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Acrylamide which is formed via reaction of reducing sugars with amino acids during food processing at high temperatures is not only neurotoxic and carcinogenic, but it also damages erythrocyte membrane and generates micronucleated erythrocytes. In the present study, effects of chronic administration of acrylamide at a dose which does not induce neurotoxicity were evaluated on blood viscosity parameters (hematocrit, erythrocyte deformability, erythrocyte aggregation and plasma viscosity). Twenty adult male Sprague-Dawley rats were divided into control and acrylamide groups. The acrylamide group received 10 mg/kg/day acrylamide, whereas the control group received saline (vehicle), both in 10 ml/kg/day volume via gastric gavage. Erythrocyte aggregation and deformability were measured with LORCA and plasma viscosity with cone-plate viscometer. Erythrocyte deformability was measured before, and at the end of the 3rd and the 5th weeks of acrylamide administration. Hematocrit, erythrocyte aggregation and plasma viscosity were measured only at the end of the 5th week. Acrylamide caused a significant decrease in the deformability index of erythrocytes (at the end of the 3rd week, control: 0.606 ± 0.003, acrylamide: 0.595 ± 0.003, p < 0.05) (at the end of the 5th week, control: 0.606 ± 0.002, acrylamide: 0.588 ± 0.002, p < 0.01). Aggregation tendency and plasma viscosity were slightly higher in the acrylamide group, however the difference was not statistically significant. These results imply that acrylamide which does not cause neurotoxicity in rats may alter blood viscosity if chronically taken.

Background/Aims: We aimed to explore the immunological outcomes of short-term mental stress in apoptosis in peripheral lymphocytes and variations by gender and hormonal status of the individuals together with possible mediators of this interaction. Methods: Acute mental stress (computerized Stroop color-word interference and cold pressor tests) was applied to men (n = 17) and women (n = 16, in both follicular and luteal phases). Heart rate and blood pressure were monitored throughout the test and after the test until baseline values were recorded. Blood samples were drawn for measuring cortisol and nitric oxide (NO) levels and flow-cytometric cell counting before and after the test. Results: Activation of the stress system was ascertained by increased heart rate, blood pressure and serum cortisol levels after the test. Relative to baseline values, acute mental stress altered the distribution of T and natural killer cells. There was a significant decrease in T helper/T cytotoxic-suppressor cell ratio and an increase in apoptotic T helper cell percentage irrespective of gender or menstrual cycle phase. An increased number of natural killer cells was detected in women, whereas it was decreased in men. After stress induction, serum NO levels remained the same in women and increased in men. Although a correlation was not found between immune system changes and NO levels, glucocorticoids seem to have a role in the observed differences. Conclusion: Acute mental stress triggers apoptotic T helper cell loss which was associated with stress system activation, and sex steroids affect the pattern of stress-related immune cell distribution.

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