Oxidative Imbalance in Pediatric Anxiety Disorders: A Preliminary Comparative Study.

Background It is important to determine the possible related factors of anxiety disorder, one of the common psychiatric disorders of childhood. Our aims in this study were to compare oxidative stress markers between anxiety disorders in pediatric patients and healthy controls and to examine the relationship between anxiety symptom severity and oxidative stress indicators. Methods The study included 25 patients and 25 healthy controls. We measured the total oxidant capacity (TOS) and total antioxidant capacity (TAS) from the collected serum samples and calculated the oxidative stress index (OSI). We evaluated the clinical severity of the anxiety symptoms by the Revised Child Anxiety and Depression Scale-Child Version (RCADS-CV). Results The groups did not exhibit a noteworthy distinction in terms of TOS (p=0.128) and TAS (p=0.329). However, OSI was markedly elevated in the group with anxiety disorder (p=0.044). In the correlation analysis between anxiety symptom severity and oxidative stress indicators in the group with anxiety disorder, we found a positive correlation between TOS and RCADS total anxiety score (p=0.08). Conclusion These results may point to an oxidative dysfunction in anxiety disorders and the potential role of oxidative stress in their aetiology. Prospective, large-scale, randomized studies are needed to investigate if oxidative stress indicators can be used in the diagnosis of anxiety disorders and as new treatment targets.

Novel N-Acyl Hydrazone Compounds as Promising Anticancer Agents: Synthesis and Molecular Docking Studies.

In this study, a new series of N-acyl hydrazones 7a-e, 8a-e, and 9a-e, starting from methyl δ-oxo pentanoate with different substituted groups 1a-e, were synthesized as anticancer agents. The structures of obtained target molecules were identified by spectrometric analysis methods (FT-IR, 11H NMR, 13C NMR, and LC-MS). The antiproliferative activity of the novel N-acyl hydrazones was evaluated on the breast (MCF-7) and prostate (PC-3) cancer cell lines by an MTT assay. Additionally, breast epithelial cells (ME-16C) were used as reference normal cells. All newly synthesized compounds 7a-e, 8a-e, and 9a-e exhibited selective antiproliferative activity with high toxicity to both cancer cells simultaneously without any toxicity to normal cells. Among these novel N-acyl hydrazones, 7a-e showed the most potent anticancer activities with IC50 values at 7.52 ± 0.32-25.41 ± 0.82 and 10.19 ± 0.52-57.33 ± 0.92 µM against MCF-7 and PC-3 cells, respectively. Also, molecular docking studies were applied to comprehend potential molecular interactions between compounds and target proteins. It was seen that the docking calculations and the experimental data are in good agreement.

Hypsarrhythmia paroxysm intensities that initiate and render physical and mental retardation irreversible in West syndrome.

PURPOSE: The present study would like to investigate the effect of hypsarrhythmia paroxysms on neurological examination findings. MATERIAL AND METHOD: This study enrolled 48 children with normal cranial magnetic resonance imaging (cMRI) findings who were previously untreated with adrenocorticotropic hormone (ACTH) and had no history of asphyxia or anoxia at birth, no underlying disease, and no history of head trauma or central nervous system infection. In these children, duration of treatment delay (DTD) was calculated, HPs in NREM sleep were counted, and neurological examination findings were identified. During the study, sometimes the 'countable hypsarrhythmia paroxysms index' (cHPI) and sometimes the 'durational hypsarrhythmia paroxysm index (dHPI)' was estimated. The onset of neurological examination findings, the onset of physical and mental retardation and the time when physical and mental retardation became irreversible were investigated. The children were stratified into 5 groups based on DTD and attempts were made to prevent the recurrence of aborted ISs by ACTH treatment. RESULTS: I- When 'cHPI = 4/min'; mild growth retardation may be noticed. II- When 'cHPI = 6/min' and 'dHPI = 25%'; reduced eye tracking and reduced movement may be observed. III- When 'cHPI = 8/min' and 'dHPI >32%'; reduced eye tracking and reduced movement become evident, and neurological examination findings are reversible. IV- When 'dHPI = 45%'; partially permanent, mild motor and psychiatric sequelae develop. V- When 'dHPI >49%'; neurological examination findings become irreversible. VI- No relationship was found between neurological examination findings the early onset of ISs. CONCLUSION: WS cannot be treated unless DCHP is elucidated.

