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Aims Type-2 Diabetes Mellitus (T2DM) is one of the most prevalent and progressive metabolic conditions affecting approximately 8.5% of the global population. Individuals with T2DM have a significantly increased risk of developing chronic conditions such as cardiovascular disease (CVD) and its associated complications, therefore, it is of great importance to establish strategies for combatting T2DM and its associated chronic conditions. Current literature has identified several biomarkers that are known to play a key role in the pathogenesis of CVD. Many of these biomarkers affecting CVD are influenced by an increase in oxidative stress as seen in T2DM. The purpose of this review is to analyse and correlate the oxidative stress-related biomarkers that have been identified in the literature to provide an updated summary of their significance in CVD risk factors. Data synthesis This review has analysed current research on T2DM, CVD, and oxidative stress. Four key cardiovascular risk factors: thrombosis, inflammation, vascular homeostasis and cellular proliferation were searched to identify potential biomarkers for this review. These biomarkers stem from seven major cellular pathways; NF-κB, Keap1-Nrf2, protein kinase-C, macrophage activation, arachidonic acid mobilisation, endothelial dysfunction and advanced glycation end products. Conclusions The pathways and biomarkers were analysed to show their role as contributing factors to CVD development and a summary is made regarding the assessment of cardiovascular risk in T2DM individuals. [ABSTRACT FROM AUTHOR]

Increased oxidant production in humans induces a number of thrombotic consequences; including platelet hyperactivity/aggregability, which could be countered through specifically developed functional foods. We sought to determine the antithrombotic properties of anthocyanin-rich Queen Garnet plum juice (QGPJ) supplementation with and without exercise-induced oxidative stress. Thirteen healthy participants were investigated in a randomised, double-blind, placebo-controlled, cross-over trial. Participants consumed 200 mL/day of QGPJ and placebo juice for 28-days, with treatments separated by a two-week wash-out period. Blood samples were collected at baseline and after 1 h of exercise (70% peak-O 2 uptake) both before and after oral supplementation and evaluated for platelet function and haemostatic activity. QGPJ supplementation inhibited adenosine diphosphate-induced platelet aggregation both without and under exercise-induced oxidative stress by 10.7% (P < 0.01) and 12.7% (P < 0.001) respectively; arachidonic acid-induced aggregation under oxidative stress by 28.8% (P < 0.05); reduced platelet activation-dependant P-selectin expression by 32.9% (P < 0.01) and 38.7% (P < 0.001) both without and under oxidative stress respectively; and exhibited favourable effects on coagulation parameters both with and without oxidative stress. The anti-thrombotic activity exhibited by anthocyanin-rich QGPJ suggests a potential for cardiovascular disease risk reduction and may be considered as complementary anti-platelet nutritional therapy in pro-thrombotic population. [ABSTRACT FROM AUTHOR]

Gilbert's syndrome (GS) is a relatively common condition, inducing a benign, non-hemolytic, unconjugated hyperbilirubinemia. Gilbert's Syndrome is associated with mutation in the Uridine Glucuronosyl Transferase 1A1 (UGT1A1) gene promoter, reducing UGT1A1 activity, which normally conjugates bilirubin allowing its elimination from the blood. Individuals with GS demonstrate mildly elevated plasma antioxidant capacity caused by elevated levels of unconjugated bilirubin (UCB), reduced thiols and glutathione. Interestingly, the development of, and risk of mortality from, cardiovascular disease is remarkably reduced in GS individuals. An explanation for this protection may be explained by bilirubin's ability to inhibit multiple processes that induce platelet hyper-reactivity and thrombosis, thus far under-appreciated in the literature. Reactive oxygen species are produced continuously via metabolic processes and have the potential to oxidatively modify proteins and lipids within cell membranes, which may encourage the development of thrombosis and CVDs. Oxidative stress induced platelet hyper-reactivity significantly increases the risk of thrombosis, which can potentially lead to tissue infarction. Here, we discuss the possible mechanisms by which increased antioxidant status might influence platelet function and link this to cardiovascular protection in GS. In summary, this is the first article to discuss the possible role of bilirubin as an anti-thrombotic agent, which inhibits platelet activation and potentially, organ infarction, which could contribute to the reduced mortality rate in mildly hyperbilirbinemic individuals. [ABSTRACT FROM AUTHOR]

One of the most commonly identified chronic illnesses in many countries is type 2 diabetes mellitus (T2DM). T2DM denotes an independent risk factor for cardiovascular disease (CVD). Heart disease is one of the causes of mortality in patients with diabetes, mainly due to the macrovascular complications. One of these macrovascular complications in diabetes is atherosclerosis, which involves a complicated pathophysiological process. Besides hyperglycemia, oxidative stress plays a significant role in the pathogenesis of diabetes and its associated risk of CVD. There are many other factors including molecular, metabolic, lipid, fibrinolytic, and platelet function disorders precipitate to thrombotic and CVD risks in T2DM. Also, Platelets have an increased response to procoagulants in patients with diabetes. Platelet hyperactivity, in the presence of oxidative stress, has a major effect on the progression of thrombotic and CVD events. This review will discuss the impact of the above factors and the potential effects of platelet hyperactivity on thrombotic and cardiovascular risks. [ABSTRACT FROM AUTHOR]