The term "oxidative stress" was coined in 1985 by Sies to describe disorders in the balance of ROS and antioxidants. However, its definition has changed over the years due to the wide variety of research results [1]. Today, OS is a state in which the balance of the pro-oxidant and antioxidant systems in the cell is disturbed [2]. ROS concentrations fluctuate in a controlled manner and persist thanks to antioxidants and other enzymes. Excess or insufficient utilization of ROS is accompanied by their accumulation, which, in turn, leads to oxidative modification of lipids, proteins, and nucleic acids [3, 4]. The process of excessive OS not only causes impaired function, but can also lead to cell death. The main role in this mechanism is given to ROS, which are large groups of derivatives of free radical processes, including superoxide anion (O2 -), hydrogen peroxide (H2O2), hydroxyl radical (- OH), hydroperoxide (ROOH) [2, 5, 6].

A violation of the ROS balance, namely an increase in their production, leads to damage to DNA, proteins, and lipid peroxidation (Pol). This condition is typical for patients with diabetes and pathology of the cardiovascular system (CVD), which is much more common in combination with diabetes than in isolation [7].

Although all the mechanisms involved in the pathophysiology of CVD are not fully understood, the negative impact of OS on their genesis is clearly elucidated. Various scientific studies have revealed a number of discrepancies that may be due to different approaches, characteristics of samples, doses of drugs and methods of their use. This requires large-scale studies to identify specific factors involved in the stages of CVD development, describe reliable biomarkers and mechanisms of OS exposure, and develop new treatments and prevention methods.

Cardiovascular diseases and oxidative stress

According to the World Health Organization (WHO), CVD is one of the leading causes of premature death and disability in the world. The development of CVD depends on both modified (cholesterol, body weight, smoking, and blood pressure – BP) and unmodified (age, gender, heredity) risk factors [8].

A number of researchers believe that cardiovascular risk factors such as diabetes, hypertension, peripheral artery disease, obesity, metabolic syndrome, dyslipidemia, and smoking lead to OS [4]. But others express the opinion that the development of functional and structural disorders of the CCC is indicated by the formation of OS as a consequence of increased ROS formation, in particular the superoxide anion, and insufficient mechanisms of antioxidant protection. OS and immunoinflammatory changes, which are links in the pathogenesis of cardiovascular dysfunction, can provoke each other according to the principle of a false circle [9]. Increased OS in the heart and cardiomyocytes occurs through a variety of mechanisms, including mitochondrial dysfunction and disconnection, increased fatty acid oxidation, increased nicotinamide adenine dinucleotide phosphate (NADP) oxidase activity, and decreased antioxidant capacity.

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