Parkinson's disease (PD) is a systemic neurodegenerative disease characterized by tremor, rigidity, bradykinesia, and stooping posture. When more than 60% of dopaminergic neurons in the substantia nigra of the brain have died, motor symptoms manifest in PD. Currently, oxidative stress (OS) is considered to be one of the leading factors provoking death of dopaminergic neurons in PD. This review is concerned with the role of polyamines in PD, especially focusing on their role in OS induction. Polyamines (putrescine, cadaverine, spermidine and spermine) are involved in many molecular mechanisms, including cell proliferation and differentiation, gene transcription and translation, modulation of the functional activity of ion channels and receptors, and other vital processes. It is worth noting that under physiological conditions polyamines are antioxidants. It has been shown that spermine oxidase (SMOX) is up-regulated in PD, activating polyamine breakdown, which leads to excessive formation of toxic aldehydes (such as acrolein), H 2 O 2 (a strong cytostatic) and ammonia (a toxic substance). Polyamines are also involved in the pathogenetic mechanism of α-synuclein modification resulting in the formation of Lewy bodies. This review provides data on the changes in polyamine levels at later stages of the disease. The review also examines the role of polyamines, as gliotransmitters, in regulating neural function and vice versa. The mechanisms of polyamine "pumping" from neurons to glia can be considered factors of OS regulation in neurons. Prolonged accumulation of polyamines in glia can lead to oxidation of polyamines and therefore potentially to gliosis in PD. The exact mechanisms of this process are, however, not clear. Answering the questions regarding the role of polyamines in gliosis development and pathogenesis of PD is necessary for treating cognitive impairment in patients with PD, which is particularly important.

The leading cause of death in developed countries is cardiovascular disease, where coronary heart disease is the main cause of death. Myocardial reperfusion is the most significant method to prevent cell death after ischemia. However, restoration of blood flow may paradoxically lead to myocardial ischemia-reperfusion injury (MI/RI) accompanied by metabolic disturbances and cardiomyocyte death. As the myocardium has an extremely limited ability to regenerate, the mechanisms of regulated cell death, including apoptosis, are the most significant for contemporary research due to their reversibility. BCL2 is a key anti-apoptotic protein. There are several signaling pathways and compounds regulating BCL2, including PI3K/AKT and MEK1/ERK1/2, JAK2/STAT3, endothelial nitric oxide synthase, PTEN, cardiac ankyrin repeat protein and microRNA, which can serve as targets for modern methods of cardioprotective therapy inhibiting intrinsic apoptosis and saving viable cardiomyocytes after MI/RI. The present review considers the mechanisms of Bcl2-regulated apoptosis in the development and treatment of MI/RI.

Background/Aim. Polyamines are important for the growth of eukaryotic cells. At high levels, they promote proliferation, invasion and migration of tumour cells. Polyamine metabolism is an important new target for anticancer therapy. Some polyamine analogues can have an inhibitory effect on tumour cells. The aim of this study was to explore the potential of certain butylated derivatives of propanediamine for prostate cancer chemotherapy. Materials and Methods. Human prostate cancer cells, LNCaP, were used for the evaluation of the antiproliferative activity of polyamine analogs and their influence on spermine oxidase. Results. Tetrabutyl propanediamine and two new polyamine analogues inhibited the growth of LNCaP cells. At the same time, a strong activation of spermine oxidase was observed. Conclusion. The investigated compounds demonstrated their potential value in the therapy of human prostate cancer. Their effect might be attributed to the activation of the polyamine catabolic pathway.

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The aim of the present study was to investigate the influence of millimeter-wave electromagnetic (MW) irradiation on normal and pathological human sperm in vitro, and to evaluate a possible role of polyamines (PA) in this process. The stability of sperm membranes, the number of apoptotic gametes, and the content of seminal plasma PA in the ejaculates of fertile and subfertile men were compared before and after short-term MW electromagnetic exposure in vitro. The ejaculate samples were collected from healthy donors [n=25, age 22-38 years old (y.o.), average age 30.6±1.1 y.o. (mean ± SEM)] and from subfertile men (n=78, age 25-48 y.o., average age 34.1±0.8 y.o.) and exposed to MW radiation. The electromagnetic field had a wavelength of 7.1 mm, a frequency of 42.194 GHz and an exposure time of 20 min. The fragility of sperm membranes was evaluated by their resistance to sodium chloride solution (Milovanov test) and to acetic acid (Joel test). Acrosin activity was assayed spectrophotometrically. Apoptosis was determined by the externalization of phosphatidylserine on the outer side of the sperm membrane and propidium iodide staining. The PA levels were determined by agar gel electrophoretic fractionation. An increase in the resistance of sperm membranes, a decrease in acrosin activity, a decrease in the number of apoptotic gametes and a decrease in the seminal plasma PA concentrations were found after exposure of the native human sperm to low-intensity MW irradiation. Two types of reactions were revealed for the subfertile samples. The results revealed positive bio-effects of specific microwaves on the human semen and the participation of PA in the realization of these effects.