Mean Thiobarbituric Acid Reactive Substances Research Articles

Wine Ingestion Has No Effect on Lipid Peroxidation Products

Objective: Moderate alcohol consumption has been associated with beneficial effects on coronary heart disease. This positive effect has been partly attributed to the flavonol contents which promote vasodilatory, anti-aggregatory and antioxidative effects and protect low-density lipoprotein (LDL) cholesterol from oxidation. Thus, the present study was carried out to determine the acute effects of different wines on LDL oxidization in healthy volunteers. Methods: Healthy male and female subjects (15/group) on a flavonol-restricted diet were randomly assigned to drink 300 ml wine from one of four different grapes and fermentation processes. Conjugated fatty acid dienes and thiobarbituric acid reactive substances (TBARS) were determined as a measure of LDL oxidation in serum at baseline and up to 96 h after wine ingestion. Results: At baseline, mean conjugated dienes in serum were 12.5 ± 6.2 µmol/l and mean TBARS in serum were 15.7 ± 8.1 µmol/l. There were no differences between the groups and no effect of any wine type on conjugated dienes (p = 0.15) or TBARS (p = 0.38) over time. 96 h following wine ingestion, the mean conjugated dienes were 12.1 ± 4.12 µmol/l and mean TBARS were 16.4 ± 8.8 µmol/l (pooled data, n = 60). Conclusion: Ingestion of 300 ml wine does not protect LDL from oxidation in vivo in healthy subjects. However, this does not exclude an effect of habitual wine consumption on LDL plasma oxidation.

Erythrocyte antioxidant enzyme activities and lipid peroxidation in patients with types IIb and IV hyperlipoproteinemias.

We measured lipid peroxidation and antioxidant enzymes in erythrocytes of types IIb and IV hyperlipoproteinemic (HLP) human subjects in comparison with age-matched controls. Thiobarbituric acid-reactive substances (TBARS), a measure of lipid peroxidation, glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), glutathione reductase (GR), and catalase (CAT) were determined in erythrocytes. We also measured lipid parameters including triglycerides (TG), total cholesterol (TC), HDL-cholesterol (HDL-C), LDL-cholesterol (LDL-C), apolipoprotein AI, and apolipoprotein B, and antioxidant related substances such as serum albumin, free iron, ferritin, ceruloplasmin. Thirty-two subjects (females 15, males 17) with type IIb (the mean age 45.6+/-8 [S.E.]), 34 with type IV (females 16, males 18) (the mean age 47+/-10 [S.E.]), and 36 normolipidemic voluntary subjects (females 18, males 18) (the mean age 46+/-8 [S.E.]) were included in the study. Erythrocytes were prepared by classical washing method (0.9% NaCl) from venous blood samples. The mean TBARS levels in plasma and erythrocyte suspensions were found to be significantly higher in both types IIb and IV hyperlipoproteinemics. Erythrocyte SOD and GSH-Px activities were decreased but erythrocyte GR activity did not change in both types IIb and IV hyperlipoproteinemics. Erythrocyte CAT activity was decreased in type IIb, but it was increased in type IV hyperlipoproteinemics. Erythrocyte SOD activity was negatively correlated with plasma TG level, whereas plasma free iron was positively correlated with plasma TBARS level in type IV hyperlipoproteinemics. These results suggest the presence of oxidative injury in patients with type IIb or IV hyperlipoproteinemia, and that the responses of erythrocyte antioxidant enzymes to oxidant stress are different in these conditions.

Role of Cadmium-Induced Lipid Peroxidation in the Kidney Response to Atrial Natriuretic Hormone

In order to investigate the role of increased lipid peroxidation in the development of cadmium-induced hypertension, 30 male albino rats were exposed to drinking water containing 15 micrograms/ml cadmium for 30 days, and the results were compared with those of 30 controls. Water containing high cadmium concentrations caused a significant accumulation of the element in blood and kidneys, associated with an obvious elevation in blood pressure. The systolic and diastolic blood pressures rose from 102.8 +/- 7.0 and 81.2 +/- 3.8 mm Hg to 128.1 +/- 4.6 and 107.9 +/- 7.4 mm Hg, respectively, in cadmium-treated rats (p < 0.01). A decreased glomerular filtration rate and increased serum creatinine levels were accompanied by elevated levels of cortical and medullary thiobarbituric acid reactive substances in cadmium-induced hypertensive rats. The mean thiobarbituric acid reactive substance level rose from a control value of 211.5 +/- 64.1 to 303.3 +/- 46.3 nmol/g protein (p < 0.01) in the renal cortex due to the high intake of cadmium. Despite its obvious diuretic and natriuretic action in control animals, the bolus injection of 1.2 and 2.4 micrograms/kg atrial natriuretic peptide corrected neither elevated blood pressure nor the reduced glomerular filtration rate in rats exposed to cadmium. However, the tubular response to atrial natriuretic peptide remained unaltered. These data suggest that a lack of vascular response to atrial natriuretic peptide is one of the many putative causes of cadmium-induced hypertension, and cadmium-mediated increased lipid peroxidation may be involved in this unresponsiveness.