Anthocyanin Addition to Kefir: Metagenomic Analysis of Microbial Community Structure.

The addition of anthocyanin to kefir for the production of more functional and bio-diversified kefir beverages has the potential to increase kefir's healthful activities. In the present study, anthocyanin extracts, obtained from black carrots, were added into kefir mixture during the fermentation process in different concentrations (1% and 5%, w/v). These kefir samples were then analyzed in terms of their microbiological qualities by metagenomic analysis. The results of the analyses show that the addition of anthocyanin has significant impacts on the community structure of kefir microbiome which in turn directly affects the expected health impacts of the beverage. Kefir with no anthocyanin included predominantly probiotic bacteria such as Lactococcus lactis (34%) and Lactobacillus kefiri (34%). On the other hand, kefir with 1% anthocyanin demonstrated a more balanced distribution of probiotic species like Lb. kefiri (17%), Leuconostoc mesenteroides (9%), and Lc. lactis (5%) at similar abundance rates. 5% anthocyanin kefir demonstrated the highest polarity in the community with a strong dominance of probiotic Lb. kefiri (72%), and distinctly less abundant bacteria such as Streptococcus salivarius subsp. thermophilus (3%). These findings provide that fortification with anthocyanins can be utilized to enhance the quality, composition, and beneficial functions of kefir.

A CASE OF MIGRAINE WITH SYMPTOMS OF PERCEPTION DISORDERS INCLUDING A FAMILY HISTORY.

Alice in Wonderland Syndrome is characterized by distortions in perception, especially with signs of micropsia or macropsia, peropia, teleopsia.The etiology of this syndrome includes migraine attacks, epilepsy, infections or substance abuse.In this case study, a 15-year-old adolescent girl was admitted to our child and adolescent psychiatry clinic with complaints of seeing objects and people as larger or smaller than they are and/or perceiving objects closer or farther than they are, before her migraine attacks.It was also stated that his father had similar complaints during his adolescence..In this case report, we present a case of migraine with aura.

Black carrot anthocyanins exhibit neuroprotective effects against MPP+ induced cell death and cytotoxicity via inhibition of oxidative stress mediated apoptosis.

Parkinson's disease (PD) is a common chronic neurodegenerative disease induced by the death of dopaminergic neurons. Anthocyanins are naturally found antioxidants and well-known for their preventive effects in neurodegenerative disorders. Black carrots (Daucus carota L. ssp. sativus var. atrorubens Alef.) are a rich source of anthocyanins predominantly including acylated cyanidin-based derivatives making them more stable. However, there have been no reports analysing the neuroprotective role of black carrot anthocyanins (BCA) on PD. In order to investigate the potential neuroprotective effect of BCA, human SH-SY5Y cells were treated with MPP+ (1-methyl-4-phenylpyridinium) to induce PD associated cell death and cytotoxicity. Anthocyanins were extracted from black carrots and the composition was determined by HPLC-DAD. SH-SY5Y cells were co-incubated with BCA (2.5, 5, 10, 25, 50, 100 µg/ml) and 0.5 mM MPP+ to determine the neuroprotective effect of BCA against MPP+ induced cell death and cytotoxicity. Results indicate that BCA concentrations did not have any adverse effect on cell viability. BCA revealed its cytoprotective effect, especially at higher concentrations (50, 100 µg/ml) by increasing metabolic activity and decreasing membrane damage. BCA exhibited antioxidant activity via scavenging MPP+ induced reactive oxygen species (ROS) and protecting dopaminergic neurons from ROS mediated apoptosis. These results suggest a neuroprotective effect of BCA due to its high antioxidant and antiapoptotic activity, along with the absence of cytotoxicity. The elevated stability of BCA together with potential neuroprotective effects may shed light to future studies in order to elucidate the mechanism and further neuro-therapeutic potential of BCA which is promising as a neuroprotective agent. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10616-021-00500-4.

