Gender-related variation expressions of neuroplastin TRAF6, GluA1, GABA(A) receptor, and PMCA in cortex, hippocampus, and brainstem in an experimental epilepsy model.

Epileptic seizures are seen as a result of changing excitability balance depending on the deterioration in synaptic plasticity in the brain. Neuroplastin, and its related molecules which are known to play a role in synaptic plasticity, neurotransmitter activities that provide balance of excitability and, different neurological diseases, have not been studied before in epilepsy. In this study, a total of 34 Sprague-Dawley male and female rats, 2 months old, weighing 250-300 g were used. The epilepsy model in rats was made via pentylenetetrazole (PTZ). After the completion of the experimental procedure, the brain tissue of the rats were taken and the histopathological changes in the hippocampus and cortex parts and the brain stem were investigated, as well as the immunoreactivity of the proteins related to the immunohistochemical methods. As a result of the histopathological evaluation, it was determined that neuron degeneration and the number of dilated blood vessels in the hippocampus, frontal cortex, and brain stem were higher in the PTZ status epilepticus (SE) groups than in the control groups. It was observed that neuroplastin and related proteins TNF receptor-associated factor 6 (TRAF6), Gamma amino butyric acid type A receptors [(GABA(A)], and plasma membrane Ca2+ ATPase (PMCA) protein immunoreactivity levels increased especially in the male hippocampus, and only AMPA receptor subunit type 1 (GluA1) immunoreactivity decreased, unlike other proteins. We believe this may be caused by a problem in the mechanisms regulating the interaction of neuroplastin and GluA1 and may cause problems in synaptic plasticity in the experimental epilepsy model. It may be useful to elucidate this mechanism and target GluA1 when determining treatment strategies.

Colchicine modulates oxidative stress in serum and leucocytes from remission patients with Family Mediterranean Fever through regulation of Ca²+ release and the antioxidant system.

We investigated the effects of colchicine on oxidative stress and Ca²+ release in serum and polymorphonuclear leucocytes (PMNs) of Familial Mediterranean Fever (FMF) patients with attack, remission and unremission periods. Eighteen FMF patients and six age-matched healthy subjects in four groups were used. The first group was a control. The second group included patients with active FMF. The third and fourth groups were patients with remission and unremission, respectively. Colchicine (1.5 mg/day) was given to the third and fourth groups for 1 month. PMN cells, serum lipid peroxidation and intracellular Ca²+-release levels in the attack and unremission groups were higher than in those in controls, although they were lower in the remission group than in the attack group. Serum vitamin E and ß-carotene concentrations were higher in the remission group than in the control and attack groups. However, PMN, serum lipid peroxidation and Ca²+-release levels were further increased in the unremission group compared to the attack group. Glutathione peroxidase, reduced glutathione and vitamin A values in the four groups did not change by FMF and colchicine. In conclusion, we observed that colchicine induced protective effects on oxidative stress by modulating vitamin E, ß-carotene and Ca²+-release levels in FMF patients with a remission period.

Effects of vitamin C and E combination on element and oxidative stress levels in the blood of operative patients under desflurane anesthesia.

We investigated effects of vitamin C and E (VCE) administration on desflurane-induced oxidative toxicity and element changes in the blood of operative patients under desflurane general anesthesia. Forty American Society of Anesthesiologists I or II Physical Status adult patients were scheduled for elective surgery. The patients were randomly divided into two groups. Control and VCE group was introduced to anesthesia with desflurane. VCE was administreted to patients in the control and VCE group before 1 hour of anesthesia with desflurane. Baseline (preoperative) and postoperative (at the 1(st), the 24(th), and 72(th) h), blood samples were taken from the first and second groups. Erythrocyte and plasma lipid peroxidation levels at the 1(st), 24(th), and 72(th) hours were higher in the control than in baseline group, although their levels at the same periods were lower in the VCE group than in the control. Vitamin E levels at the postoperative 1(st) and 24(th) hours and erythrocyte glutathione peroxidase (GSH-Px) activity at the postoperative 1(st), 24(th), and 72(th) hours was lower than in baseline values. Erythrocyte GSH-Px activity and plasma vitamins A, C, and E levels at the postoperative 1(st), 24(th), and 72(th) hours were higher in the VCE group than in the control group. Erythrocyte and plasma reduced glutathione, plasma ß-carotene, and serum copper, while zinc, selenium, aluminum, iron, magnesium, and calcium levels did not differ between preoperative and postoperative periods in both groups. In conclusion, VCE combination prevented the desflurane-induced vitamin E and GSH-Px consumptions to strengthen the antioxidant levels in the blood of operative patients.

