Is rosuvastatin protective against on noise-induced oxidative stress in rat serum?

Noise, one of the main components of modern society, has become an important environmental problem. Noise is not only an irritating sound, but also a stress factor leading to serious health problems. In this study, we have investigated possible effects of rosuvastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, thought to have an antioxidant effect, on noise-induced oxidative stress in the serum of rat models. Thirty-two male Wistar albino rats were used. In order to ease their adaptation, 2 weeks before the experiment, the rats were divided into four groups (with eight rats per each group): Noise exposure plus rosuvastatin usage, only noise exposure, only rosuvastatin usage and control. After the data had been collected, oxidant (Malondialdehyde, nitric oxide [NO], protein carbonyl [PC]) and antioxidant (superoxide dismutase [SOD], glutathione peroxidase [GSH-PX], catalase [CAT]) parameters were analyzed in the serum. Results indicated that SOD values were found to be significantly lower, while PC values in serum were remarkably higher in the group that was exposed to only noise. GSH-Px values in serum dramatically increased in the group on which only rosuvastatin was used. During noise exposure, the use of rosuvastatin caused significantly increased CAT values, whereas it resulted in reduced PC and NO values in serum. In conclusion, our data show that noise exposure leads to oxidative stress in rat serum; however, rosuvastatin therapy decreases the oxidative stress caused by noise exposure.

Possible effects of rosuvastatin on noise-induced oxidative stress in rat brain.

The problem of noise has recently gained more attention as it has become an integral part of our daily lives. However, its influence has yet to be fully elucidated. Other than being an unpleasant stimulus, noise may cause health disorders through annoyance and stress, including oxidative stress. Rosuvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, may possess antioxidant properties. Based on rat models, our project investigates the effect of rosuvastatin on noise-induced oxidative stress in the brain tissue. Thirty-two male Wistar albino rats were used. The rats were divided into four groups: Noise exposure plus rosuvastatin usage, only noise exposure, only rosuvastatin usage, and control. After the data had been collected, oxidant and antioxidant parameters were analyzed in the cerebral cortex, brain stem, and cerebellum. Results indicated that superoxide dismutase values were significantly decreased in the cerebral cortex, while malondialdehyde values in the brainstem and cerebellum were significantly increased in the group with only noise exposure. Superoxide dismutase values in the brainstem were significantly increased, but nitric oxide values in the cerebellum and brainstem and malondialdehyde values in the cerebellum and cerebral cortex were significantly decreased in the group where only rosuvastatin was used. During noise exposure, the use of rosuvastatin caused significantly increased superoxide dismutase values in the cerebral cortex and brainstem, but significantly reduced malondialdehyde values in the brain stem. Consequently, our data show that brain tissue was affected by oxidative stress due to continued exposure to noise. This noise-induced stress decreases with rosuvastatin therapy.

Neuromyelitis optica: atipic clinic presentation.

We present a patient with neuromyelitis optica who exhibited longitudinally extensive transverse myelitis and aquaporin-4 IgG positivity. Patient did not have optic neuritis clinically, but we detected it with examination of visual evoked potentials (prolonged P100 wave latans), subclinically. We argue that neuromyelitis optica may also be considered in elderly patients with isolated involvement of the longitudinally extensive transverse myelitis, and visually evoked potential evaluation is important to determine of subclinic optic neuritis and anti-AQP-4 is also important to support to determination.

The protective effect of erdosteine on short-term global brain ischemia/reperfusion injury in rats.

Experimental studies have demonstrated that free radicals play a major role on neuronal injury during ischemia/reperfusion (I/R) in rats. Erdosteine is a thioderivative endowed with mucokinetic, mucolytic and free-radical-scavenging properties. The aim of the present study was to investigate the effect of erdosteine treatment against short-term global brain ischemia/reperfusion injury in rats. The study was carried out on Wistar rats divided into four groups. (i) Control group, (ii) ischemia/reperfusion group, (iii) ischemia/reperfusion+erdosteine group, and (iv) erdosteine group. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities as well as thiobarbituric acid reactive substances (TBARSs) and nitric oxide (NO) levels were analysed in erythrocyte and plasma of rats. Plasma NO levels were significantly higher in the ischemia/reperfusion group than the other groups. The activities of SOD and GSH-Px were decreased, while TBARS levels increased in the ischemia/reperfusion group compared to other groups in both plasma and erythrocyte. The erythrocyte CAT activity was higher in erdosteine group and there was a statistically significant increase, when compared with the erdosteine plus ischemia/reperfusion group. By treating the rats with erdosteine, the depletion of endogenous antioxidant enzymes (SOD, CAT, GSH-Px) and increase of TBARS and NO levels were prevented. This study, therefore, suggests that erdosteine reduces parameters of oxidative stress is well supported by the data.