Ten-Year Experience Outcomes of a Day Treatment for Children and Adolescents with Psychiatric Disorders.

INTRODUCTION: It was aimed to evaluate the efficacy of a day treatment clinic in Turkey and which has been serving for ten years for children and adolescents with psychiatric disorders. METHODS: 262 patients who completed day treatment within ten years were tested at intake and discharge. The patients' functioning was assessed using the Children's Global Assesment Scale (CGAS), Clinical Global Impression Scale (CGIS), state-trait anxiety inventory for children, depression rating scale for children, Coopersmith self-esteem inventory for children. Pre/post treatment comparisons were made on same variables. RESULTS: Statistical analyses showed that, improvement was maintained on all measures. The high CGAS scores at discharge were showed well-being and good functioning of patients. The CGIS scores varied from moderately disturbed (4.83±0.88) to much improved (2.55±0.93) demonstrated that treatment responses showed improvement. Wilcoxon T tests showed that patients were significantly more anxious and depressive at intake and had more problems in self esteem. State-trait anxiety inventory for children and depression rating scale for children scores decreased and Coopersmith self-esteem inventory for children scores improved with day treatment. CONCLUSION: This study points that as results of ten-year experience, day treatment approach seems effective and therefore to be the treatment of choice for treating children and adolescents with psychiatric disorders. It also shows the necessity of a treatment that combines multiple modalities like day treatment and day treatment must be more generalize for these patient population.

Methylenetetrahydrofolate reductase gene polymorphisms in Turkish children with attention-deficit/hyperactivity disorder.

Attention-deficit/hyperactivity disorder (ADHD) is a common, multifactorial genetic disorder. The aim of the present study was to evaluate a possible association between 5,10-methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms and ADHD. There is evidence to suggest that MTHFR C677T and A1298C polymorphisms alter the function of the enzyme, causing reduced folate and increased homocysteine levels in plasma. Two polymorphisms of the MTHFR gene, C677T (rs1801133) and A1298C (rs1801131), were analyzed in a sample of 100 Diagnostic and Statistical Manual of Mental Disorders-IV-diagnosed ADHD and 300 healthy controls using a polymerase chain reaction-restriction fragment length polymorphism method. We did not find any association between MTHFR 677T allele, MTHFR 1298C allele, and ADHD. In addition, there was no genotype association between the MTHFR gene and ADHD (χ(2)=1.711; df=2; p=0.425; χ(2)=2.946; df=2; p=0.229). Our data suggest that neither the MTHFR C677T polymorphism nor the MTHFR A1298C polymorphism was associated with ADHD in Turkish children. Thus, the MTHFR gene does not seem to play a role in the etiopathogenesis of ADHD in the cohort studied.

Ischemia/reperfusion in rat: antioxidative effects of enoant on EEG, oxidative stress and inflammation.

PRIMARY OBJECTIVE: The present study was undertaken to evaluate whether enoant, which is rich in polyphenols, has any effect on electroencephalogram (EEG), oxidative stress and inflammation in ischemia/reperfusion (I/R) injury. METHODS: Ischemia was induced by 2-hour occlusion of bilateral common carotid artery. Animals orally received enoant. Group 1 was the ischemic control group. Group 2 was treated with enoant of 1.25 g kg⁻¹ per day for 15 days after I/R. Group 3 received the same concentration of enoant as in group 2 for 15 days before and after I/R. Group 4 was the sham operation group. EEG activities were recorded and the levels of TNF-α, IL-1ß and IL-6, TBARS and GSH were measured in the whole brain homogenate. RESULTS: There were significant changes in EEG activity in groups treated with enoant either before or after ischemia when compared with their basal EEG values. TNF-α, IL-6 and IL-1ß levels were significantly increased after I/R. GSH levels in group 3 treated with enoant in both pre- and post-ischemic periods were significantly increased and TBARS concentration was decreased compared with the ischemic group. CONCLUSION: The findings support that both pre-ischemic and post-ischemic administrations of enoant might produce neuroprotective action against cerebral ischemia.

