Oxidative stress is defined as a state when the free radical production ovecome their neutralisation via the antioxidative defense systems. Being extremely unstable, these molecules and ions tend to achieve a stable state by reacting with the surrounding molecules, which are immediately oxidised. Such chain reactions may have substantial effects on almost all cellular structures, including the lipids, the proteins and the nuclear DNA. LDL particles become atherogenic because their apoB is subjected to the oxidative modification, being recognized by the scavenger receptors. Type 2 diabetes represents a conformational disease in which proteins are subjected to the oxidative modification. The disease proceeds in several stages such as: the transition is the latent period where oxidatively modified proteins are deposited in the EPR structures, periods of accelerated redox stress when amyloid precursors are accumulated, accompanied with the insulin secretory deficiency. The process is aggravated by glycosylated proteins, which are the free radical producers. This complex cascade proceeds through the formation of early (Schiff bases and Amadori) products, while further glycation of proteins and lipids causes molecular rearrangements that lead to the generation of advanced glycation endproducts (AGEs). High glucose concentrations in non insulin-dependent tissues may follow the pathway of aldose reductase, when reduced nucleotides are used as the cofactors, leading to decreased reduced glutathione (GSH) content. Glucose fluctuations during postprandial periods exhibited a more specific triggering effect on free radical production. The superoxide overproduction is accompanied by an increased nitric oxide (NO) generation, a phenomenon favoring the formation of the stronger oxidant peroxynitrite. The increased free radical generation in accumulated fat causes dysregulated production of adipocytocines locally, leading to development of metabolic syndrome.