Effects of α-ketoglutarate on antioxidants and lipid peroxidation products in rats treated with ammonium acetate

Velvizhi, S.; Dakshayani, Kadiyala Babu; Subramanian, Perumal

doi:10.1016/s0899-9007(02)00825-0

Cited by 66 publications

(61 citation statements)

References 13 publications

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“…Kosenko et al [4] suggested ammonia toxicity as an alternate mechanism for the involvement of free radicals and oxidative damage. GPx, GSH and Vit-E (enzymatic and nonenzymatic antioxidant) are involved in reducing ammonia toxicity and the production of free radicals [64,65]. We suggested that SeMet and SeMet+Vit-E might protect against the oxidative damage of ammonia.…”

Section: Discussionmentioning

confidence: 99%

Selenium and Vitamin E Improve the <i>In Vitro</i> Maturation, Fertilization and Culture to Blastocyst of Porcine Oocytes

et al. 2012

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Abstract. Selenium (Se) and vitamin E (Vit-E), as integral parts of antioxidant systems, play important roles for sperm and embryos in vitro. In this study, the effects of Se and Vit-E on the maturation, in vitro fertilization and culture to blastocysts of porcine oocytes and accumulation of ammonia in the culture medium during different development stages were investigated. The maturation was performed in modified tissue culture medium (mTCM)-199 supplemented with 10% (v/v) porcine follicular fluid, the fertilization medium was modified Tyrode's albumin lactate pyruvate (mTALP), and the embryo culture medium was modified North Carolina State University (mNCSU)-23. Se in the form of sodium selenite (SS) and seleon-L-methionine (SeMet) and Vit-E at different concentrations were also used. The incorporation and oxidation of 14 C(U)-glucose were assessed with a liquid scintillation counter. In this study, SeMet and SeMet+Vit-E increased oocyte maturation, fertilization and incorporation and oxidation of 14 C(U)-glucose significantly (P<0.05) compared with the control and other treatments. In addition, embryo development, specifically in terms of the numbers of morulae and blastocysts, significantly increased (P<0.05) with SeMet and SeMet+Vit-E. In contrast, the accumulation of ammonia was reduced with SeMet and SeMet+Vit-E compared with other treatments. These findings indicate that SeMet and SeMet+Vit-E may play important roles in reducing the accumulation of ammonia and subsequently in increasing the rate of maturation of porcine oocytes and fertilization, as well as development of the blastocyst and utilization of glucose in in vitro maturation, fertilization and culture to blastocysts of porcine oocytes.

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Section: Discussionmentioning

confidence: 99%

Selenium and Vitamin E Improve the <i>In Vitro</i> Maturation, Fertilization and Culture to Blastocyst of Porcine Oocytes

et al. 2012

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“…13,19,20,24,25 In accordance with our findings, various studies have previously shown that administration of antioxidants such as alpha tocopherol (vitamin E) decrease the high oxidative stress and the biochemical signs of liver damage. 2,19,[24][25][26][27][28][29][30] Melatonin (N-acetyl-5-methoxytryptamine) is one of the main secretory products of the pineal gland and is also produced or found in other organs and body fluids. 31 This indolamine protects DNA, proteins and biological membrane lipids from the deleterious effects of free radicals, without the need for a specific receptor on cells.…”

Section: Discussionmentioning

confidence: 99%

Comparison of melatonin, vitamin E and L‐carnitine in the treatment of neuro‐ and hepatotoxicity induced by thioacetamide