Angiotensin-converting enzyme polymorphism in schizophrenia, bipolar disorders, and their first-degree relatives.

BACKGROUND: Family, twin and adoption studies have provided major evidence for the role of genetics in numerous psychiatric disorders including schizophrenia (SZ) and bipolar disorders (BDs). As SZ and BD have some susceptibility genes in common and since unaffected first-degree relatives of these patients carry a high likelihood of these susceptibility genes, we aimed to elucidate the role of angiotensin-converting enzyme (ACE) genetic variants in patients with SZ, BD and their first-degree relatives. METHODS: The study sample comprised 239 patients with SZ, 184 patients with BD, 284 unaffected first-degree biological relatives of patients with SZ and 301 unaffected first-degree biological relatives of patients with BD and 210 healthy controls. The ACE genotypes were determined by polymerase chain reaction. RESULTS: ACE insertion/deletion polymorphism was associated with SZ and BD. DD genotype and D allele distributions in bipolar patients and their first-degree relatives were significantly higher than those of SZ patients, their relatives, and controls. In contrast, II genotype and I allele were reduced in both the patient groups and their relatives as compared with controls. CONCLUSION: In this study, the D allele might be responsible for clustering of psychotic symptoms and results in the psychotic manifestations of BD, whereas I allele seems to be protective against development of SZ and BD. SZ and BD characterized by similar or different gene variant in ACE could be a useful marker for these psychiatric disorders, if this polymorphism is replicated in the future studies.

Are GRIK3 (T928G) gene variants in schizophrenia patients different from those in their first-degree relatives?

We examined whether the GRIK3 (T928G) polymorphic variants in patients with schizophrenia are different from those of their first-degree relatives and healthy controls. The study population was composed of 256 patients with schizophrenia, 305 first-degree relatives of schizophrenia patients and 242 healthy control subjects. The GRIK3 (T928G) polymorphism was determined by restriction fragment length polymorphism. The frequency of the TT genotype was predominant, whereas the GG genotype was rare among all groups. The frequencies of GRIK3 (T928G) genotype distributions in the patients with schizophrenia were similar to those of their relatives. The frequency of the GG genotype was significantly higher in patients than in healthy controls. Similarly, GG genotype distribution in relatives was elevated compared with that in controls, but this value did not reach statistical significance. On the other hand, the subgroups of schizophrenia patients did not show a significant association with the GRIK3 (T928G) gene. It appears that the patients share the same (GRIK3) T928G gene variants with their relatives. One interpretation of our findings is that the relatives are at risk for the development of schizophrenia in the future.

The role of solid food intake in antimuscarinic-induced convulsions in fasted mice.

Animals treated with scopolamine after fasting develop convulsions after they are allowed to eat ad libitum. This study was aimed at investigating the effect on these convulsions of liquid food intake, feeding by gavage, and placebo. Fasted mice treated with saline or scopolamine were allowed to eat solid food, slurry food or liquid food ad libitum, given placebo, or given liquid food by gavage. After 30 min, all animals were allowed to eat food pellets and observed for 30 min for the incidence and onset of convulsions. Scopolamine treatment caused convulsions only in the animals given solid food in the first 30 min; no convulsions were observed in the animals given slurry food, liquid food ad libitum, gavage, or placebo. When the animals that did not develop convulsions during the experiment were allowed to eat solid food, convulsions occurred. These findings indicate that complex mechanisms trigger scopolamine-induced convulsions in fasted animals eating solid food.

Do schizophrenia and bipolar disorders share a common disease susceptibility variant at the MMP3 gene?

