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Suppression of External NADPH Dehydrogenase-NDB1 in Arabidopsis thaliana Confers Improved Tolerance to Ammonium Toxicity via Efficient Glutathione/Redox Metabolism.
Podgórska, A, Ostaszewska-Bugajska, M, Borysiuk, K, Tarnowska, A, Jakubiak, M, Burian, M, Rasmusson, AG, Szal, B
International journal of molecular sciences. 2018;(5)
Abstract
Environmental stresses, including ammonium (NH₄⁺) nourishment, can damage key mitochondrial components through the production of surplus reactive oxygen species (ROS) in the mitochondrial electron transport chain. However, alternative electron pathways are significant for efficient reductant dissipation in mitochondria during ammonium nutrition. The aim of this study was to define the role of external NADPH-dehydrogenase (NDB1) during oxidative metabolism of NH₄⁺-fed plants. Most plant species grown with NH₄⁺ as the sole nitrogen source experience a condition known as “ammonium toxicity syndrome”. Surprisingly, transgenic Arabidopsis thaliana plants suppressing NDB1 were more resistant to NH₄⁺ treatment. The NDB1 knock-down line was characterized by milder oxidative stress symptoms in plant tissues when supplied with NH₄⁺. Mitochondrial ROS accumulation, in particular, was attenuated in the NDB1 knock-down plants during NH₄⁺ treatment. Enhanced antioxidant defense, primarily concerning the glutathione pool, may prevent ROS accumulation in NH₄⁺-grown NDB1-suppressing plants. We found that induction of glutathione peroxidase-like enzymes and peroxiredoxins in the NDB1-surpressing line contributed to lower ammonium-toxicity stress. The major conclusion of this study was that NDB1 suppression in plants confers tolerance to changes in redox homeostasis that occur in response to prolonged ammonium nutrition, causing cross tolerance among plants.
2.
Green tea supplementation increases glutathione and plasma antioxidant capacity in adults with the metabolic syndrome.
Basu, A, Betts, NM, Mulugeta, A, Tong, C, Newman, E, Lyons, TJ
Nutrition research (New York, N.Y.). 2013;(3):180-7
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Abstract
Green tea, a popular polyphenol-containing beverage, has been shown to alleviate clinical features of the metabolic syndrome. However, its effects in endogenous antioxidant biomarkers are not clearly understood. Thus, we tested the hypothesis that green tea supplementation will upregulate antioxidant parameters (enzymatic and nonenzymatic) in adults with the metabolic syndrome. Thirty-five obese participants with the metabolic syndrome were randomly assigned to receive one of the following for 8 weeks: green tea (4 cups per day), control (4 cups water per day), or green tea extract (2 capsules and 4 cups water per day). Blood samples and dietary information were collected at baseline (0 week) and 8 weeks of the study. Circulating carotenoids (α-carotene, β-carotene, lycopene) and tocopherols (α-tocopherol, γ-tocopherol) and trace elements were measured using high-performance liquid chromatography and inductively coupled plasma mass spectroscopy, respectively. Serum antioxidant enzymes (glutathione peroxidase, glutathione, catalase) and plasma antioxidant capacity were measured spectrophotometrically. Green tea beverage and green tea extract significantly increased plasma antioxidant capacity (1.5 to 2.3 μmol/L and 1.2 to 2.5 μmol/L, respectively; P < .05) and whole blood glutathione (1783 to 2395 μg/g hemoglobin and 1905 to 2751 μg/g hemoglobin, respectively; P < .05) vs controls at 8 weeks. No effects were noted in serum levels of carotenoids and tocopherols and glutathione peroxidase and catalase activities. Green tea extract significantly reduced plasma iron vs baseline (128 to 92 μg/dL, P < .02), whereas copper, zinc, and selenium were not affected. These results support the hypothesis that green tea may provide antioxidant protection in the metabolic syndrome.
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The effects of high walnut and cashew nut diets on the antioxidant status of subjects with metabolic syndrome.
Davis, L, Stonehouse, W, Loots, du T, Mukuddem-Petersen, J, van der Westhuizen, FH, Hanekom, SM, Jerling, JC
European journal of nutrition. 2007;(3):155-64
Abstract
BACKGROUND Nut consumption is associated with a protective effect against coronary heart disease, partly due to its high antioxidant content. It is hypothesized that the inclusion of nuts in the diet will improve the antioxidant status of subjects with metabolic syndrome who may be vulnerable to impaired antioxidant status. AIM: The effects of high cashew nut and high walnut diets on the antioxidant status of subjects with metabolic syndrome are investigated. METHODOLOGY Sixty-four volunteers (29 male and 35 female, 45 +/- 10y) with metabolic syndrome (diagnosed by using the ATP III criteria) received a prudent control diet, prepared in the metabolic kitchen of the North-West University, Potchefstroom campus (NWU-PC) for a period of 3 weeks (run-in). The participants were grouped according to gender and age and randomized into three groups, receiving either the walnut, cashew nut or the control diets for 8 weeks, while maintaining a stable body weight. Nuts provided 20% of daily energy intake. Fasting blood samples were taken after the run-in period (baseline) and at the end of the intervention period and analyzed for various antioxidant capacity markers. RESULTS The oxygen radical absorbance capacity (ORAC) of the walnut and cashew nut diets were significantly higher than the control diet. Despite this, the walnut and cashew nut diets had no significant effects on serum ORAC, reduced (GSH), oxidized (GSSG) glutathione, GSH:GSSG or diacron reactive metabolites (dRom) (total oxidant status) levels compared to the control group. However, all three groups showed significant improvements in antioxidant status from baseline to end (GSSG and dRom levels decreased; GSG:GSSG ratio and ORAC levels increased). This may be due to a general increased antioxidant intake from the prudent diet compared to the habitual diets. CONCLUSION Although the inclusion of walnuts and cashew nuts into a prudent diet resulted in an increased antioxidant capacity (ORAC) of the nut diets, compared to the control diet, it did not improve the serum antioxidant profiles of subjects with metabolic syndrome.