HDL has been found to protect against the oxidation of LDL by metal ions in-vitro [47,48] and by reverse cholesterol transport [49]. and ROS levels in the liver were 2-fold increased by HFD. Se supplementation, however, diminished the HFD-induced ROS levels by 29%. Furthermore, Se also improved the HFD-mediated reduction of serum PON1 enzyme activity by 34% and PON1 protein levels by 21%. However, no significant effect of Se was detected on the reduced UR 1102 PAF-AH proteins levels in HFD fed rats. mRNA expression of PON1 and PAF-AH in the liver was not affected in the Se treated groups. == Conclusion == Se supplementation appears to be protective in hypercholesterolemia by restoring the antioxidant properties of the HDL associated enzyme i.e. PON1 whereas biological system aims towards maintaining the same PAF-AH levels even on selenium supplementation indicating its probable role in both anti and pro-atherogenic activities. Therefore, Se supplementation might be a valuable approach to limit the adverse effects of hypercholesterolemia and may need further investigations. == Background == Hypercholesterolemia represents one of the important and recognized risk factor for atherosclerosis [1]. There are compelling evidences indicating the importance of type of fat than the total amount of the fat with respect to the risk of the cardiovascular diseases [2]. Cholesterol is usually transported within lipoproteins in the blood stream. High density lipoprotein (HDL) cholesterol levels are inversely related to the risk for atherosclerotic events [3] and are found to possess anti-atherogenic activity [4]. Among the UR 1102 risk factors, total cholesterol/HDL cholesterol ratio is considered to be the most predictive for atherosclerosis [5]. The protective effect of UR 1102 the HDL is usually related partly to enzymes associated with HDL [6-8] and due to its participation in reverse cholesterol transport [9]. Paraoxonase1 (PON1) is one of the enzymes associated with HDL [10]. PON1 was shown to protect against oxidative stress [11,12], a phenomenon that can be attributed to its ability to modulate oxidized lipids in LDL and HDL [13,14], in macrophages [15,16] UR 1102 and also in atherosclerotic plaques [17]. PON is capable of hydrolyzing lipid peroxides in LDL [18]. Serum HDL-associated PON1 reduces oxidative stress in lipoproteins, in macrophages and in atherosclerotic lesion, whereas PON2 acts as an antioxidant at the cellular and not humoral level. The attenuation to atherosclerosis is related to the nutritional anti-oxidative induced increase in HDL-PON activity [19]. PAF-AH is the major enzyme responsible for the catabolism of PAF and PAF like lipids that are also the potent mediators of inflammation [20,21]. Genetic deficiency of PAF-AH in defined human populations increases the severity of atherosclerosis and other syndromes [22]. Rabbit Polyclonal to PLD2 (phospho-Tyr169) PAF-AH has marked preference for phospholipids with short chain moieties at syn-2 position and, with the exception of PAF, it can equally hydrolyze oxidized phospholipids containing at syn-2 position polyunsaturated fatty acyl residues [23]. However, during hydrolysis the oxidized phospholipids, PAF-AH liberate the bioactive oxidized free fatty acids [24] and generates lysophopsphatidylcholine, both of which UR 1102 are implicated in the biological actions of ox-LDL [25]. Thus, PAF-AH could play both pro-atherogenic and anti-atherogenic role. Selenium, an essential trace element, is associated with cardiovascular diseases since years. Selenium deficiency is related to increase in plasma cholesterol levels [26,27], cardiac myopathy [28], other cardiovascular disease and ischemic heart diseases [29,30]. Selenium supplementation leads to decrease in total cholesterol and triglyceride levels [31,32]. Keeping these in view, in the present study influence of selenium was explored on HDL associated enzymes, PON1 and PAF-AH. == Results == == Selenium levels == Selenium levels were estimated in the serum of rats from all the groups after 4 months of diet feeding schedule (Figure1). Significant decrease (P < 0.05) in the Se levels in HFD group was observed in comparison to the control group. However, an apparent increase (P < 0.001) in Se was observed on HFD + Se (1 ppm) supplementation in comparison to the rats fed on only HFD diet. == Figure 1. == Serum selenium levels. *P < 0.05 represents comparison between control and HFD,aaaP < 0.001 represents comparison between HFD and HFD + Se group. == Lipid profile == Lipid profile analysis was done in serum (Table1). Total cholesterol (P < 0.001), triglycerides (P < 0.05) and HDL cholesterol (P < 0.05) levels were found to be significantly increased in HFD group in comparison to control group. A highly significant increase (P < 0.001) was observed in LDL-cholesterol and total cholesterol/HDL-cholesterol ratio in HFD group in comparison to the control group. However, no significant change in various lipid profile.