There is growing evidence of partial etiological overlap between schizophrenia (SZ) and bipolar I disorder (BD-I) from linkage analysis, genetic epidemiology and molecular genetics studies. SZ and BD-I are neurodevelopmental disorders with genetic and environmental etiologies. Recent studies have demonstrated that matrix metalloproteinase 3 (MMP3) is a key event in associative memory formation, learning and synaptic plasticity, which are important in psychiatric disorders. In the light of these findings, we analyzed the genetic variations in the MMP3-1171 5A/6A in patients with SZ, patients with BD-I and healthy controls. To the best of our knowledge, this is the first study to report an association of variation in gene encoding MMP3 with SZ. Our study group consisted of 111 unrelated patients with SZ, 141 unrelated patients with BD-I, and 121 unrelated healthy controls. The frequencies of 6A6A genotype and 6A allele distributions of MMP3 in patients with SZ were significantly decreased when compared with controls. In contrast, in patients with SZ, the distributions of 5A5A genotype and 5A allele of MMP3 gene were significantly increased as compared with healthy controls. When the frequencies of genotypes or alleles in schizophrenic patients and bipolar patients were compared, 6A6A genotype and 6A allele in patients with BD-I were significantly higher than patients with SZ. In contrast, 5A5A genotype and 5A allele distributions of MMP3 gene were significantly frequent in patients with SZ. On the other hand, no significant differences were found in the allele or genotype distribution in patients with BD-I compared with controls. In conclusion, our data have supported the hypothesis that there is a possible relationship between -1171 5A/6A polymorphism of MMP3 gene and SZ. A larger sample group is needed to confirm the potential role of this gene in the pathophysiology of psychiatric disorders.

Paraoxonase-1 55/192 genotypes in schizophrenic patients and their relatives in Turkish population.

BACKGROUND: Oxidative stress and free radical-induced toxicity have been implicated in the pathophysiology of schizophrenia. In this study, we examined paraoxonase (PON1)-55/192 polymorphisms and PON1 activity in patients with schizophrenia, first-degree relatives of schizophrenic patients, and healthy controls. METHODS: This study consisted of 292 healthy participants, 267 unrelated patients with schizophrenia and 311 first-degree relatives of schizophrenic patients. PON1 55 (rs 854560) and PON1 192 (rs 662) polymorphisms were performed by restriction fragment length polymorphism. RESULTS: The frequencies of the QQ and LL genotypes were significantly overpresented in controls compared with those of schizophrenic patients and their relatives. In contrast, the RR genotype was more prevalent in patients than their relatives and healthy controls. The frequencies of the LM and QR genotypes in relatives were higher than controls. Serum PON1 activities of controls were significantly higher when compared with both schizophrenic patients and their relatives. The RR and LL genotypes were associated with a significantly increased PON1 activity as compared with QR or QQ and MM or LM genotypes, respectively, in all groups. CONCLUSION: This is the first study that shows the association between PON1-55/192 polymorphisms and schizophrenia. Our data suggest that the subjects carrying R allele or RR genotype might be susceptible to schizophrenia and subjects with QQ or LL might be protected against schizophrenia. First-degree relatives of schizophrenic patients have higher heterozygote genotypes, suggesting that this group can shift either to patient or control group depending on their allele types and environmental factors. PON1 genetic variations are also associated with PON1 activities. Reduced PON1 activity in patients and their relatives might result from the combined effects of more than one polymorphic variant in PON1 or other genes and/or increased oxidative stress, supporting the hypothesis that reactive oxygen species-mediated cellular damage might contribute to the neuropathology of schizophrenia.

Combined impact of matrix metalloproteinase-3 and paraoxonase 1 55/192 gene variants on coronary artery disease in Turkish patients.

