Differential expression of lipid peroxidation and total antioxidant status in Indian patients with cardiovascular and cerebrovascular disease.

Data from studies examining lipid peroxidation as a mechanism involved with hyperhomocysteinemia (HHcy)-induced vascular remodeling in patients with occlusive vascular disease have been contradictory. It has not yet been studied in Indians within the context of atherogenesis. Therefore, we measured the levels of homocysteine (Hcy), malondialdehyde (MDA) as a measure of lipid peroxides (LPOs), and total antioxidant status (TAS) in the serum of 167 patients with occlusive vascular disease [coronary artery disease (CAD) = 43; cerebrovascular disease (CVD) = 82; peripheral vascular disease (PVD) = 42]. Each of these groups was further divided into groups of individuals with or without HHcy. In the case of CAD and CVD, patients with HHcy had significantly higher LPOs than those without HHcy (p = 0.009, 0.001, respectively). TAS was significantly lower in CVD patients with HHcy than in those without (p = 0.014). In patients with CAD or CVD, Hcy directly correlated with LPOs (p = 0.002, 0.001, respectively). Lipid peroxidation is a significant mechanism in HHcy-induced vascular remodeling in CAD and CVD, but not in PVD, probably because it is not relevant in thrombosis (38 of 42 patients of PVD had deep-vein thrombosis). To explain the significantly lower TAS in CVD, we hypothesized that CVD patients present very early with grave symptoms, whereas CAD and PVD occur over a longer period of time. Therefore, when CVD presents, TAS is still overwhelmed by HHcy-induced oxidative stress. Hence, adjuvant therapy with antioxidants would benefit patients with CVD.

Homocysteine-lowering exercise effect is greater in hyperhomocysteinemic people living with HIV: a randomized clinical trial.

Elevated concentration of homocysteine has been identified as an independent risk factor for the development of cardiovascular disease and is frequently associated with oxidative stress. Moreover, studies have shown that people living with human immunodeficiency virus (PLHIV) present elevated concentration of homocysteine and oxidative stress compared with people without HIV. Our purpose was to describe blood homocysteine and oxidative stress markers in PLHIV and those without HIV infection, and to examine the effects of a 16-week combined training exercise program (CTE) on oxidative stress and homocysteine concentrations of PLHIV. We included 49 PLHIV (21 men, 28 women) and 33 people without HIV infection (13 men, 20 women). After baseline evaluations, 30 PLHIV were randomized to either CTE (trained group, n = 18) or the control group (n = 12); CTE consisted of aerobic and strength exercise sessions during 16 weeks, 3 times a week. Plasma homocysteine, oxidative damage markers, folate, and vitamin B12 were assessed pre- and post-training and by hyperhomocysteinemia (homocysteine ≥ 15 µmol/L) status. At baseline, PLHIV had higher levels of homocysteine and malondialdehyde, as well as reduced circulating folate when compared with people without HIV infection. CTE resulted in a 32% reduction (p < 0.05) in homocysteine concentration and a reduction in lipid hydroperoxide in PLHIV with hyperhomocysteinemia, which was not observed in those without hyperhomocysteinemia. Hyperhomocysteinemic participants experienced a 5.6 ± 3.2 µmol/L reduction in homocysteine after CTE. In summary, 16 weeks of CTE was able to decrease elevated homocysteine concentration and enhance redox balance of PLHIV with hyperhomocysteinemia, which could improve their cardiovascular risk.