IL-6 levels in migraine patients receiving topiramate.

There is considerable evidence suggesting that cytokines play important roles in pain and in mediating neurovascular inflammation associated with migraine headaches. Although consensus exists to recommend topiramate (TPM) for migraine prevention, the mechanism of action in this regard is unknown. We measured serum interleukin-6 (IL-6) levels in 66 migraine patients. Of these patients, 23 (34.9%) were taking TPM for migraine, and 43 (65.1%) were not. The IL-6 levels were compared with those of healthy controls without migraine, from the population living in the same region. The mean IL-6 levels in migraine patients taking TPM and patients who did not were 67.06 +/- 92.09 pg/mL and 44.09 +/- 59.19 pg/mL, respectively (P > 0.05). The IL-6 levels were higher in the patients taking TPM. The IL-6 level in the controls was 8.60 +/- 7.36 pg/mL, which was significantly lower than the patient group using TPM (P = 0.001). Our results show that, although IL-6 may be involved in pain induction or inflammatory mechanisms of migraine attacks, the serum IL-6 level was not reduced in migraine patients receiving TPM therapy. In conclusion, we found high IL-6 levels in migraine patients both with and without TPM therapy, suggesting that high IL-6 levels during pain-free periods could be a conditioning factor, making patients more vulnerable to pain attacks in chronic migraine. Further studies investigating the possible mechanism of TPM in migraine are needed.

Pentylenetetrazol-induced kindling seizure attenuated by Ginkgo biloba extract (EGb 761) in mice.

Ginkgo biloba extract (EGb 761) has been used therapeutically for centuries. It has attracted great attention as agents for improving circulation, particularly cerebral circulation, which may lead to improved mental function. Many researches hypothesized on the role of the extract in the treatment of diseases involving free radicals and oxidative damage. In the present study, anticonvulsant and antioxidant effects of EGb 761 were investigated in pentylenetetrazol (PTZ)-kindled mice. Valproic acid (VA), a major antiepileptic drug, was also tested for comparison. EGb 761-treated mice displayed a significant attenuated response to PTZ on the test day (day 26) compared with saline-treated and VA-treated animals. Valproic acid significantly increased seizure latency. Pretreatments with EGb 761 significantly protected against PTZ-induced convulsive behaviors (seizure latency, seizure score). EGb 761 and VA significantly decreased PTZ-induced oxidative injury in brain tissue. EGb 761 was found to be the most effective in preventing PTZ-induced oxidative damage among both substances studied. The data obtained support our speculation that neuroprotective action of EGb 761 may correlate with its ability to inhibit not only excessive reactive oxygen species (ROS) formation but also seizure generation. Taken together, the results of the present study show that the effect of EGb 761 on ROS production contributes to their neuroprotective action. It might be concluded that the suppression of seizure-induced ROS generation may be involved in the mechanism of action of antiepileptic drugs.

Median and Ulnar Neuropathy Assessment in Parkinson's Disease regarding Symptom Severity and Asymmetry.

Background. While increasing evidence suggests comorbidity of peripheral neuropathy (PNP) and Parkinson's disease (PD), the pathogenesis of PNP in PD is still a debate. The aim of this article is to search the core PD symptoms such as rigidity and tremor as contributing factors to mononeuropathy development while emphasizing each individual patient's asymmetric symptom severity. Methods. We studied 62 wrists and 62 elbows of 31 patients (mean age 66.48 ± 10.67) and 64 wrists and 64 elbows of 32 age-gender matched healthy controls (mean age 62.03 ± 10.40, p = 0.145). The Hoehn and Yahr disability scale and Unified Parkinson's Disease Rated Scale were used to determine the severity of the disease. Results. According to electrodiagnostic criteria, we confirmed median neuropathy in 16.12% (bilateral in two-thirds of the patients) and ulnar neuropathy in 3.22% of the PD group. While mean age (p = 0.003), age at PD onset (p = 0.019), and H&Y scores (p = 0.016) were significant, tremor and rigidity scores were not. The comparison of the mean indices of electrophysiologic parameters indicated subclinical median and ulnar nerve demyelination both at the wrist and at the elbow in the patient groups where a longer disease duration and mild tremor and rigidity scores are prominent, remarkably. Conclusion. A disease related peripheral neurodegeneration beyond symptom severity occurs in PD.

Antiepileptogenic and antioxidant effects of Nigella sativa oil against pentylenetetrazol-induced kindling in mice.

