According to the WHO, cancer is the second leading cause of death globally and the third most common cancer is colorectal. A significant etiological factor for carcinogenesis might be oxidative stress. Chemoprevention by consuming natural antioxidants has great perspectives in the struggle to control cancer because it is available and affordable for the wide population. Studies by diverse research groups discovered that grapes, as well as grape-based products, are exceptional sources of the polyphenolic compound resveratrol, which has powerful antioxidant properties. Despite the great number of publications on the anticancer effectiveness of resveratrol, they were all aimed at studying its action once the condition was established. This experiment was the first to study the dynamics of the anticancer activity of resveratrol in the development of chemically induced colorectal cancer. Administrating resveratrol along with 1,2-dimethylhydrazine (DMH) during 30 weeks led to the inhibition of oxidative stress manifestations, in particular, lipid peroxidation. Our research showed that the level of thiobarbituric acid reactive substances in blood serum was 85.1%, 214.6%, and 276.9% lower on the third, fifth, and seventh months of the experiment in the group of rats that obtained resveratrol, compared with the animals affected only by DMH. In the fifth month of the experiment, we noticed that the GPx activity in blood serum was 1.54 times higher than the DMH-control level. During the next 8 weeks, this indicator decreased. The activity of glutathione reductase increased by 2 times in the seventh month, compared with the DMH-control. Histologically resveratrol decelerated the development of the tumor. After 30 weeks of experiment, rats that were receiving only DMH had developed colon adenocarcinoma in situ. In contrast to them, morphological changes in the colon tissue of the animals that obtained resveratrol + DMH could be characterized as signs of mucous colitis.

BACKGROUND: Cardiovascular (CV) diseases are the most spread cause of mortality in the world. Essential arterial hypertension (EAH), as a major risk factor for the development of CV diseases, is a multifactorial disease involving environmental and genetic factors together with risk-conferring behaviors. AIM: The purpose of this study was to analyze lipid metabolism changes in patients with EAH depending on the Vitamin D receptor (VDR rs2228570 (aka rs10735810)) and angiotensinogen (AGT rs699) genes polymorphism. MATERIALS AND METHODS: The single-stage study involved 100 patients suffering from Stage 2 EAH, 1–3 degrees of blood pressure increase, high and very high CV risks, 21% (21) men, and 79% (79) women. The average age of patients was 59.86 ± 6.22 years old. The control group included 60 practically healthy individuals of an appropriate age and sex distribution. To examine the VDR gene (rs10735810, rs2228570) and AGT gene (rs699) polymorphism, a qualitative real-time polymerase chain reaction was made. The lipid metabolism was studied by determining the blood plasma content of total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TGs). RESULTS: Т allele of AGT gene is associated with reduced HDL-C level in men and increased TGs level in women. The EAH risk increases 4.5 times as much among the ТС-genotype carriers and lowered HDL-C level (odds ratio [OR] = 6.43; p = 0.01). The EAH risk increases as far as the HDL-C level reduction, irrespective of the VDR gene alleles condition 1.83 times (OR = 2.37; OR 95% confidence interval [CI]: 1.02–5.51; p = 0.04) and 1.9 times (OR=2.43; OR 95% CI: 0.99–5.97; p = 0.04). HDL-C reduction and LDL-C elevation in women increase the EAH risk 2.4 times (OR = 3.27; p = 0.01) and 1.24 times (OR = 3.67; p = 0.01), respectively. CONCLUSIONS: The EAH risk increases with a reduced HDL-C level in the TC genotype carriers of the AGT gene and irrespective of VDR gene polymorphic variants.

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КЛючОВІ СЛОВА: вперше діагностований туберкульоз легень; маркери цитолітичного синдрому.