Effects of platelet-activating factor and hyperbaric oxygenation on antioxidant defense and duodenal contractility.

Platelet-activating factor (PAF) is a phospholipid mediator with potent biological effects on organisms. Some investigators have previously postulated that PAF exerts its effects by producing oxygen free radicals. The aim of this study was to investigate the effects of PAF on intracellular antioxidant enzyme activities and on duodenal muscle contractility. The effects of hyperbaric oxygenation (HBO2) on the response to PAF were also investigated. Two experimental sets were designed. Each experimental set comprised two groups and each group consisted of six animals. The first group of the first experimental set to which only isotonic NaCl solution (serum physiologic, SP) was injected was named the control group. The second group of the first experimental set to which only PAF was administrated was named the PAF group. Blood samples and duodenum segments of both groups were obtained 2 h after the administration of PAF or SP. We observed that acetylcholine (ACh)-induced duodenal muscle contractions were more effective in the PAF group than those in the control group. Erythrocyte catalase and glutathione peroxidase (GPx) activities were found to be lower. In the second experimental set, rats administered PAF, and rats administered SP were exposed to HBO2. In both groups of this set, contractile responses to ACh were found to be significantly increased. We found that erythrocyte GPx activities were lower and erythrocyte superoxide dismutase activities were higher than in the control group. These data support the hypothesis that PAF produces free oxygen radicals and that HBO2 enhances this effect.

Does the platelet-activating factor affect the antioxidant defense system? The possible role of hyperbaric oxygenation.

The platelet-activating factor (PAF) is an inflammatory mediator and it may exert some of its effects by reactive oxygen species (ROS). We investigated the effects of PAF and hyperbaric oxygenation (HBO) on copper (Cu) and zinc (Zn) levels in plasma and the intracellular antioxidant enzyme activities of rats. PAF administration caused a decrease in erythrocyte catalase (CAT) and glutathione peroxidase (GPx) activities and in the plasma zinc level. Following PAF administration, exposure to HBO also caused a decrease in erythrocyte GPx activity. These results support the hypothesis that PAF may produce free oxygen radicals and HBO enhances this effect. The enzyme activities of the antioxidant defense system were found to be affected by these oxidative processes. This is likely to be the result of excessive production of ROS or overutilization and/or inhibition of the antioxidant enzymes.

The effect of altered selenium and vitamin E nutritional status on learning and memory of third-generation rats.

It has been proposed that selenium (Se) and Vitamin E (Vit E) are involved synergistically in protection of cell membrane lipids from peroxidation. However, little is known about the effect of both deficiencies of Se and Vit E and toxic status of those antioxidants on the peroxidation potentiality of the brain. We aimed to study the effects of both Se and Vit E inadequate diet and Se rich diet on the learning and memory processes of third-generation young rats. Their ancestors were also fed by the same diets starting from their births. To test the learning and memory, the rats aged 60 days were trained by using automated two ways active avoidance shuttle box. The acquisition tests were terminated with training the rat from each group to be 25 trials per day during three days. Ten days after the last acquisition test, the retention test was performed and the acquisition of the conditioned avoidance responses (CAR) of the rats were evaluated. It is demonstrated that the CAR of all rats from three groups showed a significant increase in three consecutive days while the differences observed in CAR of same sessions was not significantly different among three groups. The memory process of these young rats also was not affected significantly by two types of diets. Under the light of our results one can suggest that, in the case of alterations in antioxidant defense status, the learning and the memory mechanisms seems to be not affected. Further researches are needed to be able to explain the possible role of oxidative stress on the mechanisms of learning and memory.

Superoxide dismutase activity in healthy and inflamed pulp tissues of permanent teeth in children.

The free radicals play an important role in the tissue damage. Oxygen-derived free radicals are controlled by various cellular defense mechanisms consisting of enzymatic such as superoxide dismutase, catalase, glutathion peroxidase and nonenzymatic scavenger components. Superoxide dismutase (SOD) is responsible for the dismutation of the superoxide radicals into hydrogen peroxide and molecular oxygen. In this study, pulp samples extirpated from the teeth of the 27 children between 10-15 ages which diagnosed to be healthy, reversible pulpitis or symptomatic irreversible pulpitis were evaluated for the activity of superoxide dismutase enzyme. There were statistically significant differences between healthy and reversible pulpitis, and between reversible and symptomatic irreversible pulpitis groups. The SOD activity of the reversible pulpitis group were significantly lower than the irreversible pulpitis and healthy pulp groups. The evaluation of the data revealed that the quantity of SOD as a vitality protector enzyme is low at the beginning of the inflammation as a consequence of rapidly depletion and/or destruction of this enzyme, but as the inflammation proceeds the pulp tissue showed adaptation to this situation.

Platelet aggregation and release function in hyperbaric oxygenation.

The aim of the study was to investigate the acute and chronic effects of hyperoxygenation on platelet aggregation and adenosine triphosphate (ATP) release. To observe the acute effects of hyperbaric oxygen (HBO2), seven New Zealand rabbits were exposed to 2.4 atm abs oxygen for 90 min (group 1). Eight other rabbits were further exposed to O2 daily for 20 days (group 2) to observe the chronic effects of HBO2. Adenosine diphophate (ADP) and collagen-induced platelet aggregation and ATP release were evaluated before and after oxygenation in groups 1 and 2. It was found that the maximal rate of ADP and collagen-induced platelet aggregation decreased after hyperbaric oxygenation in group 1. No significant alteration was observed in platelet responses at the end of 20 days of oxygenation in group 2. The adaptation of platelets of 2.4 atm abs O2 after 20 days of exposure seems to need further investigation.