Nigella sativa oil (NSO), a herbaceous plant, has been used for thousands of years for culinary and medical purposes. This study aimed to investigate the anticonvulsant and antioxidant activities of NSO on pentylenetetrazol (PTZ) kindling seizures in mice. Nigella sativa oil was tested for its ability (i) to suppress the convulsive and lethal effects of PTZ in kindled mice (anti-epileptogenic effect), (ii) to attenuate the PTZ-induced oxidative injury in the brain tissue (antioxidant effect) when given as a pretreatment prior to each PTZ injection during kindling acquisition. Valproate, a major antiepileptic drug, was also tested for comparison. Both substances studied significantly decreased oxidative injury in the mouse brain tissue in comparison with the PTZ-kindling group. Nigella sativa oil was found to be the most effective in preventing PTZ-induced seizures relative to valproate. Nigella sativa oil showed anti-epileptogenic properties as it reduced the sensitivity of kindled mice to the convulsive and lethal effects of PTZ; valproate was ineffective in preventing development of any of these effects. The data obtained support the hypothesis that neuroprotective action of NSO may correlate with its ability to inhibit not only excessive reactive oxygen species (ROS) formation but also seizure generation.

The related causes in very early morning onset of stroke.

We investigated the influence of early awakening and related factors on onset of cerebrovascular disease (CVD). Totally 1199 stroke patients, in whom the onset time was known, at 3 reference hospitals were included in this study. The effects of demographic, medical, and pathophysiological factors on the circadian pattern of an unselected series of patients with ischemic stroke were analyzed. Nine-hundred seventeen CVD patients with cerebral infarction (CI), 240 patients with intracerebral hemorrhage (CH), and 42 patients with subarachnoid hemorrhage (SAH) were identified. The greatest portion of strokes (32.5%) occurred between 03:00 and 06:00 a.m. Nearly one half of the strokes in this series occurred in the very early- to mid-morning hours. This analysis of strokes provides strong evidence with a higher risk in the early morning hours (03:00 a.m. to 06:00 a.m.), and lower risk during the night time period (21:00 p.m. to midnight). Approximately 1 of every 3 strokes (1 of 3 ischemic strokes, 1 of 6 hemorrhagic strokes, and 1 of 8 subarachnoid hemorrhages) is attributable to the early morning excess. This difference tried to be explained by three ways: cold weather, religious factors, and physiological mechanisms.

Erdosteine ameliorates PTZ-induced oxidative stress in mice seizure model.

The role of oxygen-derived free radicals has been suggested in genesis of epilepsy and in the post seizure neuronal death. The aim of this study was to investigate whether erdosteine has a preventive effect against epilepsy and postepileptic oxidative stress. The mice (n=27) were divided into three groups: (i) PTZ-induced-epilepsy group (n=9); (ii) PTZ-induced-epilepsy+erdosteine group (n=9); (iii) control group (n=9). The animals were observed for a period of 30 min for latency to first seizure onset, total seizure duration, the number of seizure episodes. Then they were sacrificed and the brains were quickly removed, and frozen for biochemical analysis. Malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD) and xanthine oxidase (XO) activities were carried out in the brain tissue. The latent period between PTZ induction and seizure are longer in the PTZ+erdosteine group than in PTZ-induced-epilepsy group (P<0.05). Biochemical analyses of brain tissue, revealed a significant increase in the MDA, XO and NO levels in the PTZ group according to erdosteine group. SOD level did not change in this group. While MDA and XO levels are significantly lower, SOD level is significantly higher in the PTZ+erdosteine group compared to PTZ and control groups (P<0.01). The present study demonstrated that erdosteine treatment both may increase latent interval between seizures and may decrease oxidative stress, thus may ameliorate neuronal death in brain during seizures. It may be used as an adjunct therapy in epilepsy.

A comparison of hair and serum trace elements in patients with Alzheimer disease and healthy participants.

BACKGROUND/AIM: To determine whether there was a difference between serum and hair trace elements' concentrations in patients with Alzheimer disease (AD) and healthy participants. MATERIALS AND METHODS: Hair and serum copper, selenium, zinc, magnesium, manganese, and iron levels were measured by inductively coupled plasma-mass spectrometry in patients with AD and healthy participants, and the obtained results were statistically compared. RESULTS: The mean hair selenium and zinc levels of patients with AD were significantly lower than the levels found for control participants (P < 0.05). Patients with AD had significantly higher mean hair copper and manganese levels than the controls. There were no significant differences between AD patients and controls with respect to the hair iron and magnesium levels (P > 0.05). Hair and serum trace element (copper, selenium, zinc, magnesium, manganese, and iron) levels in patients with AD showed no significant difference according to mini mental test scores or sex (P > 0.05). CONCLUSION: Some trace element levels may change in patients with AD. Due to the more permanent status, the analysis of these element levels in hair might be superior to blood analysis.

