Ramazan Amanvermez

Pre-eclampsia and eclampsia associated with increased lipid peroxidation and decreased serum vitamin E levels

Objective: To evaluate lipid peroxidation and the serum levels of the antioxidant vitamin E in pre‐eclampsia according to the disease severity. Method: Serum malondialdehyde (MDA) and vitamin E levels were measured in 18 pre‐eclamptic, 15 eclamptic and 25 normotensive pregnant women in Ondokuz Mayis University Hospital. The correlation of these levels with the factors indicating disease severity was tested. Mann–Whitney U‐test and correlation coefficients were used for the statistical analysis. Result: Both the pre‐eclamptic and the eclamptic patients had higher MDA and lower vitamin E levels compared with control (P<0.05); but these values were not significantly different from each other (P>0.05). MDA levels were significantly correlated with the systolic and diastolic blood pressure (BP) and with serum uric acid levels. There was significant but negative correlation with the vitamin E levels. Conclusion: There is an imbalance between lipid peroxidation and serum vitamin E levels in pre‐eclampsia and eclampsia. Increased lipid peroxidation is well correlated with the increase in systolic and diastolic BP measurements and serum uric acid levels.

The effects of ethanol consumption on the lipid peroxidation and glutathione levels in the right and left brains of rats

The effects of ethanol consumption on the levels of lipid peroxidation and reduced glutathione (GSH) in the cerebral hemispheres of male rats were investigated. The rats were randomly divided into eight groups: control, 10%, 25%, 35% ethanol-consuming groups, and four groups given vitamin E. The level of lipid peroxidation increased 34.32% (right brain), 35.67% (left brain) in 10% ethanol-consuming rats; 32.05% (right brain), 31.81% (left brain) in 25% ethanol-consuming rats; and 33.45% (right brain), 39.72% (left brain) in 35% ethanol-consuming rats. The GSH level of the right and left brains significantly decreased: 19.39%, 19.56%; 27.58%, 29.34%; 35.34%, 33.22% in rats consuming 10%, 25%, and 35% ethanol, respectively. These effects were partly antagonized by administration of vitamin E (100 mg/kg/day i.p.) to ethanol-consuming rats for 20 days. The results suggested that the cerebral hemispheres of adult rats are susceptible to the oxidative neurotoxic effects of ethanol, which may be blocked by vitamin E

Alcohol-induced oxidative stress and reduction in oxidation by ascorbate/L-cys/ L-met in the testis, ovary, kidney, and lung of rat

Chronic exposure to high doses of alcohol results in many pathophysiologic changes in cellular function caused by the alcohol itself and the effects of its metabolism (ie, generation of acetaldehyde, nicotinamide adenine dinucleotide [NADH], free radicals, and oxidative stress). However, the role of each of these effects on the testis, ovary, kidney, and lung in chronic alcoholism must be investigated. It is hypothesized that cysteine-methionine and vitamin C might neutralize harmful compounds and potentiate the antioxidant capacity of the cell or tissue. In this study, rats were fed regular diets and were maintained in the following groups for 90 days: control group; alcoholic group (2.5 g of 50% ethanol/kg body wt administered intragastrically every other day); and alcoholic with antioxidant supplement group (2.5 g of 50% ethanol plus a solution containing 200 mg vitamin C, 100 mg cysteine, and 100 mg methionine/kg body wt administered intragastrically every other day). After treatment had been completed, rat blood, testis, ovary, kidney, and lung were taken for biochemical analysis. Mean alcohol level in the alcoholic group was raised (by 40%) compared with that in the control group, but it was lower (by 30%) in the antioxidantsupplemented group than in the alcoholic group. In accordance with the levels of alcohol, oxidized protein and lipid content in the testis, ovary, kidney, and lung were low in the control group, higher in the antioxidant-supplemented group, and highest in the alcoholic group. It is interesting to note that levels of glutathione in the testis and lung of the alcoholic group were lower than those in both the control and antioxidant-supplemented groups. In conclusion, chronic alcohol administration led to a significant increase in the level of protein oxidation in the ovary and kidney of rats. Simultaneous intake of ascorbate/l-cys/l-met, along with ethanol, partly attenuated the amount of lipid and protein oxidation that occurred in tissues with oxidative stress caused by alcohol consumption.

