The aim of this study was examine the effects of high starch (HS) vs. high fat (HF) feeding on blood glycated hemoglobin (GHbA(1c)) level, thiobarbituric acid-reactive species (TBA-RS) concentration and delta-aminolevulinate dehydratase (delta-ALA-D) activity in mice. The GHbA(1c) level was significantly higher in mice fed the HF diet compared with those fed the HS diet. Hepatic, renal, and cerebral TBA-RS concentrations in mice fed the HF diet were significantly greater than in mice fed the HS diet. In addition, positive correlations were found between the GHbA(1c) and TBA-RS levels for hepatic (P < 0.05; r = 0.46), renal (P < 0.003; r = 0.65), and cerebral (P < 0.001; r = 0.69) tissues. The delta-ALA-D hepatic, renal and cerebral activities of mice fed the HF diet were significantly lower than those of mice fed the HS diet. Furthermore, a negative correlation was found between the GHbA(1c) level and delta-ALA-D activity in hepatic (P < 0.001; r = -0.77), renal (P < 0.007; r = -0.60), and cerebral (P < 0.007; r = -0.60) tissues. The results of this study indicate that consumption of a high fat diet promotes oxidative stress related to hyperglycemia, which in turn can stimulate glycation of proteins leading to delta-ALA-D inhibition in mice.

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The heme pathway enzyme delta-aminolevulinate dehydratase is a good marker for oxidative stress and metal intoxication. This sulfhydryl enzyme is inhibited in such oxidative pathologies as lead, mercury and aluminum intoxication, exposure to selenium organic species and diabetes. Oxidative stress is a complicating factor in diabetes, inducing non-enzymatic glucose-mediated reactions that change protein structures and impair enzyme functions. We have studied the effects of high glucose, fructose and ribose concentrations on delta-ALA-D activity in vitro. These reducing sugars inhibited delta-ALA-D with efficacies in the order fructose=ribose>glucose. The possible mechanism of glucose inhibition was investigated using lysine, DTT, and t-butylamine. Oxidation of the enzyme's critical sulfhydryl groups was not involved because DTT had no effect. We concluded that high concentrations of reducing sugars or their autoxidation products inhibit delta-ALA-D by a mechanism not related to thiol oxidation. Also, we are not able to demonstrate that the formation of a Schiff base with the critical lysine residue of the enzyme is involved in the inhibition of delta-ALA-D by hexoses.

The effect of parboiled rice (PR) and white rice (WR) diets on oxidative stress (OS) parameters was investigated in the kidneys of rats with streptozotocin-induced diabetes (40 mg kg(-1), iv). The experimental groups (n=8) were control fed with PR (CPR), control fed with WR, diabetic fed with PR, and diabetic fed with WR. After 30 days of treatment, all animals were anesthetized and exsanguinated before removal of kidneys, which were used to determine thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides, carbonyl protein, superoxide dismutase, catalase, glutathione peroxidase (GPx), glutathione reductase, glutathione-S-transferase activities, and levels of glutathione (GSH). Total phenolic compounds were determined in WR and PR grains. Our data indicated that diabetes induced increase in TBARS and lipid hydroperoxides levels. Although PR has not prevented the rise in the levels of these measurements, its consumption by our animals resulted in higher GPx activity and GSH content than that of the CPR. Moreover, PR also presented concentration of total phenolic compounds 127% higher than WR grains. Thus, its consumption in this diabetic condition is suggested because this seems to confer greater protection against OS in the renal tissue of diabetic animals.

This study aimed to evaluate oxidative stress parameters in juvenile tambaqui (Colossoma macropomum) exposed to 3.88 mg l(-1) Mn(2+) for 96 hours. Biomarkers of oxidative stress, such as thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase (CAT), and glutathione-S-transferase (GST) activities, as well as content of reduced glutathione (GSH), were analyzed in gill, liver, brain, and kidney. The presence of Mn(2+) in the water corresponded to increased levels of Mn(2+) accumulation according to the following sequence: gill > kidney > brain > liver. There was a significant increase in TBARS levels (40 %) and SOD activity (80 %) in addition to a significant decrease in GSH content (41 %) in gills of fish exposed to waterborne Mn(2+). In hepatic tissue of the exposed animals, TBARS levels decreased significantly (35 %), whereas SOD (82 %) and GST activities (51 %) as well as GSH content (43 %) increased significantly. In brain of exposed juvenile fish, only significant decreases in SOD (32 %) and CAT activities (65 %) were observed. Moreover, the kidney of exposed fish showed a significant increase in TBARS levels (53 %) and a significant decrease in SOD activity (41 %) compared with the control. Thus, the changes in biomarkers of oxidative stress were different in the tissues, showing a specific toxicity of this metal to each organ.