Effects of Ascorbic Acid and its 2-Sulfate on Rabbit Aortic Intimal Thickening

Verlangieri, Anthony J.; Hollis, Theodore M.; Mumma, Ralph O.

doi:10.1159/000158123

Cited by 6 publications

(5 citation statements)

References 16 publications

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“…Therefore, the higher spe cific activity o f C 4 -S in nonsupplemented animals suggests increased degradation o fC-4-S, with concomitant increased de novo synthesis. These observations may be part of the reduced intimal thickening mechanism reported by Verlangieri et aL (21) previously. Changes in G A G turnover may have a profound effect on maintaining the structural and permeability characteristics o f the intima and result in a reduced rate o f atherogenesis.…”

Section: Discussionsupporting

confidence: 70%

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L-Ascorbic Acid: Effects on Aortic Glycosaminoglycan 35S Incorporation in Rabbit-Induced Atherogenesis

Verlangieri¹,

Stevens²

1979

J Vasc Res

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The effects of L-ascorbic acid on ³⁵S-incorporation into thoracic aorta glycosaminoglycans and upon aorta cholesterol levels were determined in hypercholesterolemic rabbits. No significant difference was observed in serum free or esterified cholesterol levels between animals receiving L-ascorbic acid supplementation or saline while maintained on a cholesterol diet (0.5%). A 15-fold higher serum cholesterol was observed in animals on the cholesterol diet to those animals which received a normal rabbit (Purina) diet. L-Ascorbic acid increased sulfated glycosaminoglycans concentrations in hypercholesterolemic rabbits which paralleled lower tissue free and esterified cholesterol levels. The ³⁵S-specific activity of glycosaminoglycans in hypercholesterolemic animals receiving saline was much greater than in those animals receiving L-ascorbic acid. This suggests that L -ascorbic acid plays a role in the maintenance of adequate levels of aortic sulfated glycosaminoglycans. This then is a suggested biochemical mechanism of L-ascorbic acids interaction in the atherogenic process.

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Section: Discussionsupporting

confidence: 70%

“…The remaining piece o f aorta was divided in half. The half originally most proximate to the bifurcation was designated the middle section, the distal remaining piece the lower section as described by Verlangieri et al (21). The upper and lower sections were frozen immediately at 10 °C for further analysis.…”

Section: A Nimal Proceduresmentioning

confidence: 99%

L-Ascorbic Acid: Effects on Aortic Glycosaminoglycan 35S Incorporation in Rabbit-Induced Atherogenesis

Verlangieri¹,

Stevens²

1979

J Vasc Res

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“…Ascorbate can increase the oxidation, however, of partially oxidized LDL [29,30]. Some studies have shown an anti-atherogenic effect of ascorbate in cholesterol fed-rabbits [33,34], but others have demonstrated that ascorbate had no protective effect in these animals [35]. Similarly to a-tocopherol, there is no strong evidence that ascorbate decreases cardiovascular disease in clinical trials [8,9,36,37].…”

Section: Introductionmentioning

confidence: 99%

Vitamins E and C do not effectively inhibit low density lipoprotein oxidation by ferritin at lysosomal pH

Ojo

Leake

2021

Free Radical Research

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Low density lipoprotein (LDL) might be oxidized by iron in the lysosomes of macrophages in atherosclerotic lesions. We have shown previously that the iron-storage proteinferritin can oxidize LDL at lysosomal pH. We have now investigated the roles of the most important antioxidant contained in LDL, a-tocopherol (the main form of vitamin E) and of ascorbate (vitamin C), a major water-soluble antioxidant, on LDL oxidation by ferritin at lysosomal pH (pH 4.5). We incubated LDL with ferritin at pH 4.5 and 37 C and measured its oxidation by monitoring the formation of conjugated dienes at 234 n min a spectrophotometer. a-Tocopherol is well known to inhibit LDL oxidation at pH 7.4, but enrichment of LDL with a-tocopherol was unable to inhibit LDL oxidation by ferritin at pH 4.5. Ascorbate had a complex effect on LDL oxidation by ferritin at lysosomal pH and exhibited both antioxidant and pro-oxidant effects. It had no antioxidant effect on partially oxidized LDL, only a pro-oxidant effect. Ascorbate completely inhibited LDL oxidation by copper at pH 7.4 for a long period, but in marked contrast did not inhibit LDL oxidation by copper at lysosomal pH. Dehydroascorbate, the oxidation product of ascorbate, had a pronounced pro-oxidant effect on LDL incubated with ferritin at pH 4.5. The inability of a-tocopherol and ascorbate to effectively inhibit LDL oxidation by ferritin at lysosomal pH might help to explain why the large clinical trials with these vitamins failed to show protection against cardiovascular diseases.

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“…Ascorbate supplementation of cholesterol-fed animals has been shown to be anti-atherogenic [15][16][17], although other studies have reported no significant biological effect [18,19]. Some epidemiological studies in man [20,21], but not all [22], have shown that individuals who consume high concentrations of ascorbate through diet or supplements tend to have lower risks of cardiovascular disease, however, large clinical trials have found no benefits of antioxidant supplementation on cardiovascular disease risk [23].…”

Section: Introductionmentioning

confidence: 99%

Ascorbate does not protect macrophages against apoptosis induced by oxidised low density lipoprotein

Harris

Mann

Ruiz

et al. 2006

Archives of Biochemistry and Biophysics

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Apoptosis of macrophages and smooth muscle cells is observed in atherosclerotic lesions and may play an important role in the disease progression. Oxidised low density lipoprotein (LDL) is cytotoxic and induces apoptosis in a variety of cell types. We reported previously that ascorbate protects arterial smooth muscle cells from apoptosis induced by oxidised LDL containing the peak levels of lipid hydroperoxides. We now demonstrate that macrophages undergo apoptosis when treated with this species of oxidised LDL, as detected by increased annexin V binding and DNA fragmentation. Ascorbate treatment of macrophages did not protect against the cytotoxicity of oxidised LDL, and modestly increased the levels of annexin V binding and DNA fragmentation. Oxidised LDL treatment also increased the expression of the antioxidant stress protein heme oxygenase-1 in macrophages; however, this increase was markedly attenuated by ascorbate pretreatment. Although apoptosis induced by oxidised LDL was modestly promoted by ascorbate, ascorbate apparently decreased the levels of oxidative stress in macrophages, suggesting that this pro-apoptotic effect was not mediated by a pro-oxidant mechanism, but may instead have been due to intracellular protection of the apoptotic machinery by ascorbate.

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Effects of Ascorbic Acid and its 2-Sulfate on Rabbit Aortic Intimal Thickening

Cited by 6 publications

References 16 publications

<i>L</i>-Ascorbic Acid: Effects on Aortic Glycosaminoglycan <sup>35</sup>S Incorporation in Rabbit-Induced Atherogenesis

<i>L</i>-Ascorbic Acid: Effects on Aortic Glycosaminoglycan <sup>35</sup>S Incorporation in Rabbit-Induced Atherogenesis

Vitamins E and C do not effectively inhibit low density lipoprotein oxidation by ferritin at lysosomal pH

Ascorbate does not protect macrophages against apoptosis induced by oxidised low density lipoprotein

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