Moderate Hypothermia Prevents Brain Stem Oxidative Stress Injury after Hemorrhagic Shock

BACKGROUND The purpose of this study was to investigate the effects of temperature on oxidative stress in brain stem tissue induced by hemorrhagic shock. We researched the hemorrhagic oxidative stress at various core temperatures using reduced glutathione (GSH) levels and thiobarbituric acid-reactive substances (TBARS) as markers of lipid peroxidation in brain stem homogenate. METHODS Forty rats were divided into four groups, of which one constituted the nonbleeding normothermia control group. In all of the three study groups, 40% of estimated blood volume was removed while they were being held at normothermia, mild hypothermia (32 degrees C), or moderate hypothermia (28 degrees C). Parameters including mean arterial pressure, rectal temperature, and heart and breathing rates were monitored and recorded during the procedures. After an hour at shock state, tissue samples were removed by craniectomy. RESULTS The tissue levels of TBARS increased significantly in normothermic and mild hypothermic hemorrhagic shock groups (10.74 nmol/g and 8.26 nmol/g) as compared with the control group (3.50 nmol/g) (p < 0.001). However, the tissue TBARS level in the moderate hypothermia group was only minimally increased (4.53 nmol/g). GSH showed a slight decrease in normothermic and mild hypothermic bleeding rats, and were unchanged in the moderate hypothermic rats. CONCLUSION Moderate systemic hypothermia (28 degrees C) appears to protect brain stem tissue from oxidative stress during severe hemorrhagic shock in rats, as indicated by insignificant change in tissue TBARS and GSH concentrations. These results suggest antioxidant protective effects of moderate systemic hypothermia in metabolically active brain stem tissue during hemorrhagic shock. Similar effects in humans remain to be studied.

Serum Nitric Oxide and Glutathione Levels in Preeclamptic and Normotensive Women during Labor

This study was performed on 38 preeclamptic women, including 26 severely preeclamptic and eclamptic cases, as well as 50 normotensive pregnant controls. Twenty cases in the preeclamptic group and 34 cases in the control group were in labor. Serum nitric oxide levels were measured as total nitrites after reduction of nitrates to nitrites. Among the control subjects, nitric oxide levels were significantly lower in the cases in labor when compared to those not in labor (p < 0.05), but glutathione levels were not significantly different (p >0.05). Among the preeclamptic patients, although nitric oxide levels were not significantly different between the cases in and not in labor (p > 0.05), glutathione levels were significantly higher in the latter group (p < 0.05). Thus, in preeclamptic patients there might be a compensatory increase in nitric oxide production during labor in order to maintain the systemic circulation. Glutathione levels might also be increased to compensate for the marked oxidative stress.

Does ascorbate/L-Cys/L-Met mixture protect different parts of the rat brain against chronic alcohol toxicity?

Chronic ingestion of high levels of alcohol may cause oxidative stress that results in the formation, through alcohol metabolism, of excess free radicals, acetaldehyde, lipid and protein oxidation, and their reactivity products. These harmful molecules may trigger oxidative damage to neurons and can cause cell death. It is hypothesized that cysteine-methionine and vitamin C may neutralize these harmful compounds while potentiating the antioxidant capacity of the cell or tissue. In the present study, rats were fed regular diets and were maintained for 90 days in (1) the control group, (2) the alcoholic group, which was given 2.5 g of 50% ethanol/kg body weight administered intragastrically every other day, or (3) the alcoholic with antioxidant supplement group, to whom 2.5 g of 50% ethanol/kg body weight + a solution that contained 200 mg vitamin C, 100 mg cysteine, and 100 mg methionine was administered intragastrically every other day. The mean blood alcohol level was raised by 40% in the alcoholic group compared with the control group, but, compared with the alcoholic group, the alcohol level was decreased by 30% in the antioxidant-supplemented group. In keeping with blood alcohol levels, oxidized protein and lipid content in the cerebrum, brain stem, and cerebellum were low in the control group, higher in the antioxidant-supplemented group, and highest in the alcoholic group. The mean total thiol level was higher in the antioxidant-supplemented group than in the alcoholic and control groups. It is interesting to note that the level of total glutathione in the cerebrum and cerebellum in the alcoholic group was lower than in the control and antioxidant-supplemented groups. In conclusion, long-term alcohol administration led to increased levels of oxidized protein and lipids in the cerebrum, brain stem, and cerebellum of rats. Simultaneous intake of ascorbate/ l-cys/l-met and ethanol attenuated the amount of oxidation that occurred, which suggested that cysteine, methionine, and vitamin C may play a protective role in the central nervous system against oxidative damage caused by alcohol consumption. In addition, the mean alcohol level was increased in the alcoholic group compared with the control group. The level of total glutathione was significantly decreased in the cerebellum of the alcoholic group, and oxidative damage was noted in various parts of the brain in this group. These findings suggest that oxidative stress plays a pathogenetic role in brain damage related to chronic alcoholism.

