Plasma high-density lipoprotein cholesterol(HDL-C) levels do not predict functionality and composition of high-density lipoprotein(HDL). Traditionally, keeping levels of low-density lipoprotein cholesterol(LDL-C) down and HDL-C up have been the goal of patients to prevent atherosclerosis that can lead to coronary vascular disease(CVD). People think about the HDL present in their cholesterol test, but not about its functional capability. Up to 65% of cardiovascular death cannot be prevented by putative LDL-C lowering agents. It well explains the strong interest in HDL increasing strategies. However, recent studies have questioned the good in using drugs to increase level of HDL. While raising HDL is a theoretically attractive target, the optimal approach remains uncertain. The attention has turned to the quality, rather than the quantity, of HDL-C. An alternative to elevations in HDL involves strategies to enhance HDL functionality. The situation poses an opportunity for clinical chemists to take the lead in the development and validation of such biomarkers. The best known function of HDL is the capacity to promote cellular cholesterol efflux from peripheral cells and deliver cholesterol to the liver for excretion, thereby playing a key role in reverse cholesterol transport (RCT). The functions of HDL that have recently attracted attention include anti-inflammatory and anti-oxidant activities. High antioxidant and anti-inflammatory activities of HDL are associated with protection from CVD.This review addresses the current state of knowledge regarding assays of HDL functions and their relationship to CVD. HDL as a therapeutic target is the new frontier with huge potential for positive public health implications.

The endothelium is the primary target for biochemical or mechanical injuries caused by the putative risk factors of atherosclerosis. Endothelial dysfunction represents the ultimate link between atherosclerotic risk factors that promote atherosclerosis. HDL-C is thought to exert at least some parts of its antiatherogenic facilities via stimulating endothelial NO production, nearby inhibiting oxidative stress and inflammation. HDL-C is capable of opposing LDL's inductive effects and avoiding the ox-LDL's inhibition of eNOS. Paraoxonase 1 (PON1) is an HDL-associated enzyme esterase which appears to contribute to the antioxidant and antiatherosclerotic capabilities of HDL-C. “Healthy HDL,” namely the particle that contains the active Paraoxonase 1, has the power to suppress the formation of oxidized lipids. “Dysfunctional HDL,” on the contrary, has reduced Paraoxonase 1 enzyme activity and not only fails in its mission but also potentially leads to greater formation of oxidized lipids/lipoproteins to cause endothelial dysfunction. The association of HDL-C PON1 and endothelial dysfunction depends largely on the molecules with exact damaging effect on NO synthase coupling. Loss of nitric oxide bioavailability has a pivotal role in endothelial dysfunction preceding the appearance of atherosclerosis. Analyses of HDL-C and Paraoxonase1 would be more important in the diagnosis and treatment of atherosclerosis in the very near future.

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Background: Impaired oxidative/antioxidative status plays an important role in the pathogenesis of many diseases like cancer. The aim of this study was to evaluate the levels of the novel marker ischemia modified albumin (IMA) and albumin adjusted-IMA (Adj-IMA) in patients with bladder cancer (BC) as well as its association with total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI). Materials and Methods: Forty male patients with BC (mean age, 67.4±12 years) and forty age-sex matched healthy persons (mean age 56.0±1.7 years) were included in this study. Serum levels of IMA, TAS, TOS were analyzed and Adj-IMA and OSI was calculated. Results: Serum IMA, TOS and OSI values were significantly higher in patients with BC compared to controls (p<0.0001, p=0.01 and p=0.01, respectively), whereas TAS was significantly lower in BC patients (p=0.04). There was no significant difference for serum albumin-adjusted IMA levels between groups (p=0.4). Conclusions: In this study, it was found that there was an impaired oxidative/antioxidant status in favor of oxidative stress in BC patients. This observation was not confirmed by Adj-IMA calculation. There is no published report about serum concentrations of IMA in patients with BC. Further studies are needed to establish the relationship of IMA and oxidative stress parameters in BC and the significance of IMA to other cancers.

We observed impaired oxidant/antioxidant status in favor of oxidative stress in CIHF patients. Oxidative stress may be a key factor in the development of hypoalbuminemia in CIHF. Further studies are needed to establish the relationships among IMA, albumin, and redox balance in CIHF.

Increased oxidative stress, alterations of lipid metabolism and induction of thrombosis have been suggested to be pathogenic links which are present between hyperhomocysteinaemia and atherosclerosis. However, the mechanism by which homocysteine (Hcy) can promote atherogenesis is far from clear and it has been debated. In the presence of cardiovascular risk factors, endothelial dysfunction is the central commodity which converges a plenty of factors, which have been named as atherogenic. Now-a-days, there are only few studies which have presented the correlation between antioxidant enzyme HDL-associated-paraoxonase 1(PON1) and Hcy in atherosclerosis. Both PON 1 and Hcy have been implicated in human diseases which are related to endothelial dysfunction.Although paraoxonases have the ability to hydrolyze a variety of substrates, only one of them, Hcy-thiolactone, is known to occur naturally. It seems very likely that the involvement of Hcy in atherosclerotic disease is mediated through its interactions with PON1. OveRviewThe healthy endothelium plays a pivotal role in regulating vascular homeostasis. A plethora of factors converge to generate endothelial dysfunction, which seems to be the main road to atherosclerosis. Our journey down the rabbit hole starts with the well-known gate keeper, nitric oxide (NO); and we will take a look at the struggle between the good (Paraoxonase) and the bad (Homocysteine), to seek dominion over the microworld which is guarded by NO.

We show that the OP group had reduced TAS, whereas the elevated TPx was different from that in the NOP group. Slightly elevated homocysteinemia may contribute to increasing TPx and reducing TAS in the OP group. However, our results suggest a weak but negative relationship between TAS and BMD. Further investigations are needed to examine the relationship of oxidative stress as an endogenous bioactive agent to bone loss in post-menopausal women. Since oxidative stress is the imbalance between total oxidants and antioxidants in the body, any single oxidant/ antioxidant parameter may not reflect overall oxidative stress. Further studies are needed to understand the underlying mechanisms of these findings.

Introduction:Oligodendrocytes need iron in processes of energy generation and myelination. However, excessive levels of iron may exert iron induced oxidative stress and thus lead to tissue degeneration. Monitoring oxidative stress will be of paramount importance in follow-up of patients with many diseases including multiple sclerosis (MS). The aim of this study was to measure total anti-oxidative status (TAS), total oxidative status (TOS) and ischemia modified albumin (IMA) in stable relapse remitting MS (RRMS) patients.Materials and methods:Thirty-five RRMS patients (15 males and 20 females; median age 42 (20–55) years) and thirty-five age-sex matched healthy controls (13 males and 22 females; median age 37 (21–60) years) were included in this study. All patients were diagnosed with MS according to the criteria of McDonald.Results:IMA levels were significantly higher in RRMS patients (P < 0.001), while TAS and TOS did not show any significant difference between groups (P = 0.870 and P = 0.460, respectively).Conclusions:Our results suggest IMA as a more efficient serum marker than TAS and TOS in detecting the oxidative stress in MS patients. Serum oxidative stress markers should be included in future study protocols besides clinical and radiological parameters.