Senescence is a permanent cell cycle arrest that is accompanied by changes in cell morphology and physiology occurring in vitro and in vivo. Senescence evolved as a beneficial response to damage promoting wound healing, limiting fibrosis, fighting against cancer and helping embryonic development. However, excessive accumulation of senescent cells is considered to play a substantial role in the development of aging-related diseases and other morphological and physiological changes associated with aging. Therefore, the aim of many researchers is to find out a way to eliminate senescent cells and improve the health condition of aging people. Bioactive compounds e.g. polyphenols, vitamins, phenols, carotenoids, ginsenosides, omega-3 fatty acids, and compounds isolated from algae (phloroglucinol, sargachromal) are known to affect important biological functions. Recent in vitro studies have revealed that they can protect different types of cells against stress induced senescence (SISP), delay replicative senescence, rejuvenate senescent cells and exert senolytic effects. This review summarizes how the biological compounds listed above affect cell morphology, cell proliferation, specific cell functions, the activity of senescence-associated β-galactosidase (SA-β-gal), the shortening of telomeres and reduction of telomerase activity, production of intracellular reactive oxygen species (ROS) and lipid peroxidation products, expression of antioxidant enzymes, expression of p53 and p21 – key effectors of cell cycle arrest leading to senescence – and expression of some key components of senescence associated secretory phenotype (SASP) in replicative senescence, stress induced senescence (SISP) and under conditions which may lead to the development of senescence such as UV-A and UV-B irradiation of cells and the production of matrix metalloproteinases (a component of the SASP) in cells. Finally, future perspectives of this research are discussed.

We have focused on determining the range of oxidative stress biomarkers and their dynamic changes in patients at different time points after the acute ischemic stroke (AIS). 82 patients with AIS were involved in our study and were tested: within 24 h from the onset of the attack (group A); at 7‐day follow‐up (group B); and at 3‐month follow‐up (group C). 81 gender and age matched volunteers were used as controls. Stroke patients in group A had significantly higher concentrations of plasma lipid peroxides and urine 8‐isoprostanes when compared with controls. Protein carbonyls were not significantly different in any experimental group compared to controls. Antioxidant capacity of plasma was increased only in experimental group C. Activities of superoxide dismutase and catalase were elevated in all three experimental AIS groups compared to controls. Paraoxonase activity was reduced in groups A and B and unchanged in group C when compared to controls. Glutathione peroxide activity was elevated only in group A. Our results suggest that free radical damage is the highest within 24 h after the attack. During the next 3 months oxidative damage to lipids caused by free radicals is reduced due to activated antioxidant system.

In this study we investigated effects of natural extract from the black tea Camellia sinensis (BTE) against human colon carcinoma cell line HT-29, human breast carcinoma cell line MCF-7, human alveolar carcinoma cell line A549 and healthy cell line NIH-3T3. We identified concentration range for cytotoxic/antiproliferative effects using MTT assay and the trypan blue assay, gel electrophoresis we employed to determine the type of cell death induced by BTE and DNA damage we determined by comet assay. Different concentrations of the extract (0.00078 - 5 μg/mL) we added to the cultured cells and incubated for 216 h. BTE showed cytotoxic effects against all carcinoma cell lines, however HT-29 and MCF-7 cells were more sensitive than A549. BTE showed no antiproliferative effect against healthy cells NIH-3T3 at tested concentrations. We found no apoptotic cell death in HT-29 and MCF-7 cells after 72 h of incubation in case of single administration of BTE but in case of repetitive administration of BTE (BTE was added to the cells each day) we found apoptotic cell death in HT-29 after 72 h incubation. BTE induced also DNA strand breaks and oxidative damage to DNA in carcinoma cells HT-29 and MCF-7.

Background: Obstructive sleep apnea (OSA) is a disorder with a significant risk for cardiovascular diseases. Dyslipidemia and redox imbalance belong to potential mechanisms linking OSA with the development of vascular diseases. The main aim of this study was the evaluation of the presence of lipid abnormalities in OSA patients, focusing on small dense low-density lipoprotein (LDL) and high-density lipoprotein (HDL) subfractions and determination of the redox imbalance by evaluating the marker of oxidative damage to plasma lipids - lipoperoxides. Methods: The study included 15 male subjects with polysomnographically confirmed OSA and 16 male healthy controls. Plasma levels of total cholesterol, LDL and HDL and their subfractions, triacylglycerols and lipoperoxides were determined in all study individuals. Plasma LDL and HDL subfractions were separated by the Lipoprint system which is a polyacrylamide gel electrophoresis. Lipoperoxide levels were determined spectrophotometrically. Results: OSA patients had significantly higher triacylglycerols, total cholesterol and LDL-cholesterol compared to healthy controls. HDL cholesterol was not significantly different. Of the LDL and HDL subfractions, OSA patients had significantly lower levels of atheroprotective LDL1 and large HDL subfractions and significantly higher levels of atherogenic small dense LDL3–7 and HDL8–10 subfractions. Lipoperoxide levels in patients with OSA were significantly elevated compared to healthy individuals. Conclusion: The lipoprotein pro-atherogenic phenotype was found in individuals with OSA characterized by increased levels of atherogenic lipoprotein subfractions and reduced levels of atheroprotective subfractions. In addition, a plasma redox imbalance was found in patients with OSA compared to controls by detecting higher oxidative damage to lipids. Abnormalities in lipoprotein levels in patients with OSA, as well as the redox imbalance, could lead to an acceleration of the atherosclerotic process in predisposed individuals and thus represent a significant risk factor for vasular diseases.

Objective: In this study, we examined the relationships between perimenopausal symptoms, biochemical parameters, and markers of oxidative stress in women in perimenopause and compared them with those of premenopausal women. Methods: Sixty-two women (age, 53.2 ± 5.7 y) with perimenopausal symptoms were recruited to participate in our study. The control group consisted of 18 women without perimenopausal symptoms (age, 40 ± 5 y). Clinical perimenopausal symptoms were evaluated via the questionnaire of the Menopausal Rating Scale. Our participants were checked for basic biochemical parameters. The oxidative status of our samples was determined through the examination of lipoperoxides, 8-oxoguanine (8-oxoG) levels, and the total antioxidant status (TAS). Results: Perimenopausal women had higher total cholesterol values and lower paraoxonase-1 (PON1) activity compared to reference values. Other biochemical parameters as well as 8-oxoG levels were unchanged compared with those of healthy control women. Lipoperoxide levels were significantly increased compared with those of premenopausal women. We found an indirect correlation between PON1 arylesterase (PON1 A) activity and lipoperoxide levels, between PON1 A activity and atherogenic index, between age and TAS, and between age and 8-oxoG levels. DNA repair ability and the total antioxidant status of women in perimenopause were significantly increased compared with women in premenopause. Hypercholesterolemic women had significantly increased low-density lipoprotein cholesterol levels when compared with normocholesterolemic individuals, but these values were still within the reference range. Normocholesterolemic women had significantly decreased high-density lipoprotein cholesterol levels, below the reference range. We found no correlations between perimenopausal symptoms and biochemical parameters or oxidative stress markers. Conclusions: We found that women in perimenopause are under increased oxidative stress manifested by reduced PON1 A activity and elevated lipoperoxidation, DNA repair ability, and TAS. Nutritional antioxidant supplementation may be an effective approach in improving menopausal symptoms.