Túnez

Muñoz

Medina

et al. 2005

Cell Biochemistry & Function

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This study was designed to evaluate and compare the effect of melatonin, vitamin E and L-carnitine on brain and liver oxidative stress and liver damage. Oxidative stress and hepatic failure were produced by a single dose of thioacetamide (TAA) (150 mg kg(-1)) in Wistar rats. A dose of either melatonin (3 mg kg(-1)) vitamin E (20 mg kg(-1) ) or L-carnitine (100 mg kg(-1)) was used. Blood samples were taken from the neck vasculature in order to determine ammonium, blood urea nitrogen (BUN) and liver enzymes. Lipid peroxidation products, glutathione (GSH) content and antioxidative enzymes were determined in cerebral and hepatic homogenates. The results showed a decrease in BUN and in the antioxidant enzymes activities and GSH in the brain and liver. Likewise, TAA induced significant enhancement of lipid peroxidation products levels in both liver and brain, as well as in ammonia values. Melatonin, vitamin E and L-carnitine, although melatonin more significantly, decreased the intensity of the changes produced by the administration of TAA alone. Furthermore melatonin combined with TAA, decreased the ammonia levels and increased the BUN values compared with TAA animals. Also it was more effective than vitamin E or L-carnitine in these actions. These data show the protective effect of these agents, especially melatonin, against oxidative stress and hepatic damage present in fulminant hepatic failure.

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“…Increasing data from the literature have indicated that a-ketoglutarate, an intermediate of Krebs cycle, can inhibit oxidative stress in vitro when induced by hydrogen peroxide in human erythrocytes (1) and cultured striatal neurons (2), and after in vivo treatment with ammonium acetate (3) or chronic ethanol administration (4). In the same way, a-ketoglutarate and oxaloacetate can prevent damage to mitochondrial DNA and seizures induced by kainic acid in mice (5).…”

Section: Introductionmentioning

confidence: 99%

Krebs Cycle Intermediates Modulate Thiobarbituric Acid Reactive Species (TBARS) Production in Rat Brain In Vitro

2005

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The aim of this study was to investigate the effect of Krebs cycle intermediates on basal and quinolinic acid (QA)- or iron-induced TBARS production in brain membranes. Oxaloacetate, citrate, succinate and malate reduced significantly the basal and QA-induced TBARS production. The potency for basal TBARS inhibition was in the order (IC50 is given in parenthesis as mM) citrate (0.37) > oxaloacetate (1.33) = succinate (1.91) > > malate (12.74). alpha-Ketoglutarate caused an increase in TBARS production without modifying the QA-induced TBARS production. Cyanide (CN-) did not modify the basal or QA-induced TBARS production; however, CN- abolished the antioxidant effects of succinate. QA-induced TBARS production was enhanced by iron ions, and abolished by desferrioxamine (DFO). The intermediates used in this study, except for alpha-ketoglutarate, prevented iron-induced TBARS production. Oxaloacetate, citrate, alpha-ketoglutarate and malate, but no succinate and QA, exhibited significantly iron-chelating properties. Only alpha-ketoglutarate and oxaloacetate protected against hydrogen peroxide-induced deoxyribose degradation, while succinate and malate showed a modest effect against Fe2+/H2O2-induced deoxyribose degradation. Using heat-treated preparations citrate, malate and oxaloacetate protected against basal or QA-induced TBARS production, whereas alpha-ketoglutarate induced TBARS production. Succinate did not offer protection against basal or QA-induced TBARS production. These results suggest that oxaloacetate, malate, succinate, and citrate are effective antioxidants against basal and iron or QA-induced TBARS production, while alpha-ketoglutarate stimulates TBARS production. The mechanism through which Krebs cycle intermediates offer protection against TBARS production is distinct depending on the intermediate used. Thus, under pathological conditions such as ischemia, where citrate concentrations vary it can assume an important role as a modulator of oxidative stress associated with such situations.

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Effects of α-ketoglutarate on antioxidants and lipid peroxidation products in rats treated with ammonium acetate

Cited by 66 publications

References 13 publications

Selenium and Vitamin E Improve the <i>In Vitro</i> Maturation, Fertilization and Culture to Blastocyst of Porcine Oocytes

Selenium and Vitamin E Improve the <i>In Vitro</i> Maturation, Fertilization and Culture to Blastocyst of Porcine Oocytes

Comparison of melatonin, vitamin E and L‐carnitine in the treatment of neuro‐ and hepatotoxicity induced by thioacetamide

Krebs Cycle Intermediates Modulate Thiobarbituric Acid Reactive Species (TBARS) Production in Rat Brain In Vitro

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