Reduction of energy metabolism in rat hippocampus by arginine administration

Delwing, Débora; Tagliari, Bárbara; Streck, Emílio L.; Wannamacher, Clovis Milton Duval; Wajner, Moaçir; Wyse, Ângela T. S.

doi:10.1016/s0006-8993(03)03029-4

Cited by 25 publications

(29 citation statements)

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“…Results showed that acute administration of Arg significantly reduced glucose uptake and increased lactate production in rat cerebellum, indicating that Arg compromised aerobic glycolysis (lower glucose uptake) and increased anaerobic glycolysys (higher lactate release from glucose). These results are in agreement with our previous study showing that Arg administration impairs the same parameters of energy metabolism in rat hippocampus (Delwing et al, 2003).…”

Section: Discussionsupporting

confidence: 94%

“…In addition, it has been demonstrated that inhibition of NOS ameliorates striatal damage caused by malonate (Maragos and Silverstein, 1995), is neuroprotective against cerebral ischemia (Carreau et al, 1994;Ding-Zhou et al, 2002) and prevents rats and mice against convulsions (Bitterman and Bitterman, 1998;Demchenko et al, 2000;Demchenko et al, 2003;Oury et al, 1992;Zhang et al, 1993), which are thought to be caused by peroxynitrite generated from NO. Similarly, we have previously demonstrated that L-NAME, an inhibitor of NOS, prevents the reduction of Na + , K + -ATPase, acetylcholinesterase, catalase, energy metabolism Delwing et al, 2003;Reis et al, 2002;Wyse et al, 2001;Wyse et al, 2004), as well as memory impairment in rats provoked by Arg administration (Reis et al, 2002).…”

Section: Discussionmentioning

confidence: 59%

“…In this context, we have shown that Arg administration impairs energy metabolism in rat hippocampus that was prevented by co-administration of N ω -nitro-L-arginine methyl ester (L-NAME), a competitive inhibitor of NOS (Delwing et al, 2003). We have also demonstrated that Arg administration to rats increases lipid peroxidation and decreases the nonenzymatic antioxidant defenses, and that these effects were prevented by L-NAME (Wyse et al, 2001) and α-tocopherol and ascorbic acid (Bavaresco et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

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α-Tocopherol and Ascorbic Acid Administration Prevents the Impairment of Brain Energy Metabolism of Hyperargininemic Rats

et al. 2006

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1. We have previously demonstrated that arginine administration induces oxidative stress and compromises energy metabolism in rat hippocampus. In the present study we initially investigated the influence of pretreatment with alpha-tocopherol and ascorbic acid on the effects produced by arginine on hippocampus energy metabolism. We also tested the effect of acute administration of arginine on various parameters of energy metabolism, namely glucose uptake, lactate release and on the activities of succinate dehydrogenase, complex II and cytochrome c oxidase in rat cerebellum, as well as the influence of pretreatment with alpha-tocopherol and ascorbic acid on the effects elicited by arginine on this structure. 2. Sixty-day-old female Wistar rats were treated with a single i.p. injection of saline (control) or arginine (0.8 g/kg) and were killed 1 h later. In another set of experiments, the animals were pretreated for 1 week with daily i.p. administration of saline (control) or alpha-tocopherol (40 mg/kg) and ascorbic acid (100 mg/kg). Twelve hours after the last injection of the antioxidants the rats received one i.p. injection of arginine (0.8 g/kg) or saline and were killed 1 h later. 3. Results showed that arginine administration significantly increased lactate release and diminished glucose uptake and the activities of succinate dehydrogenase and complex II in rat cerebellum. In contrast, complex IV (cytochrome c oxidase) activity was not changed by this amino acid. Furthermore, pretreatment with alpha-tocopherol and ascorbic acid prevented the impairment of energy metabolism caused by hyperargininemia in cerebellum and hippocampus of rats.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 59%

Section: Introductionmentioning

confidence: 99%

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α-Tocopherol and Ascorbic Acid Administration Prevents the Impairment of Brain Energy Metabolism of Hyperargininemic Rats

et al. 2006

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“…l-Arginine is a substrate for NOS, and increased l-arginine levels have been associated with increased NO production (Buchmann et al 1996; Wu and Morris 1998). l-Arginine has been shown to induce oxidative stress (Wyse et al 2001) and decrease energy metabolism in brain (Delwing et al 2003). l-Arginine-induced oxidative stress has been shown to inhibit the activity of Na + , K + -ATPase (dos Reis et al 2002;da Silva et al 1999), a transporter which is vital to maintain neuronal excitability (Delwing et al 2008).…”