BACKGROUND: We investigated the association of matrix metalloproteinase-3 (MMP-3) and paraoxonase 1 (PON1) 55/192 polymorphisms with coronary artery disease (CAD) and the number of diseased vessels in patients with CAD. MATERIAL/METHODS: One hundred thirty-nine CAD patients and 119 healthy control subjects were included in the study. Genotypes for PON1 55/192 and MMP-3 5A/6A polymorphisms were determined by restriction fragment length polymorphism. RESULTS: Although distributions of the RR genotype of PON1 192 and the 5A5A genotype of MMP-3 were more frequent in patients, frequencies of the QQ genotype of PON1 192, the MM genotype of PON1 55, and the 6A6A genotype of MMP-3 were significantly lower in patients compared with healthy control subjects. The combined genotypes of RR/LL and/or 5A5A are increased the risk of CAD when compared with subjects who possess neither the MMP-3 5A5A nor the PON1 RR/LL genotype. While the MMP-3 5A/6A genetic variants were not associated with the number of diseased vessels, PON1 55/192 variants were associated with the number of diseased vessels. CONCLUSIONS: The combined PON1 55/192 and MMP-3 5A/6A genetic variants are associated with CAD; PON1 seems to be connected with the number of diseased vessels, and hypertension and hyperlipidemia are related with PON1 192 and MMP-3 in CAD patients.

Effect of the methylenetetrahydrofolate reductase gene polymorphisms on homocysteine, folate and vitamin B12 in patients with bipolar disorder and relatives.

We investigated the effect of polymorphic variants of c.1298A>C (Glu429Ala) and c.677C>T (Ala222Val) in methylenetetrahydrofolate (MTHFR) gene on the total homocysteine (tHcy), folate and B12 levels in patients with bipolar disorder, first-degree relatives of patients, and controls. The c.677C>T and c.1298A>C polymorphisms in MTHFR were determined by polymerase chain reaction-restriction fragment length polymorphism in 197 bipolar patients, 278 relatives and 238 controls. tHcy and folate and vitamin B12 levels were measured by Fluorescence Polarization Immunoassay and Electrochemiluminescence, respectively. The tHcy was significantly increased in patients and relatives. In contrast, folate and B12 were significantly lower in patients and relatives. Gender was not considered as a significant determinant in the multivariate analysis. Genotypes of c.1298A>C and c.677C>T were correlated with tHcy, folate and B12. Patients and relatives carrying TT and/or AA and AC genotypes had elevated tHcy and reduced folate and B12 levels. High tHcy but low folate and vitamin B12 levels may be a risk factor for development of bipolar disorder.

Methylenetetrahydrofolate reductase gene polymorphisms are associated with ischemic and hemorrhagic stroke: Dual effect of MTHFR polymorphisms C677T and A1298C.

Hyperhomocysteinemia is an independent risk factor for ischemic stroke. The enzyme methylenetetrahydrofolate reductase (MTHFR) plays a critical role in modulating the levels of plasma homocysteine. Two polymorphisms in the MTHFR gene, C677T, A1298C result in reduced enzyme activity. The mechanisms of ischemic and hemorrhagic stroke are not well understood. Although controversial, previous studies have shown evidence of causality of both stroke subtypes in patients with methylenetetrahydrofolate reductase gene polymorphisms. Therefore, we examined whether the C677T and A1298C polymorphisms of MTHFR gene are genetic risk factors for both ischemic and hemorrhagic stroke in a Turkish Caucasian population. In a case-control study, 120 total unrelated stroke patients (92 ischemic stroke, 28 hemorrhagic stroke), and 259 healthy controls were genotyped for C677T and A1298C polymorphisms of the MTHFR gene using a PCR-RFLP based-method. The MTHFR 1298C allele (chi(2)=8.589; P=0.014), C1298C genotype (OR=2.544; P=0.004), and C677C/C1298C compound genotype (OR=3.020; P=0.001) were associated with overall stroke. The MTHFR 1298C allele (chi(2)=11.166; P=0.004), C1298C genotype (OR=2.950; P=0.001), and C677C/C1298C compound genotype (OR=3.463, P=0.0001) were strongly associated with ischemic stroke. Interestingly however, the MTHFR 677T allele (chi(2)=6.033; P=0.049), T677T genotype (OR=3.120; P=0.014), and T677T/A1298A compound genotype (OR=4.211; P=0.002) were associated with hemorrhagic stroke. In conclusion, the C677T and A1298C polymorphisms of the MTHFR gene are genetic risk factors for hamorrhagic and ischemic stroke respectively, independent of other atherothrombotic risk factors.