Ankaferd Blood Stopper: Does it have a role in fracture healing?

* Correspondence: aramazan@omu.edu.tr

Heart-type fatty acid-binding protein as a potential biomarker of acute carbon monoxide poisoning☆☆☆

BACKGROUND The aim of this study was to investigate the role of serum heart-type fatty acid-binding protein (H-FABP) in the evaluation of patients with carbon monoxide (CO) poisoning. METHODS Forty patients with acute CO poisoning admitted to the emergency department and 15 healthy adults as the control group were included in the study. Serum H-FABP levels of patients were studied on admission and at the 6th, 12th, and 18th hours. Patients were divided into 3 groups according to clinical severity as mild, moderate, and severe. Patients were also divided into 2 groups according to treatment with hyperbaric oxygen (HBO) or normobaric oxygen. RESULTS Serum H-FABP levels of the patients were higher than those of the control group. There was a negative correlation between H-FABP levels and Glasgow Coma Scale score on admission. Heart-type fatty acid-binding protein levels were significantly higher in patients in the severe compared with mild group. Heart-type fatty acid-binding protein levels in patients treated with HBO were significantly higher than in those treated with normobaric oxygen. The cutoff value of serum H-FABP as an indicator for HBO treatment was determined as 1.5 ng/mL or higher, with a sensitivity of 85.7% and specificity of 69.7%. Serial measurement revealed that H-FABP level peaked at the sixth hour and reduced over time but remained higher than in the control group at the 18th hour. CONCLUSION Heart-type fatty acid-binding protein may be a promising novel biomarker in the evaluation of clinical severity and in the selection of patients for HBO therapy in acute CO poisoning.

The changes in lipid peroxidation and GSH levels in the cerebellum of rats induced by ethanol consumption are prevented by vitamin E

The present study used male Wistar rats to investigate changes in glutathione (GSH) and lipid peroxidation (TBARS) in the cerebellum of 10%, 25%, 35% ethanol-consuming rats with or without vitamin E treatment when compared to the control group, the level of lipid peroxidation was increased 58.3%, 68.7%, 66.7% in rats consuming10%, 25%, 35% ethanol, respectively. Ethanol decreased GSH levels in the cerebellum. This decrease was dose-dependent with 23.7%, 27.6%, 28% decreases in GSH in the cerebellum of rats consuming 10%, 25% or 35% ethanol, respectively. Vitamin E (100 mg/kg/day, i.p) treatment prevented the increase in the lipid peroxidation and decreases in cerebellum GSH levels of ethanol-consuming rats.

Pentraxin 3, ischemia-modified albumin, and myeloperoxidase in predicting a cardiac damage in acute carbon monoxide poisoning.

BACKGROUND Carbon monoxide (CO) poisoning is associated with cardiac injuries or manifestations, frequently attributing to direct hypoxic damage at cellular level. For this, the aims were to evaluate the role of serum pentraxin 3 (PTX 3), ischemia-modified albumin (IMA), and myeloperoxidase (MPO) as an early biomarker for cardiac damage when compared to cardiac troponin I (cTnI) and creatine kinase-MB fraction (CK-MB) in adult patients with acute CO poisoning. METHODS Forty patients with acute CO poisoning admitted to the emergency department. The patients were divided into 2 main groups as follows: cardiac injury (group I, n=19) and nonsuspected cardiac injury (group II, n=21). Pentraxin 3, IMA, MPO, cTnI, CK-MB, and the other assays in the circulation were measured on admission. RESULTS Upon measuring the serum PTX 3, IMA, MPO, cTnI, and CK-MB levels as well as large electrocardiography and echocardiography abnormalities of patients with cardiac injury on admission, no statistical difference for PTX 3, IMA, and MPO was found between the groups (P>.05). However, cTnI, CK-MB, and leukocyte count (white blood cell) were higher determined in patients of group I compared to group II (P<.05). Receiver operating characteristic curve was also performed to evaluate the diagnostic performance of these tests in patients with cardiac injury. CONCLUSIONS Our results suggest that PTX, IMA, and MPO assays are not superior to cTnI and CK-MB in predicting a cardiac damage in patients with acute CO intoxication.