Section: Pathophysiology and Pathobiochemistrymentioning

confidence: 99%

Hyperargininemia due to arginase I deficiency: the original patients and their natural history, and a review of the literature

et al. 2015

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Hyperargininemia is caused by deficiency of arginase 1, which catalyzes the hydrolysis of L-arginine to urea as the final enzyme in the urea cycle. In contrast to other urea cycle defects, arginase 1 deficiency usually does not cause catastrophic neonatal hyperammonemia but rather presents with progressive neurological symptoms including seizures and spastic paraplegia in the first years of life and hepatic pathology, such as neonatal cholestasis, acute liver failure, or liver fibrosis. Some patients have developed hepatocellular carcinoma. A usually mild or moderate hyperammonemia may occur at any age. The pathogenesis of arginase I deficiency is yet not fully understood. However, the accumulation of L-arginine and the resulting abnormalities in the metabolism of guanidine compounds and nitric oxide have been proposed to play a major pathophysiological role. This article provides an update on the first patients ever described, gives an overview of the distinct clinical characteristics, biochemical as well as genetical background and discusses treatment options.

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“…In this context, we have demonstrated that Arg administration decreases the activities of the enzymes Na + ,K + -ATPase [24] and acetylcholinesterase [25] in rat brain. We also have reported that Arg acute administration reduces energy metabolism in hippocampus and cerebellum of rats [26,27] and impairs memory of rats [17]. Some of these results were Fig.…”

Section: Discussionmentioning

confidence: 77%

NTPDase and 5′-nucleotidase Activities of Synaptosomes from Hippocampus of Rats Subjected to Hyperargininemia

et al. 2007

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ATP is an important excitatory neurotransmitter and adenosine acts as a neuromodulatory structure inhibiting neurotransmitters release in the central nervous system. Since the ecto-nucleotidase cascade that hydrolyzes ATP to adenosine is involved in the control of brain functions and previous studies realized in our laboratory have recently reported that acute administration of Arg decreases the NTPDase and 5'-nucleotidase activities of rat blood serum, in the present study we investigated the effect of arginine administration on NTPDase and 5'-nucleotidase activities by synaptosomes from hippocampus of rats. First, sixty-days-old rats were treated with a single or a triple intraperitoneal injection of arginine (0.8 g/Kg) or an equivalent volume of 0.9% saline solution (control) and were killed 1 h later. Second, rats received an intracerebroventricular injection of 1.5 mM arginine solution or saline (5 microL) and were killed 1 h later. We also tested the in vitro effect of arginine (0.1-1.5 mM) on nucleotide hydrolysis in synaptosomes from rat hippocampus. Results showed that intraperitoneal arginine administration did not alter nucleotide hydrolysis. On the other hand, arginine administered intracerebroventricularly reduced ATP (32%), ADP (30%) and AMP (21%) hydrolysis, respectively. In addition, arginine added to the incubation medium, provoked a decrease on ATP (19%), ADP (17%) and AMP (23%) hydrolysis, respectively. Furthermore, kinetic studies showed that the inhibitory effect of arginine was uncompetitive in relation to ATP, ADP and AMP. In conclusion, according to our results it seems reasonable to postulate that arginine alters the cascade involved in the extracellular degradation of ATP to adenosine.

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Reduction of energy metabolism in rat hippocampus by arginine administration

Cited by 25 publications

References 26 publications

α-Tocopherol and Ascorbic Acid Administration Prevents the Impairment of Brain Energy Metabolism of Hyperargininemic Rats

α-Tocopherol and Ascorbic Acid Administration Prevents the Impairment of Brain Energy Metabolism of Hyperargininemic Rats

Hyperargininemia due to arginase I deficiency: the original patients and their natural history, and a review of the literature

NTPDase and 5′-nucleotidase Activities of Synaptosomes from Hippocampus of Rats Subjected to Hyperargininemia

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