Potential genetic biomarkers in the early diagnosis of Alzheimer disease: APOE and BIN1.

BACKGROUND/AIM: Alzheimer disease (AD) is triggered by interactions of multiple genetic and environmental factors. The APOE gene E4 allele is the best-known risk factor for AD, yet it represents a small ratio of genetic factors. According to genome-wide association studies, the BIN1 gene is the second important risk factor for AD, following the APOE gene. We aimed to identify a novel biomarker indicating susceptibility to AD by investigating APOE alleles and BIN1 gene polymorphisms in a Turkish population. MATERIALS AND METHODS: Fifty-three AD patients and 56 controls were included to examine polymorphism and allele frequency of the APOE and BIN1 genes. Genomic DNAs were isolated from whole blood by SDS/proteinase K treatment, phenol-chloroform extraction, and ethanol precipitation. RFLP was done for identification of polymorphisms in the APOE gene and allele-specific PCR was used for the BIN1 gene. RESULTS: Frequency of the APOE E4 allele was higher in the AD patient group, while the frequency of the E2 allele was higher in controls. The E4/E4 genotype was detected in the AD patient group, while this genotype was not observed in the controls. The frequencies of BIN1 alleles were similar in both groups. CONCLUSION: There was a strong association between AD and the APOE E4 allele, while no such relation was observed with BIN1 gene polymorphism.

The effects and interactions of APOE and APH-1A polymorphisms in Alzheimer disease.

BACKGROUND/AIM: Alzheimer disease (AD) is characterized by the accumulation of senile plaques composed of amyloid ß-peptide, which is derived from ß-amyloid precursor protein through degradation by ß-secretase and y-secretase complexes. One of the major components of y-secretase complex, anterior pharynx-defective-1 (APH-1), is responsible for the activity of the γ-secretase complex. In this study, we searched for not only the most known common genetic risk factor, APOE, but also the APH-1a gene polymorphism in AD patients in a Turkish population. MATERIALS AND METHODS: In this study, 49 AD patients and 45 healthy controls were included. The genetic polymorphisms and allele frequencies of APOE and APH-1a were investigated. Patients were evaluated for behavioral, cognitive, and functional domains by detailed neurocognitive tests, and comparison between the above-mentioned polymorphisms and disease severity was made. RESULTS: Although there was an increased tendency of the APO ε4 allele in the AD group, no statistically significant difference was detected either in APOE or APH-1a polymorphisms, not suggesting a strong susceptibility to the development of AD. CONCLUSION: While searching for the pathogenesis of AD in order to develop novel diagnostic as well as therapeutic approaches, analysis of other genes with a possible role in AD is warranted.

Protective effects of caffeic acid phenethyl ester against experimental allergic encephalomyelitis-induced oxidative stress in rats.

Because oxidative damage has been known to be involved in inflammatory and autoimmune-mediated tissue destruction, modulation of oxygen free radical production represents a new approach to the treatment of inflammatory and autoimmune diseases. Central nervous system tissue is particularly vulnerable to oxidative damage, suggesting that oxidation plays an important role in the pathogenesis of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). Caffeic acid phenethyl ester (CAPE), an active component of honeybee propolis, has been determined to have antioxidant, anti-inflammatory, antiviral, and anticancer activities. We have previously reported that CAPE inhibits ischemia-reperfusion injury and oxidative stress in rabbit spinal cord tissue. The present study, therefore, examined effects of CAPE on oxidative tissue damage in EAE in rats. Treatment with CAPE significantly inhibited reactive oxygen species (ROS) production induced by EAE, and ameliorated clinical symptoms in rats. These results suggest that CAPE may exert its anti-inflammatory effect by inhibiting ROS production at the transcriptional level through the suppression of nuclear factor kappaB activation, and by directly inhibiting the catalytic activity of inducible nitric oxide synthase.

The protective effect of nebivolol on ischemia/reperfusion injury in rabbit spinal cord.

