Reduction of elevated lipids and low‐density lipoprotein oxidation in serum of individuals with subclinical hypoxia and oxidative stress supplemented with lycosome formulation of docosahexaenoic acid

Abstract

Thirty two individuals aged 40–65 years old with a moderate hyperlipidemia (serum triglycerides > 150 mg/dl and LDL from 130 to 160 mg/dl) were supplemented once daily for 30 days with a 250 mg conventional formulation of docosahexaenoic acid ( DHA ) without lycopene ( CF ‐ DHA ) or 250 mg of lycosome‐formulated DHA containing 7 mg of lycopene ( LF ‐ DHA ). It was shown that ingestion of CF ‐ DHA led to a transient increase in serum DHA level after 2 weeks of the trial, whereas LF ‐ DHA did not cause significant changes in serum DHA . However, there was a noticeable increase in serum eicosapentaenoic acid levels exceeding the pretreatment value by 42.8% and 39.1% after the 2nd and 4th weeks of LF ‐ DHA ingestion. Patients supplemented with LF ‐ DHA showed a significant (19.5 mg/dl, p < 0.05) decline in LDL , which was accompanied by a corresponding decrease in total serum cholesterol and a much stronger reduction in serum triglyceride levels (reduction of medians by 27.5 mg/dl). No changes in HDL were observed. LF ‐ DHA caused a significant decline in the serum level of malonic dialdehyde ( MDA ), whereas the components of LF ‐ DHA , lycopene and DHA , ingested as two separate formulations had a less significant effect on serum MDA . Moreover, LF ‐ DHA increased both the plasma oxygen transport and tissue oxygen saturation by the end of the observational period, while lycopene or DHA taken alone, or both of them co‐ingested separately had none or a much less effect on the oxygen turnover parameters.

Selenium nanoparticles are more efficient than sodium selenite in reducing the toxicity of aflatoxin B1 in Japanese quail

“…Adding Se supplements to the diet largely alleviated these harmful effects of AFB 1 by a 14.1% decrease in triglycerides, 12.6% decrease in total cholesterol, 6.5% decrease in LDL cholesterol and 34.7% increase in HDL cholesterol, which might be mediated by changes in the antioxidant status of the birds. It is generally accepted that LDL oxidation is the primary mechanism contributing to lipid disorders such as hypertriglyceridemia and hypercholesterolemia (Menéndez‐Carreño et al., 2008 ; Petyaev et al., 2019 ) and fatty acid distribution changes (Yamaoka et al., 2008 ). Se plays a fairly well‐recognized role in preventing LDL oxidation as part of the enzyme phospholipid‐hydroperoxide GPx that is transported in the bloodstream by HDL (Steinbrenner & Sies, 2009 ).…”

Evaluation of Antioxidant Therapeutic Value of ACE Inhibitor as Adjunct Therapy on Type 2 Diabetes Mellitus Patients with Cardiovascular Disease

“…Even LDLs subjected to a very mild oxidative stress can acquire important biological properties, including the ability to stimulate the release of chemokines from endothelial cells. 30 Oxidation of LDL can be caused by enzymes such as lipooxygenase that are produced by endothelial cells and monocytes/macrophages, which convert polyunsaturated fatty acids into lipid hydroperoxides and then oxidize LDL. 31 Oxidized LDL (ox-LDL) may induce vasoconstriction through inhibition of NO production.…”

“…The extent of the changes in the LDL particle induced by oxidation depends on the peroxidation conditions in the LDL bio-environment. Even LDLs subjected to a very mild oxidative stress can acquire important biological properties, including the ability to stimulate the release of chemokines from endothelial cells . Oxidation of LDL can be caused by enzymes such as lipooxygenase that are produced by endothelial cells and monocytes/​macrophages, which convert polyunsaturated fatty acids into lipid hydroperoxides and then oxidize LDL .…”