The effect of ingested sulfite on active avoidance in normal and sulfite oxidase-deficient aged rats.

The aim of this study was to investigate the possible toxic effects of sulfite on neurons by measuring active avoidance learning in normal and sulfite oxidase (SOX)-deficient aged rats. Twenty-four months of age Wistar rats were divided into four groups: control (C), sulfite-treated group (S), SOX-deficient group (D) and SOX-deficient + sulfite-treated group (DS). SOX deficiency was established by feeding rats with a low molybdenum (Mo) diet and adding 200 ppm tungsten (W) to their drinking water. Sulfite in the form of sodium metabisulfite (25 mg/kg) was given by gavage for six weeks. Active avoidance responses were determined by using an automated shuttle box. Hepatic SOX activity was measured to confirm SOX deficiency. The hippocampus was used for determining the activity of cyclooxygenase (COX) and caspase-3 enzymes and the level of prostaglandin E2 (PGE2) and nitrate/nitrite. SOX-deficient rats had an approximately 10-fold decrease in hepatic SOX activity compared with normal rats. Sulfite did not induce impairment of active avoidance learning in SOX-deficient rats and in normal rats compared with their control groups. Sulfite had no effect on the activity of COX and caspase-3 in the hippocampus. Treatment with sulfite did not significantly increase the level of PGE2 and nitrate/nitrite in the hippocampus.

The effect of docosahexaenoic Acid on visual evoked potentials in a mouse model of Parkinson's disease: the role of cyclooxygenase-2 and nuclear factor kappa-B.

This study aimed to investigate the effect of docosahexaenoic acid (DHA) on visual evoked potentials (VEPs) in a mice model of Parkinson's disease (PD). Mice model was created by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and DHA was given by gavage. Cyclooxygenase-2 (COX-2), caspase-3 activities, nuclear factor kappa-B (NF-κB) and prostaglandin E2 (PGE2) levels were determined in substantia nigra (SN) and retina. Cyclooxygenase-2 intensities were also determined immunohistochemically. The tyrosine hydroxylase (TH) immunolabelling was significantly decreased in MPTP group compared to control. Docosahexaenoic acid decreased dopaminergic neuron death in MPTP + DHA group when compared to MPTP group. Mice treated with MPTP showed motor deficits as compared to control. Significant improvement was observed in MPTP + DHA group when compared to MPTP group. Treatment with MPTP significantly increased the activity of COX-2 and total COX in SN when compared to the control group. Docosahexaenoic acid caused a significant decrease in total COX and COX-2 activity in SN of mice given MPTP. Cyclooxygenase-2 showed strong immunostaining in MPTP group when compared to other groups in SN. Levels of PGE2 increased in MPTP group when compared to control in SN. Docosahexaenoic acid treatment in MPTP group reduced PGE2 in SN. Nuclear factor kappa-B levels were found to be decreased in SN of MPTP group. The mean latencies of P1, N1, P2, N2, P3, N3, P4, N4, and P5 VEP components were significantly prolonged in MPTP group when compared to control. In MPTP + DHA group, the mean latencies of all components except P5 returned to control values. Current data shows that DHA treatment improves prolonged VEPs latencies and locomotor activity.

Plasma and erythrocyte magnesium, manganese, zinc, and plasma calcium levels in G-6-PD-deficient and normal male children.

Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency is the most common human enzymopathy in the world. Trace elements are important for normal hematopoiesis and can play a role in acute hemolytic anemia induced by G-6-PD deficiency. For this purpose, we studied two groups consisting of 10 male children who are G-6-PD-deficient and 12 age-matched normal male children to compare plasma and erythrocyte magnesium, manganese, zinc, and plasma calcium levels between G-6-PD-deficient and normal children. All assays were performed under normal conditions free of any oxidative attack that may result in hemolytic crisis in G-6-PD-deficient subjects. All parameters in each group did not differ significantly except for erythrocyte G-6-PD activities. These data show that plasma and erythrocyte trace element contents of G-6-PD-deficient subjects do not differ in normal conditions.

Does massive proximal small bowel resection influence prostaglandin E2 synthesis in the stomach and ileum during adaptive process in rats?

It is unclear whether massive small bowel resection (SBR) affects prostaglandin E2 synthesis in the gastrointestinal tracts. Thus the aim of this study was to investigate possible changes over tissue levels of prostaglandin E2 in the stomach and ileum after massive proximal SBR. Female Swiss-Albino rats underwent control operation (groups 1, 3, 5) or an 80% SBR (groups 2, 4, 6). The specimens were obtained during relaparotomy at 3 days in groups 1 and 2, at 9 days in groups 3 and 4, at 15 days in groups 5 and 6. Group 2 vs. groups 1 and 6, group 4 vs. groups 3 and 6 had significant increase in the levels of gastric acid (P < 0.01, P < 0.05, respectively). Gastric prostaglandin E2 levels markedly increased in group 2 compared to group 1 (P < 0.01). Ileal prostaglandin E2 levels showed to be significantly higher in group 6 when compared with groups 2, 4, and 5 (P < 0.05). Gastric acidity increased at 3 and 9 days, decreased thereafter at 15 days following massive proximal SBR. While resected rats had increased levels of gastric prostaglandin E2 at 3 days, ileal prostaglandin E2 was markedly elevated at 15 days. Therefore, we conclude that prostaglandin E2 may have a possible role in regulating intestinal adaptation at the end of the adaptive process, and contribute to cytoprotective barrier function in the ileum and stomach at early and late periods of the intestinal adaptation, respectively.

The effects of pentoxifylline on renal function and free radical production in unilateral ureteral obstruction.

There is an ongoing discussion about ureteral obstruction-related renal dysfunction. In this study, we aimed to test the effect of pentoxifylline (PTX) on both kidneys in unilateral ureteral obstruction (UUO), and to determine its interaction of with prostaglandin E2 (PGE2), and diclofenac sodium (DIS). A sham operation was performed in group 1. Placebo, PTX, DIS, and PTX+DIS were administrated to groups 2, 3, 4 and 5, respectively. The left ureter was ligated in all groups except group 1. At 24 h, technetium 99m diethylenetriamine penta-acetic acid scintigraphy was performed to determine renal function. Additionally, the tissue levels of thiobarbituric acid reactive substances (TBARS) and PGE2 in both kidneys were measured to determine cytotoxic and cytoprotective mechanisms. When the ipsilateral kidneys were evaluated: (1) UUO significantly reduced DTPA uptake and none of the medications used prevented the reduction, (2) UUO significantly increased TBARS production, and only PTX prevented the increase, (3) UUO caused a significant increase in PGE2 production, and only DIS significantly decreased this. When the contralateral kidneys were evaluated: (1) UUO significantly increased DTPA uptake but DIS and PTX+DIS prevented this, (2) UUO significantly elevated TBARS levels and DIS and PTX+DIS caused an additional elevation, (3) UUO significantly increased PGE2 production, and only DIS prevented this. In conclusion, UUO caused ipsilateral renal hypofunction and contralateral hyperfunction, which are related to increased TBARS and PGE2 levels. PTX markedly decreased free radical activity in the ipsilateral kidney. While PTX showed a placebo effect, DIS prevented the compensatory contralateral renal response through increased TBARS and decreased PGE2 levels. The beneficial effect of PTX on the ipsilateral kidney, and the hazardous effect of DIS on the contralateral kidney may be explained by more complex interactions among TBARS, PGE2, PTX, DIS and UUO-related renal dysfunction.