The aim of this experimental study was to investigate whether nebivolol has protective effects against neuronal damage induced by spinal cord ischemia/reperfusion (I/R). Twenty-one rabbits were divided into three groups: group I (control, no I/R), group II (only I/R) and group III (I/R+nebivolol). Spinal cord ischemia was induced by clamping the aorta both below the left renal artery and above the aortic bifurcation. Seventy-two hours postoperatively, the motor function of the lower limbs was evaluated in each animal. The animals were sacrificed at 72 h, and histopathological and biochemical analyses were carried out in the lumbar spinal cords. The motor deficit scores in nebivolol group were different from I/R group at 72 h (3.25+/-0.70 vs. 1.75+/-1.28, p=0.01). I/R produced a significant increase in the superoxide dismutase (SOD), xanthine oxidase (XO), adenosine deaminase (ADA) and myeloperoxidase (MPO) activities in spinal cord tissue when compared with control group. Nebivolol treatment prevented the increase of all those enzymes activities produced by I/R. A significant decrease in spinal cord glutathione peroxidase (GSH-Px) level was seen in I/R group and nebivolol treatment prevented the decrement in the spinal cord tissue GSH-Px contents. On the other hand, I/R produced a significant increase in the spinal cord tissue malondialdehyde (MDA) and nitric oxide (NO) contents, this was prevented by nebivolol treatment. In conclusion, this study demonstrates a considerable neuroprotective effect of nebivolol on neurological, biochemical and histopathological status during periods of spinal cord I/R in rabbits.

The comparison of nail and serum trace elements in patients with epilepsy and healthy subjects.

The objective of this prospective study was to determine the levels of manganese (Mn), copper (Cu), and zinc (Zn) levels in both nail and serum from patients with epilepsy. For this purpose, levels of these elements were measured in 31 patients with epilepsy and 19 healthy subjects. Element analyses were carried out by atomic absorption spectrophotometer (AAS). Increased Mn levels were detected in nail of patients with epilepsy compared to healthy controls (P<.008). The main nail Zn and Cu levels were found to be unchanged in epileptic patients compared to control subjects. There were no significant differences in serum Mn and Zn levels between epileptic patients and control subjects. However, there was a statistically significant increase in serum Cu levels in patients with epilepsy in comparison with control group (P<.009). Our results demonstrate that some trace element levels may vary in epileptic patients, and because of the more stable status, the analysis of these element levels in some tissues such as nail might be superior to serum analysis.

Ginkgo biloba prevents mobile phone-induced oxidative stress in rat brain.

BACKGROUND: The widespread use of mobile phones (MP) in recent years has raised the research activities in many countries to determine the consequences of exposure to the low-intensity electromagnetic radiation (EMR) of mobile phones. Since several experimental studies suggest a role of reactive oxygen species (ROS) in EMR-induced oxidative damage in tissues, in this study, we investigated the effect of Ginkgo biloba (Gb) on MP-induced oxidative damage in brain tissue of rats. METHODS: Rats (EMR+) were exposed to 900 MHz EMR from MP for 7 days (1 h/day). In the EMR+Gb groups, rats were exposed to EMR and pretreated with Gb. Control and Gb-administrated groups were produced by turning off the mobile phone while the animals were in the same exposure conditions. Subsequently, oxidative stress markers and pathological changes in brain tissue were examined for each groups. RESULTS: Oxidative damage was evident by the: (i) increase in malondialdehyde (MDA) and nitric oxide (NO) levels in brain tissue, (ii) decrease in brain superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and (iii) increase in brain xanthine oxidase (XO) and adenosine deaminase (ADA) activities. These alterations were prevented by Gb treatment. Furthermore, Gb prevented the MP-induced cellular injury in brain tissue histopathologically. CONCLUSION: Reactive oxygen species may play a role in the mechanism that has been proposed to explain the biological side effects of MP, and Gb prevents the MP-induced oxidative stress to preserve antioxidant enzymes activity in brain tissue.

The increase of mean platelet volume in patients with Alzheimer disease.

BACKGROUND/AIM: Vascular risk factors play an important role in the progression of Alzheimer disease (AD). Mean platelet volume (MPV) is a determinant of platelet functionality and increased MPV is associated with an increased risk of vascular inflammation. Here we aimed to examine whether MPV could be used as a marker of vascular damage in AD and to discuss the relation between MPV and other vascular risk factors. MATERIALS AND METHODS: A total of 109 outpatients with AD and 81 healthy controls were included in this study. Diagnosis of AD was made according to defined criteria. The Turkish version of the Mini Mental State Examination (MMSE) was used for cognitive assessment. According to the test results, patients were divided into 2 subgroups, mild (MMSE ≥ 18) and moderate (MMSE < 18), and their MPV levels were compared. RESULTS: MPV levels were higher in the AD group. There was no statistically significant difference between the moderate group and the mild group according to MPV values. CONCLUSION: Increased MPV in patients with AD may point to platelet dysfunction. MPV is an indicator of increased in vivo platelet activation. Hence, platelets could be the link between vascular risk factors and AD. The assessment of MPV in patients with AD may help identify the patients that could benefit from additional antiplatelet therapy.