Background/Aims: Increased oxidative stress in chronic kidney disease (CKD) was suggested to be both a cause and an effect of renal injury. However, the evolution of oxidant stress from early stages of renal function decline is not fully clear. This study aimed to determine the oxidant-antioxidant balance across the whole range of renal function. Methods: A total of 116 patients with CKD (85 predialysis patients divided into groups according to CKD stage, and 31 patients with end-stage renal disease (ESRD) on hemodialysis treatment), as well as 29 healthy subjects were evaluated. Plasma levels of 15-F2t-isoprostane (15-F2t-IsoP), a valid marker of oxidant stress, as well as total antioxidant capacity (TAC) and serum levels of vitamin E were measured in all participants. Results: Plasma 15-F2t-IsoP levels were higher in predialysis and ESRD patients compared to healthy subjects and were progressively increasing with advancing CKD stages (p < 0.001). In contrast, plasma TAC was similar between healthy subjects and predialysis patients, and presented a small reduction in ESRD patients (p < 0.001). Vitamin E levels were higher in healthy subjects compared to any other group (p < 0.001) and slightly higher in ESRD patients compared to predialysis patients (p < 0.01), but did not differ significantly between the groups of predialysis patients. Plasma 15-F2t-IsoP levels were inversely correlated with estimated glomerular filtration rate in predialysis patients (r = –0.65, p < 0.001). Conclusions: This study shows that 15-F2t-IsoP levels increase progressively with advancing CKD stages, whereas TAC and vitamin E levels remain rather stable with the loss of renal function and change only in patients with ESRD.
Twenty-five 12-week-old turkeys randomly divided into five groups were given a basal diet, or a basal diet supplemented with 200 mg alpha-tocopheryl acetate/kg, or 100 mg oregano oil/kg or 200 mg oregano oil/kg, or 100 mg oregano oil plus 100 mg alpha-tocopheryl acetate/kg diet, for 4 weeks prior to slaughter. Breast, thigh, liver and heart tissues were subjected to iron-induced lipid oxidation, the extent of which was determined by third-order derivative spectrophotometry. Results showed that dietary oregano oil at the inclusion level of 200 mg oregano oil/kg diet was more effective in delaying lipid oxidation compared with the inclusion level of 100 mg/kg, but equivalent to the inclusion of 200 mg alpha-tocopheryl acetate/kg diet, which in turn was inferior to the combined inclusion of 100 mg oregano oil plus 100 mg alpha-tocopheryl acetate/kg, which was superior to all dietary treatments. Thigh tissue was more susceptible to oxidation than breast tissue, although it contained alpha-tocopherol at higher concentrations. Also, lipid oxidation in heart was relatively high, although it contained the highest alpha-tocopherol levels. This indicates that tissue alpha-tocopherol is one important factor influencing the level of lipid oxidation, but the distribution of lipids, iron and oregano oil in tissues must also be taken into consideration. Tissue alpha-tocopherol levels responded to dietary intake of 30-200 mg alpha-tocopheryl acetate/kg in the order heart > liver > thigh > breast. Breast, thigh and heart tissues from the oregano groups presented significantly (p < 0.05) higher levels of alpha-tocopherol compared with the control, the increase being positively correlated with the supplementation level. The increased levels of alpha-tocopherol in these tissues indicated that the dietary oregano oil exerted a protective action on alpha-tocopherol.
The effect of intramuscular administration of high (30 mg/kg body weight for 3 days) or very high (300 mg/kg body weight for 3 days) doses of a-tocopherol to Wistar rats subjected to total severe warm hepatic ischemia and reperfusion was investigated. After a 60-minute period of total hepatic ischemia and 120 minutes of reperfusion, animals were killed, and liver samples were taken for determination of malondialdehyde (MDA) and histological examinations. Blood samples were also taken for assay of serum a-tocopherol, alanine transaminase (ALT), aspartate transaminase (AST), and lactic dehydrogenase (LDH). Additional animals were followed for a 7-day survival rate determination. Results showed that ischemia and reperfusion decreased the survival rate to 10%, whereas the levels of AST, ALT, and LDH in serum were increased compared with levels in animals that were sham operated. The MDA concentrations in liver were also increased, from 1.142 to 1.567 nmoles/g, whereas the levels of a-tocopherol in serum were decreased from 10.20 to 1.80 mmol/L. Pretreatment with a-tocopherol increased the viability to 50% and 70%, for the high and very high doses, respectively, and decreased the levels of AST, ALT, and LDH in serum. It also decreased the MDA concentrations in liver to 0.975 and 0.774 nmoles/g for the high and very high doses of a-tocopherol, respectively, whereas it increased the level of a-tocopherol in serum to 11.25 and 13.02 mmol/L for the high and very high doses, respectively. Histological examinations showed protection of the liver parenchyma in the animals treated with a-tocopherol.
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