Artichoke leaf extract reduces oxidative stress and lipoprotein dyshomeostasis in rats fed on high cholesterol diet.

Hypercholesterolemia and lipid peroxidation play complementary role in atherosclerosis. Artichoke leaf extract (ALE) is rich in natural antioxidants and has a cholesterol-reducing effect. However, there is no study investigating the effect of ALE on lipid levels and lipid peroxidation in experimental hypercholesterolemic conditions. Rats were fed on 4% (w/w) cholesterol and 1% (w/w) cholic acid supplemented diet for 1 month. ALE (1.5 g/kg/day) was given by gavage during the last 2 weeks. Serum lipid composition, malondialdehyde (MDA) and diene conjugate (DC) levels and plasma antioxidant activity (AOA) were measured. In addition, endogenous DC and copper-induced MDA levels were determined in apo B-containing lipoproteins (LDL+VLDL fraction). Serum cholesterol and triglyceride levels and the ratio of cholesterol to HDL-cholesterol decreased due to ALE treatment in rats fed on HC diet. Significant decreases in serum MDA and DC levels and increases in plasma AOA were detected in serum in ALE-treated hypercholesterolemic rats. Endogenous DC and copper-induced MDA levels were also lower in LDL+VLDL fraction due to ALE-treatment in hypercholesterolemic rats. Our results indicate that ALE may be useful for the prevention of hypercholesterolemia-induced pro-oxidant state in LDL+VLDL fraction and the reduction of increased serum cholesterol and triglyceride levels.

Mitochondrial lipid peroxides and antioxidant enzymes in the liver following phorone-induced glutathione depletion.

The levels of lipid peroxidation product (malondialdehyde = MDA) and vitamin C and the activities of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were determined in the liver and its mitochondrial fraction, in the rats 2 and 18 hr after the injection of phorone, a glutathione (GSH) depleting agent. GSH levels decreased in liver homogenate and its mitochondrial fraction after 2 hr of phorone treatment, but these values returned to normal levels at 18 hr. In GSH depleted conditions, hepatic vitamin C levels increased, GSH-Px and SOD activities remained unchanged in mitochondrial and post-mitochondrial fractions. These results indicate that GSH depletion per se does not influence lipid peroxidation and GSH-Px and SOD activities in the liver and the mitochondrial fraction.

Endogenous and copper-induced lipid peroxidation and antioxidant activity of serum in hypercholesterolemic subjects.

Endogenous malondialdehyde and diene conjugate levels were increased in hypercholesterolemic subjects with serum cholesterol levels above 240 mg/dl as compared to normocholesterolemic subjects (below 20 mg/dl). A decrease in vitamin E/cholesterol and vitamin C/cholesterol ratios was observed in serum of hypercholesterolemic individuals. However, the susceptibility of serum to copper-induced lipid peroxidation and antioxidant activity were found unchanged. The present study indicates that hypercholesterolemic subjects have a high level of circulating lipid peroxides and that a higher tendency towards atherosclerosis in these subjects may be related to increased baseline levels of serum lipid peroxides.

Evidence for oxidative stress in the hepatic mitochondria of bile duct ligated rats.

Lipid peroxidation increased both in the liver homogenates and in the hepatic mitochondrial fraction of bile duct ligated (BDL)-rats. Although mitochondrial superoxide dismutase (SOD) activity did not change in the liver, glutathione (GSH) levels and glutathione peroxidase (GSH-Px) activity decreased in hepatic mitochondrial fraction of BDL-rats as compared to sham-operated rats. In addition, GSH-Px and glutathione transferase (GST) activities decreased but SOD activity remained unchanged in the post-mitochondrial fraction of the liver from BDL-rats. However, erythrocyte lipid peroxide and GSH levels did not change in BDL-rats. In conclusion, our results show that the disturbance of oxidant-antioxidant balance especially in mitochondria may be responsible for cholestatic liver injury in BDL-rats.

Age-related changes in plasma lipid peroxidation and antioxidant system in humans and rats.

This study was carried out on young (20-35 years) and old (60-85 years) men and rats (6 vs 22 months) to investigate the effect of aging on plasma lipid peroxidation and the antioxidant system. Plasma polyunsaturated fatty acid (PUFA), total fatty acid (TFA) and malondialdehyde (MDA) levels increased in aged humans and rats compared with young groups. However, plasma MDA/TFA ratios did not increase in aged humans and rats. Plasma vitamin E/TFA, and total thiol content were found to decrease both in aged humans and rats. Plasma antioxidant activity (AOA) decreased only in aged rats. In addition, the susceptibility of VLDL+LDL, apolipoprotein B containing lipoproteins to copper-induced peroxidation increased with aging. It is concluded that aging is associated with some variations in plasma oxidant-antioxidant balance.

Peroxidation potential and antioxidant activity of serum in patients with diabetes mellitus and myocard infarction.

Endogen malondialdehyde (MDA), diene conjugate levels, the susceptibility to copper-induced lipid peroxidation and antioxidant activity of serum were determined in patients with atherosclerotic diseases such as diabetes mellitus and myocard infarction. Lipid peroxidation susceptibility and antioxidant activity did not change, however, an increase in endogen MDA and diene conjugate levels was observed in serum of these patients. These results indicate the presence of oxidative stress in diabetes mellitus and myocard infarction.