ABSTRACT
Objective@#In this study, we aimed to examine thiol/disulfide homeostasis and oxidative DNA damage in patients with OCD and compare them with healthy controls. @*Methods@#Thirty-five patients previously diagnosed with OCD in Van Yuzuncu Yil University Department of Psychiatry and thirty-three healthy volunteers were included in the study. The severity of the symptoms was measured using the Yale-Brown Obsessive-Compulsive Scale. Five ml of blood samples were taken from the patient and control groups. The samples were stored at appropriate conditions until use. Leukocyte DNA was isolated and the levels of 8-hydroxy-2-deoxyguanosine (8-OHdG) and deoxyguanosine were detected to assess the oxidative DNA damage. The level of oxidative DNA damage was expressed as 8-OHdG/106 dG. Total thiolative thiol levels were measured for thiol/disulfide homeostasis. The level of disulfide was determined by subtracting the native thiol value from the total thiol value and the result was divided by two. Results were given as percentages. @*Results@#The total and native thiol levels in patients with OCD were significantly lower, and the disulfide levels were significantly higher in patients with OCD than healthy control subjects. In addition, 8-OHdG, an indicator of DNA damage, was significantly lower in the control group compared to the patient group. @*Conclusion@#Increased levels of disulfideative thiol and disulfide/total thiol in patients with OCD show that levels of oxidative stress were elevated and therefore, higher 8-OHdG levels in patients with OCD is a marker of oxidative DNA damage.
ABSTRACT
Objective@#Insufficient number of oxidative stress studies have been conducted in patients with adult attention deficit hyperactivity disorder (ADHD). The objective of the current study is to examine the thiol/disulfide homeostasis as well as oxidative DNA damage levels in adult ADHD patients and to compare them with the results of healthy control subjects. @*Methods@#The study was inclusive of forty-nine patients who were diagnosed with adult ADHD, as well as thirty-three healthy volunteers to be used as the control group. The diagnosis of the patients was conducted according to the DSM-5 diagnostic criteria. Blood were stored under appropriate laboratory conditions. For the purpose of detecting the oxidative DNA damage level, an extraction of genomic DNA from leukocytes was carried out, and furthermore the levels of 8-hydroxy-2-deoxyguanosine (8-OHdG), apart from deoxyguanosine, were measured accordingly. @*Results@#Total thiol and the native thiol levels were observed to be statistically lower in adult ADHD patients as compared to the subjects in the healthy control group (p = 0.001). It was observed that the disulfide levels were higher in adult ADHD patients as compared to the healthy control subjects (p = 0.001). In addition, the levels of 8-OHdG, which are considered as a marker for assessing DNA damage, were found to be significantly lower in the control group as compared to the adult ADHD patients (p = 0.001). @*Conclusion@#It was observed that the thiol/disulfide homeostasis had shifted towards disulfide, and 8-OHdG levels were increased in adult ADHD patients.
ABSTRACT
The role of inflammation has been shown in the pathogenesis of epilepsy, while glucocorticoids and adrenaline have anti-inflammatory effects. The aim of the present study was to investigate the effects of adrenaline, prednisolone, and indomethacin on caffeine-induced epilepsy [epileptiform activity] in rats and to examine the mechanism of the pro-epileptic effect of indomethacin. The adrenalectomized rats that had been given only adrenaline [the control group] did not die; however, adrenaline did not prevent the adrenalectomized rats which were given prazosin, phenoxybenzamine, yohimbine, metoprolol, and propranolol from dying. In the rats given propranolol + adrenaline, the rate of death was 100%, while this rate was 50% in the groups receiving prazosin + adrenaline, phenoxybenzamine + adrenaline, and metoprolol + adrenaline. The rate was 75% in the group given yohimbine + adrenaline. Prednisolone increased the degree of convulsion in adrenalectomized rats. Over-reduction in the blood catecholamine level made epileptogenesis more severe. It was observed that adrenaline pressed epileptogenesis via its own receptors [alpha -1, alpha - 2, beta - 1, beta - 2]. It was also revealed that all of the adrenergic receptors were responsible due to antiepileptic activity; beta - 2 receptors played the most important role. It was observed that both acute and chronic indomethacin administration reduced the catecholamine levels. The situation in which acute administration of indomethacin did not affect epileptogenesis might originate from the fact that the structure of indomethacin did not significantly increase the corticosterone level
ABSTRACT
In this study, we investigated the effects of treatment with chronic antihypertensive drugs [clonidine, methyldopa, amlodipine, ramipril and rilmenidine] on oxidant-antioxidant parameters and toxic effects on DNA in rat uterus tissue. In addition, uterus tissues were examined histopathologically. A total of 36 albino Wistar rats were divided into the following six groups: 0.075 mg/kg clonidine group; 100 mg/kg methyldopa group; 2 mg/kg amlodipine group; 2.5 mg/kg ramipril group; 0.5 mg/kg rilmenidine group; and the healthy group. Rats underwent chronic drug administration for 30 days and at the end, biochemical and histopathological examinations were performed. All data were subjected to one-way ANOVA test. We divided these drugs into the following three groups according to their effects on rat uteri: [I] mild negative effects [clonidine], [II] moderate negative effects [rilmenidine, methyldopa] and [III] drugs which had severe negative effects [amlodipine, ramipril]. These data may help with selection of antihypertensive drugs, in order to determine which drugs have the lowest toxicity in pregnant and non-pregnant [pre-pregnancy] women