Acetaminophen at different doses protects brain microsomal Ca2+-ATPase and the antioxidant redox system in rats.

Acetaminophen, an analgesic and antipyretic drug, rescues neuronal cells from mitochondrial redox impairment and reactive oxygen species (ROS). Excessive administration of acetaminophen above the recommended daily dose range has some negative effects on the brain. We investigated the effects of different doses of acetaminophen on Ca(2+)-ATPase and the antioxidant redox system in rats. Seventy rats were randomly divided into seven equal groups. The first was used for the control. One dose of 5, 10, 20, 100, 200, and 500 mg/kg acetaminophen was intraperitoneally administered to rats constituting the second, third, fourth, fifth, sixth, and seventh groups, respectively. After 24 h, brain cortical samples were taken and brain microsomal samples were obtained by ultracentrifugation. Brain and microsomal lipid peroxidation (LP) and brain calcium levels in the sixth and seventh groups were increased compared to control. LP levels in the second, third, and forth groups; brain vitamin E levels; brain and microsomal glutathione peroxidase (GSH-Px); and Ca(2+)-ATPase activity in the sixth and seventh groups were lower than in control, although brain vitamin E concentrations in the second, third, fourth, and fifth groups and microsomal GSH-Px activity in the third and fourth groups were higher than in control. Brain cortical beta-carotene and vitamin A concentrations did not differ in the seven groups. In conclusion, 5-100 mg/kg acetaminophen seems to have protective effects on oxidative stress-induced brain toxicity by inhibiting free radicals and supporting the antioxidant redox system.

Venlafaxine modulates depression-induced oxidative stress in brain and medulla of rat.

Venlafaxine is an approved antidepressant that is an inhibitor of both serotonin and norepinephrine transporters. Medical treatment with oral venlafaxine can be beneficial to depression due to reducing free radical production in the brain and medulla of depression-induced rats because oxidative stress may a play role in some depression. We investigated the effect of venlafaxine administration and experimental depression on lipid peroxidation and antioxidant levels in cortex brain, medulla and erythrocytes of rats. Thirty male wistar rats were used and were randomly divided into three groups. Venlafaxine (20 mg/kg) was orally supplemented to depression-induced rats constituting the first group for four week. Second group was depression-induced group although third group was used as control. Depressions in the first and second groups were induced on day zero of the study by chronic mild stress. Brain, medulla and erythrocytes samples were taken from all animals on day 28. Depression resulted in significant decrease in the glutathione peroxidase (GSH-Px) activity and vitamin C concentrations of cortex brain, glutathione (GSH) value of medulla although their levels were increased by venlafaxine administration to the animals of depression group. The lipid peroxidation levels in the three tissues and nitric oxide value in cortex brain elevated although their levels were decreased by venlafaxine administration. There were no significant changes in cortex brain vitamin A, erythrocytes vitamin C, GSH-Px and GSH, medulla vitamin A, GSH and GSH-Px values. In conclusion, cortex brain within the three tissues was most affected by oxidative stress although there was the beneficial effect of venlafaxine in the brain of depression-induced rats on investigated antioxidant defenses in the rat model. The treatment of depression by venlafaxine may also play a role in preventing oxidative stress.