Astaxanthin prevents changes in the activities of thioredoxin reductase and paraoxonase in hypercholesterolemic rabbits

Paula R Augusti, Andréia Quatrin, Sabrina Somacal, Greicy Mm Conterato, Rocheli Sobieski, Amanda R Ruviaro, Luana H Maurer, Marta Mf Duarte, Miguel Roehrs, Tatiana Emanuelli, Paula R Augusti, Andréia Quatrin, Sabrina Somacal, Greicy Mm Conterato, Rocheli Sobieski, Amanda R Ruviaro, Luana H Maurer, Marta Mf Duarte, Miguel Roehrs, Tatiana Emanuelli

Abstract

This study explored the effects of the antioxidant astaxanthin on paraoxonase and thioredoxin reductase activities as well as on other oxidative stress parameters and on the lipid profile in hypercholesterolemic rabbits. Rabbits were fed a standard or a hypercholesterolemic diet alone or supplemented with 50, 100 and 500 mg/100 g of astaxanthin for 60 days. Antioxidant enzymes activities, lipid profile and oxidative stress markers were evaluated in the serum. The hypercholesterolemic diet increased lipids, including unsaturated fatty acids level, whereas it decreased saturated fatty acids level. These changes were accompanied by increased levels of oxidized low-density lipoprotein and oxidized low-density lipoprotein antibodies, as well as lipid and protein oxidation. Astaxanthin (100 and 500 mg/100 g) prevented hypercholesterolemia-induced protein oxidation, whereas 500 mg/100 g of astaxanthin decreased protein oxidation per se. The activities of superoxide dismutase and thioredoxin reductase were enhanced, whereas paraoxonase activity was inhibited in hypercholesterolemic rabbits. All astaxanthin doses prevented changes in thioredoxin reductase and paraoxonase activities. This effect was not related to a direct effect of astaxanthin on these enzymes, because in vitro astaxanthin enhanced thioredoxin reductase and had no effect on paraoxonase activity. Astaxanthin could be helpful in cardiovascular diseases by restoring thioredoxin reductase and paraoxonase activities.

Keywords: atherosclerosis; fatty acids; oxidative stress.

Figures

Fig. 1
Fig. 1
Total cholesterol (A), triglycerides (B), HDL (C) and non-HDL cholesterol (D) levels of rabbits fed with a cholesterol and/or ASX enriched diet (means ± SEM, n = 6). *Different from control groups (p<0.05).
Fig. 2
Fig. 2
TBARS levels (A), protein carbonyl content (B), LDLox (C) and LDLoxAB (D) levels of rabbits fed with a cholesterol and/or ASX enriched diet (means ± SEM, n = 6). *Different from control groups (p<0.05). #Different from ASX 0-Chol group (p<0.05). &Different from ASX 0-control group (p<0.05). MDA = malondialdehyde.
Fig. 3
Fig. 3
PON1 (A), SOD (B) and TrxR-1 (C) activities of rabbits fed with a cholesterol and/or ASX enriched diet (means ± SEM, n = 6). *Different from control groups (p<0.05). #Different from ASX 0-Chol group (p<0.05).
Fig. 4
Fig. 4
In vitro effect of ASX on serum TrxR-1 (A) and PON1 (B) activities from rabbits. Serum was preincubated for 1 h in the presence of 0, 3, 10, 30 or 100 µg/ml of ASX. Then, the activities of TrxR-1 and PON1 were determined as described in Materials and Methods section. Data are means ± SEM (n = 4). *Different from control (0 µg ASX/ml) at p<0.05.

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