Electroencephalographic characterization of scopolamine-induced convulsions in fasted mice after food intake.

The present study was conducted to evaluate scopolamine-induced convulsions in fasted mice after food intake effects on the cortical electroencephalogram (EEG). Continuous EEG recordings were taken with Neuroscan for 10 min in freely moving mice with six chronic cortical electrode implants. Animals were weighed and deprived of food for 48 h. EEG recordings were taken at the 24th and 48th hour after their food deprivations. Later, all animals were treated with saline or scopolamine of 3mg/kg i.p. and EEG recordings were repeated for 10 min. Twenty minutes later, they were given food pellets and were allowed to eat ad libitum. All animals were observed for 60 min to determine the incidence and onset of convulsions and EEG recordings were taken simultaneously. The present results demonstrate that food deprivation causes differences in EEG in the elapsed time. The changes in EEG induced after food deprivation become different with scopolamine administration. In scopolamine treatment group, eating caused a series of high-voltage polyspikes and synchronized spikes with a predominant frequency in the 1-3 Hz range and fast activity that represents a typical epileptiform manifestation. It was concluded that the EEG properties and the behavioral patterns of these convulsions are in accordance with each other.

PON1 55/192 polymorphism, oxidative stress, type, prognosis and severity of stroke.

We investigated the association of PON1 55/192 polymorphisms with type, severity and prognosis of stroke and oxidative markers. Paraoxonase1 (PON1), Glutathione Reductase (GSH-Rd) and Malondialdehyde (MDA) levels were measured at day 1 and at day 5 following the onset of stroke. Genotypes were determined by polymerase chain reaction and restriction digestion. The frequencies of QQ and MM genotypes of PON1 192 and PON1 55, respectively, were significantly higher in controls than in patients. However, the allele frequencies of PON1 192 R and PON1 55 L were significantly more frequent in patients compared to controls. The frequency of combined genotype of RR/LL was significantly higher in cardioembolic group than in atherothrombotic group. PON1 activities were significantly diminished in stroke patients compared to controls. In contrast, serum MDA levels were significantly greater in patients than the values in controls. GSH-Rd activity was higher in patients with small lesion and good prognosis than those with large and poor prognosis. Low density lipoprotein (LDL) levels in patients with large lesions were higher than those with small lesions. PON1 55/192 polymorphisms influence activity of the enzyme. PON1 55/192 genotypes have been associated with MDA levels. In conclusion, PON1 genetic variations are associated with risk factors, severity, type and prognosis of stroke and oxidative stress.

Evaluation of the angiotensin-converting enzyme insertion/deletion polymorphism and the risk of ischaemic stroke.

Angiotensin-converting enzyme (ACE) gene polymorphism has been associated with increased incidence of stroke in some populations, although contradictory results have been reported. The aim of this study was to determine the allelic frequency and the genotypic distribution for ACE gene polymorphism in Turkish patients with ischemic stroke compared to appropriate healthy controls and to correlate the genetic findings with stoke type. One hundred and eight patients with ischemic stroke versus 79 healthy controls were studied for the presence of ACE gene polymorphism detected by PCR. Genotypes were defined as DD, II and ID according to the presence of the D (deletion) and I (insertion) alleles. There was no statistically significant difference in either the genotypic distribution or allelic frequency between the patients versus healthy controls (chi2 = 0.105; df = 1; p = 0.430). There was also no significant difference for ACE genotype distribution and allelic frequency within the stroke group classified according to Bamford criteria (chi2 = 4.827; df = 3; p = 0.185). Our data supports lack of association between DD genotype and/or D allele and ischemic stroke or subtypes of ischaemic stroke in the Turkish population.