Positive Health Online | Research - RELEVY and COLLEAGUES

Research: RELEVY and COLLEAGUES

Abstract

RELEVY and COLLEAGUES, 1. The Bert W. Strassburger Lipid Center, Sheba Medical Center, 5265601 Tel-Hashomer, Israel ; Sackler Faculty of Medicine, Tel-Aviv University, Israel; 2. The Bert W. Strassburger Lipid Center, Sheba Medical Center, 5265601 Tel-Hashomer, Israel; 3. N.B.T., Eilat, Israel; 4. Department of Biochemistry and Molecular Biology, University of Debrecen, Debrecen, Hungary studied the effect of vitamin A deficiency on atherogenesis.

Background

Vitamin A is involved in regulation of glucose concentrations, lipid metabolism, and inflammation, which are major risk factors for atherogenesis. However, the effect of vitamin A deficiency on atherogenesis has not been investigated. Therefore, the objective of the current study was to examine whether vitamin A deficiency accelerates atherogenesis in apolipoprotein E-deficient mice (apoE(-/-)).

Methodology

ApoE(-/-) mice were allocated into the following groups: control, fed vitamin A-containing chow diet; BC, fed chow diet fortified with Dunaliella powder containing βc isomers; VAD, fed vitamin A-deficient diet; and VAD-BC group, fed vitamin A-deficient diet fortified with a Dunaliella powder.

Results

Following 15 weeks of treatment, liver retinol concentration had decreased significantly in the VAD group to about 30% that of control group. Vitamin A-deficient diet significantly increased both plasma cholesterol concentrations and the atherosclerotic lesion area at the aortic sinus (+61%) compared to the control group. Dietary βc fortification inhibited the elevation in plasma cholesterol and retarded atherogenesis in mice fed the vitamin A-deficient diet.

Conclusion

The results imply that dietary vitamin A deficiency should be examined as a risk factor for atherosclerosis and that dietary βc, as a sole source of retinoids, can compensate for vitamin A deficiency.

References

Relevy NZ1, Harats D1, Harari A2, Ben-Amotz A3, Bitzur R1, Rühl R4, Shaish A2. Vitamin A-deficient diet accelerated atherogenesis in apolipoprotein E(-/-) mice and dietary β-carotene prevents this consequence. Biomed Res Int. 2015:758723. doi: 10.1155/2015/758723. Epub Feb 23 2015. 2015.

ZHANG and COLLEAGUES,1. Department of Cardiology, Xuzhou Central Hospital, Affiliated Xuzhou Hospital, Medical school of Southeast University, Xuzhou, Jiangsu, China. mwlj521@163.com study the roles of oxidative damage and antioxidant protection in cardiovascular diseases.

BACKGROUND: Atherosclerosis, the hardening of arteries under oxidative stress is related to oxidative changes of low density lipoproteins (LDL). The antioxidants prevent the formation of oxidized LDL during atherogenesis. Perhaps more than one mechanism is involved in the atherosclerosis disease where LDL is oxidized in all the cells of arterial wall during the development of this disease.

METHODOLOGY: The oxidation of LDL produces lipid peroxidation products such as isoprostans from arachidonic, eicosapentaenoic and docosahexaenoic acids, oxysterols from cholesterol, hydroxyl fatty acids, lipid peroxides and aldehydes. The lipid peroxidation bioassay can serve as a marker for the risk of cardiovascular. An in vivo test of levels of oxidative lipid damage is an early prediction of development of cardiovascular disease (CVD). Serum paraoxonase (PON) activity is correlated to severity of the coronary artery disease.

RESULTS: The antioxidants level in the serum and serum paraoxonase activity provides information for the risk of CVD. The antioxidant enzyme superoxide dismutase is responsible for dismutation of superoxide, a free radical chain initiator. The subcellular changes in the equilibrium in favour of free radicals can cause increase in the oxidative stress which leads to cardiomyopathy, heart attack or cardiac dysfunction. The oxidative damage and defence of heart disease has been reported where dietary antioxidants protect the free radical damage to DNA, proteins and lipids. The ascorbic acid, vitamin C is an effective antioxidant and high vitamin E intake can reduce the risk of coronary heart disease (CHD) by inhibition of atherogenic forms of oxidized LDL.

CONCLUSIONS: The vitamin A and beta-carotene protect lipid peroxidation and provitamin-A activity. It has been recently suggested that the protection of oxidative damage and related CVD is best served by antioxidants found in the fruits and vegetables. The oxidative damage and antioxidant protection of CVD have been described here.

Zhang PY1, Xu X, Li XC. Cardiovascular diseases: oxidative damage and antioxidant protection. Eur Rev Med Pharmacol Sci. 18(20):3091-6. Oct 2014. Comment in The combination of hydralazine and isosorbide dinitrate: the only antioxidant treatment recommended in the guidelines. [Eur Rev Med Pharmacol Sci. 2015].

Relevy NZ1, Harats D1, Harari A2, Ben-Amotz A3, Bitzur R1, Rühl R4, Shaish A2. Vitamin A-deficient diet accelerated atherogenesis in apolipoprotein E(-/-) mice and dietary β-carotene prevents this consequence. Biomed Res Int. 2015:758723. doi: 10.1155/2015/758723. Epub Feb 23 2015. 2015.

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