Abstract

Objective Cholesterol oxidation products have an established proatherogenic and cytotoxic effect. An increased exposure to these substances may be associated with the development of atherosclerosis and cancers. Relatively little, though, is known about the effect of phytosterol oxidation products, although phytosterols are present in commonly available and industrial food products. Thus, the aim of the research was to assess the effect of 5α,6α-epoxyphytosterols, which are important phytosterol oxidation products, on redox state in rats. Material and Methods The animals were divided into 3 groups and exposed to nutritional sterols by receiving feed containing 5α,6α-epoxyphytosterols (ES group) and 5α,6α-epoxycholesterol (Ech group) or sterol-free feed (C group). The levels of malondialdehyde (MDA), conjugated dienes (CD), and ferric reducing antioxidant potential (FRAP) were assayed in the plasma; anti-7-ketocholesterol antibodies and activity of paraoxonase-1 (PON1) were determined in serum, whereas the activity of catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), S-glutathione transferase (GST), and superoxide dismutase (SOD) were assayed in RBCs. Results During the experiment, the levels of lipid peroxidation products increased, such as CD and anti-7-ketocholesterol antibodies. At the same time, the plasma levels of FRAP and serum activity of PON1 decreased alongside the reduced activity of GPx, GR, and SOD in RBCs. There was no effect of the studied compounds on the plasma MDA levels or on the activity of CAT and GST in RBCs. Conclusions Both 5α,6α-epoxyphytosterols and 5α,6α-epoxycholesterols similarly dysregulate the redox state in experimental animal model and may significantly impact atherogenesis.

Highlights

  • Cholesterol is the most common animal sterol

  • In terms of antioxidant enzyme activity in red blood cells (RBCs), significant differences in the activity of glutathione peroxidase (GPx), glutathione reductase (GR), and superoxide dismutase (SOD) were demonstrated between the study groups, with no differences in the activity of CAT and glutathione S-transferase (GST)

  • There was a significant decrease in GPx, GR, and SOD activity in RBCs demonstrated in ES and ECh groups as compared to controls, with no difference between the ES and ECh groups

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Summary

Introduction

Cholesterol is the most common animal sterol. It is present in every cell, as a plasma membrane component, and in the extracellular space, as a plasma lipoprotein component. Its wide bioavailability and chemical structure (monounsaturated alcohol) make cholesterol prone to oxidation, which leads to oxycholesterol formation [1]. Apart from endogenous production, oxycholesterols can be sourced from nutrition, in particular, from cholesterol-rich foods after. Food products containing phytosterols and phytostanols have been widely promoted. Animal experimental studies and epidemiological studies demonstrated their positive effect on lipoprotein status by, e.g., inhibiting intestinal absorption of exogenous cholesterol. Population studies show that increased intake of phytosterols and phytostanols leads to a significant decrease in total cholesterol and LDL cholesterol levels, as well as favourably affects HDL cholesterol and triacylglycerol levels [3, 4]

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