Introduction: Intracellular adhesion molecule-1 is one of the factors associating obesity and inflammatory lesions like atherosclerosis. This study examined the effects of resistance (R) and endurance (E) training on serum levels of sICAM-1 and lipid profiles in sedentary obese women. Materials and Methods: Participants included 24 (8 control, 8 RT and 8 ET) obese (BMI≥30) women, studied before and after 10 weeks of resistance training (40-60% of 1RM) and swimming endurance training (at 50-60% of HRmax), 3 days/week. Serum levels of sICAM-1, lipid profiles and anthropometric indices were measured at baseline and again 48 hours after training. Statistical analysis was done by paired t-test. ANOVA and Pearson correlation, and P value<0.05 was considered significant. Results: Levels of sICAM-1 (P=0.042), cholesterol (P=0.006) and HDL-C (P=0.006) changed significantly following 10 weeks of endurance and resistance training compared to those of the control group. There was significant decrease in serum levels of sICAM-1 in the both RT (P=0.012, 21.7%) and ET groups (P=0.017, 18.4%). Although significant changes did not exist in lipid profiles after resistance training (p>0.05), TG (P=0.001), cholesterol (P=0.043) and HDL-C (P=0.002) changed significantly in the endurance training group. Hence there were significant correlations between the primary level of sICAM-1 and primary values of BF% (P=0.031), pelvic (P=0.005) and waist (P=0.006) circumferences following endurance training, whereas changes in the levels of sICAM-1 or lipid profiles and anthropometric markers did not correlate significantly in the resistance training group (p>0.05). Conclusion: Although decrease in sICAM-1  level may be associated with the beneficial effects of training on body composition or/and lipid profile, further studies are needed to elucidate the mechanisms responsible for the effects of resistance training on ICAM-1 level.

Introduction: The intercellular adhesion molecule-1 (ICAM-1) plays a pivotal role in inflammation and linkage between monocytes and endothelium. LDL-induced ICAM-1 expression may include the possibility of an atherogenic stimulation due to a binding between lipoprotein and ICAM-1. To evaluate of this hypothesis, the present study investigated the effect of sICAM-1 on susceptibility of LDL and HDL to oxidation and Paraoxonase-1 (PON-1) activity. Materials and Methods: LDL and HDL were purified from serum via ultracentrifugation and 25 and 100 µg-protein/ml of LDL and HDL, in the presence of sICAM-1 (0, 2, 5 ng/ml), were exposed to oxidative stress (5 µM copper) and assayed through monitoring of formation of conjugated dienes using a spectrophotometer. Electrophoresis was performed to determine the mobility of incubated-lipoproteins with sICAM-1. The activity of PON-1 was assayed in the presence of of sICAM-1. Results: In presence of different concentrations of sICAM-1, Vmax increased significantly (P<0.05), while electrophoretic mobility of LDL decreased (↓ 25%). PON-1 activity increased at low levels of sICAM-1 but decreased at higher levels (P<0.05 P<0.005). Conclusion: The results indicate that sICAM-1 in dosages over than 2  ng/ml affects some kinetical parameters of LDL oxidation and PON-1 activity that can be interpreted as a positive stimulus in atherogenesis. Overall the results may support the hypothesis of a lipoprotein-mediated role for ICAM-1 in atherogenesis. of