of erythrocyte LPO and changes the activities of antioxidant enzymes, suggesting that reactive oxygen species may be involved in the toxic effects of diazinon.

NMDA receptor subunits 2A and 2B decrease and lipid peroxidation increase in the hippocampus of streptozotocin-diabetic rats: effects of insulin and gliclazide treatments.

Recent studies indicate that diabetes mellitus changes N-methyl-D-aspartate (NMDA) receptor subunit composition and impairs cognitive functions. It also has been known that diabetes mellitus causes lipid peroxidation. This study examined the effects of streptozotocin-diabetes and insulin or gliclazide treatment on the hippocampal NMDA receptor subunit 2A and 2B (NR2A and NR2B) concentrations. In addition, malondial dehyde (MDA) levels were measured as a marker for lipid peroxidation. Eight weeks after the induction of diabetes MDA, levels were increased, and NR2A and NR2B concentrations were reduced. Insulin and gliclazide treatment partially prevented the reduction of NR2A and NR2B expression and prevented the elevation of MDA levels. There was no significant difference between the effects of insulin and gliclazide. The results suggest that the elevation of lipid peroxidation can be the primary biochemical disturbances in diabetes progression, and that changes in NMDA receptor subunit compositions can be involved in cognitive decline in diabetes.

Unilateral nostril breathing in intraocular pressure of right-handed healthy subjects.

The effects of unilateral forced nostril breathing on the intraocular pressures of right and left eyes was studied in 24 male and 26 female right-handed adults. In men, the forced breathing through both the right and left nostrils significantly decreased the intraocular pressures of both right and left eyes. For women, the forced breathing through right nostril did not affect the intraocular pressures of right and left eyes, and the forced breathing through left nostril also had no effect on the intraocular pressure of right eye, although it decreased the intraocular pressure of left eye significantly. These results show that unilateral forced nostril breathing decreases intraocular pressure especially in men, perhaps increasing sympathetic nervous system activity.