Breast cancer and benign breast disease patients evaluated in relation to oxidative stress.

In this study, breast cancer (n = 23) and benign breast disease (n = 15) patients were evaluated in relation to oxidative stress. The extent of lipid peroxidation was assessed by measuring thiobarbituric acid reactive substances (TBARS) in plasma. Erythrocyte glutathione peroxidase (GSH Px), CuZn speroxide dismutase (CuZn SOD), glutathione (GSH) and plasma vitamin E, cholesterol Fe, Zn, Cu levels were analysed in both groups GSH Px (p < 0.01), vitamin E (p < 0.001), Zn (p < 0.01), Cu (p < 0.05) and cholesterol (p < 0.01) concentrations were found to be significantly increased, TBARS level (p < 0.01) significantly decreased in breast cancer patients in comparison to benign breast disease group.

Lipid peroxidation and antioxidant status in experimental animals: effects of aging and hypercholesterolemic diet.

Effects of aging and hypercholesterolemic diet on lipid peroxidation and antioxidant status were investigated in rats. The rats were divided into four groups of ten: Group I; young rats receiving standard lab chow; Group II; young rats on hypercholesterolemic diet (0.4 g/rat/day); Group III; aged rates receiving standard lab chow; Group IV; aged rats on hypercholesterolemic diet (0.4 g/rat/day). Plasma lipid peroxidation end product level was determined as thiobarbutiric acid reactive substances (TBARS). Plasma cholesterol concentration was analyzed by a kinetic enzymatic method. Erythrocyte superoxide dismutase (CuZn SOD), glutathione peroxidase (GSH Px) and glutathione (GSH) levels were determined spectrophotometrically. Cholesterol values were found to be significantly high (p < 0.001), TBARS (0.05 > p > 0.02) and GSH (p < 0.001) levels significantly low in aged rats in comparison with young rats. Hypercholesterolemic diet induced significant increases in GSH (p < 0.001) and CuZn SOD (p < 0.001) levels, whereas a significant decrease in GSH Px activity (0.05 > p > 0.02) was observed in aged rats. In young rats hypercholesterolemic diet caused a significant increase in both GSH and CuZnSOD levels. Our results indicate an imbalance between radical production and destruction in favour of prooxidant conditions in the young rats and the induction by hypercholesterolemic diet of the antioxidative response in erythrocytes.

The effect of iron supplementation on GSH levels, GSH-Px, and SOD activities of erythrocytes in L-thyroxine administration.

Our aim was to study the effect of iron supplementation on the following aspects of erythrocyte metabolism in experimental hyperthyroidism: glutathione (GSH) levels, glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) activities. Hyperthyroidism induced by L-thyroxine administrations significantly raised erythrocyte GSH, GSH-Px and SOD levels of the rats (P < 0.001). Likewise, we observed that iron supplementation induced significant rises in erythrocyte GSH, GSH-Px and SOD levels (P < 0.001) as compared with the control group. The erythrocyte GSH, GSH-Px and SOD levels of hyperthyroidism-induced iron-supplemented animals were significantly higher when compared with either the iron-supplemented group (P < 0.001) or the only L-thyroxine-administered hyperthyroid group (P < 0.001, P < 0.05, P < 0.01, respectively). The results of this study show that L-thyroxine administration and/or iron supplementation increases GSH, GSH-Px and SOD levels of erythrocytes.

Calcium, magnesium, and zinc status in experimental hyperthyroidism.

In this study, experimental hyperthyroidism was established and used to investigate possible alterations in the calcium (Ca), magnesium (Mg), and zinc (Zn) homeostasis by assessing their concentrations in plasma and erythrocytes. In the L-thyroxine-induced hyperthyroidism condition, the experimental animals show a significant decrease in erythrocyte Ca, Mg, and Zn concentrations, and a significant decrease in plasma Mg concentration. Significant positive correlations were found for Mg and Zn both in plasma and in erythrocytes. The results suggest that the homeostasis of Ca, Mg, and Zn is altered during experimental hyperthyroidism.

Could L-carnitine be an acute energy inducer in catabolic conditions?

Serum free carnitine levels in five children (aged between 2.5 months and 4 years) with the findings of septic shock without disseminated intravascular coagulopathy and seven children (aged between 1.5 and 6.5 years) with the first attack of idiopathic status epilepticus were compared with those of eight healthy children (aged between 2.5 months and 5 years). Serum free carnitine levels showed a statistically significant decrease in the sepsis (mean 51.5 +/- 19 mg/L) and status epilepticus groups (mean 4.1 +/- 12.4 mg/L) (P = 0.006 and P = 0.001, respectively) when compared with the controls (mean 90.8 +/- 17.2 mg/L).

Calcium, magnesium, and zinc status in experimental hypothyroidism.

In this study, experimental hypothyroidism was established and used to investigate possible alterations in the calcium, magnesium, and zinc homeostasis by assessing their concentration in plasma and erythrocytes. Hypothyroidism was induced by administration of methimazole an iodine blocker at a dose of 75 mg/100 g food for 3 wk. In the methimazole-induced hypothyroid state, the experimental animals showed a significant decrease in plasma zinc concentration, whereas a significant increase in plasma magnesium concentration occurred. No change was observed in plasma calcium concentration. The erythrocyte zinc and calcium concentrations were found to be increased, whereas magnesium concentration decreased. Erythrocyte magnesium concentration showed a significant positive correlation with T4 values. The study provides evidence for marked alterations in homeostatis of zinc, magnesium, and calcium.

Antioxidant status in experimental hyperthyroidism: effect of vitamin E supplementation.

Free radical-mediated oxidative stress has been implicated in the genesis and exacerbation of degenerative diseases. In view of the role of oxidative processes in hyperthyroidism, in this study, we investigated the antioxidant status of erythrocytes in experimental hyperthyroidism and the effect of vitamin E supplementation on defense systems. Our findings of significantly increased T4 and T3 and undetectable TSH values in thyroxine administered rats confirmed the establishment of hyperthyroidism. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione (GSH) values were found to be significantly increased in hyperthyroid rats in comparison to the control group. Vitamin E supplementation to hyperthyroid rats induced a significant decrease in GSH-Px activity and a significant increase in GSH level. These findings show that hyperthyroidism increases the components of the antioxidant system in the erythrocytes. Furthermore, vitamin E supplementation reduces the burden of oxidative stress in hyperthyroidism.