Inhibition of arginase in sheep brain homogenates by some L-amino acids

Reddy, P. U. M.; Rao, J. Venkateswara

doi:10.1007/bf01985654

Cited by 6 publications

(3 citation statements)

References 13 publications

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“…Changes in the aminoacid pool in the brain may also affect arginase activity. Valine, leucine, isoleucine and ornithine all have inhibitory effects on arginase activity [19].…”

Section: Resultsmentioning

confidence: 99%

Effect of caffeine on metabolism of L-arginine in the brain

Nikolić

Bjelaković

Stojanović

2003

Guanidino Compounds in Biology and Medicine

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Methylxanthines are widely consumed because of their stimulating effect primarily on the central nervous system. Their diuretic and respiratory stimulant action is used in clinical medicine. L-Arginine metabolism in the brain is very important for normal brain function. In addition to brain protein synthesis, arginine is a substrate for the production of urea, creatine, nitric oxide, agmatine, glutamic acid, ornithine, proline and polyamines. As known, many of these compounds are very important in brain function. There is no information relating to effects of caffeine on arginine metabolism in the brain, however, there is a lot of new information about arginine metabolism and caffeine action on the central nervous system. So, we have hypothesized the existence of a relationship that may be of interest in understanding mechanisms of caffeine effects on the central nervous system that may have utility in the clinical applications.In our experiment protocol we used male Wistar rats weighing about 200 g. Caffeine was added to the drinking water in gradually increasing amounts, from 2 gil over the first 3 days, to 4 gil over the last 7 days. A control group was given drinking water without caffeine. The level of lipid peroxidation, arginase and diarnine oxidase (DAO) activity in the brain was measured. The results of our study show that arginase and diamine oxidase were decreased in animals treated with caffeine. The level of lipid peroxidation (MDA) was decreased also.The inhibitory effect of caffeine on arginase activity indicates that caffeine provides more arginine for consumption in other metabolic pathways. Considering the central stimulant effects of caffeine and the decreased lipid peroxidation level, it can be assumed that moderate short-term consumption of caffeine may be beneficial for brain function. (Mol Cell Biochem 244: 125-128,2003)

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“…Changes in the aminoacid pool in the brain may also affect arginase activity. Valine, leucine, isoleucine and ornithine all have inhibitory effects on arginase activity [19].…”

Section: Resultsmentioning

confidence: 99%

Effect of caffeine on metabolism of L-arginine in the brain

Nikolić

Bjelaković

Stojanović

2003

Guanidino Compounds in Biology and Medicine

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“…In experiments lasting for 7-8 h, the persistence of the nitrergic relaxation may involve the conversion of Lcitrulline to L-arginine via AS and AL. The cationic amino acid L-lysine has been shown to be an inhibitor of the enzyme arginase that catalyses the hydrolysis of Larginine to L-ornithine [27,28]. It is thus clear that, potentially, there are several ways in which the amino acids might influence the supply of substrate to nNOS.…”

Section: Discussionmentioning

confidence: 98%

The effects of exogenous amino acids on the relaxant responses of pig urethral smooth muscle evoked by stimulation of the inhibitory nitrergic nerves

Durlu

Brading

2004

Pflugers Arch - Eur J Physiol

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Inhibitory innervation of urethral smooth muscle is mediated partly through release of NO. We investigated the mechanisms involved in the supply of the substrate L: -arginine to NO synthase by examining the relaxant response of the muscle to electrical field stimulation (EFS) and the effects of addition of amino acids to the bathing medium. Relaxant responses persisted during hours of repetitive stimulation but were enhanced rapidly by addition of L: -arginine (the "arginine paradox"). Addition of L: -lysine (competes with L: -arginine for transport on the y(+) carrier) and L: -glutamine (competing on the y(+)L carrier) attenuated the enhancement. Enhancement persisted after washing but was reversed by application of L: -lysine, suggesting that exogenous L: -arginine fills an intracellular pool and that L: -lysine can trans-stimulate its efflux from the pool. After prolonged depolarization in high-K(+), Na(+)-free solution the relaxant response became purely nitrergic. Addition of L: -arginine during the exposure continued to enhance the subsequent responses but L: -glutamine added with L: -arginine, could no longer reduce this enhancement. The results show the arginine paradox in inhibitory nerves and suggest the involvement of y(+) and y(+)L carriers in the transport of L: -arginine.

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“…The assay was essentially that of Moore et al [35] modified by adding L-valine to the incubation mixture at a final concentration of 60 mM to inhibit non-specific arginase [36]. Treated supernatant (25 ll) was added to 75 ll of a solution containing (at final concentrations after supernatant addition) 0.75 mM CaCl 2 , 0.5 mM NADPH, 60 mM valine and 120 nM [ 3 H]-L-arginine (0.5 lCi; Sigma-Aldrich, Castle Hill, NSW, Australia).…”

Section: Nos Activitymentioning

confidence: 99%

Inhibition of Nitric Oxide Synthase with 7-Nitroindazole does not Modify Early Metabolic Recovery Following Focal Cerebral Ischemia in Rats

Helps

Sims

2006

Neurochem Res

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Nitric oxide has been strongly implicated in the development of tissue infarction in response to focal cerebral ischemia. Nitric oxide and its derivatives can inhibit components of the electron transport chain, providing a likely target for these substances in ischemic and post-ischemic brain. Lactate content is increased during post-ischemic reperfusion in tissue destined to become infarcted, consistent with impairment of mitochondrial respiration. To investigate the possible involvement of nitric oxide in generating these changes, we have tested the effect of 7-nitroindazole, a nitric oxide synthase (NOS) inhibitor, on the content of lactate and other metabolites during early reperfusion following temporary focal ischemia. This treatment inhibited total NOS by approximately 50%. However, the treatment did not significantly affect the marked increases in lactate in post-ischemic brain nor did it alter the recovery of other energy-related metabolites. These findings indicate that inhibition of oxidative metabolism is probably not the primary site of the deleterious effects of nitric oxide and derivatives during early post-ischemic reperfusion.

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Inhibition of arginase in sheep brain homogenates by some L-amino acids

Cited by 6 publications

References 13 publications

Effect of caffeine on metabolism of L-arginine in the brain

Effect of caffeine on metabolism of L-arginine in the brain

The effects of exogenous amino acids on the relaxant responses of pig urethral smooth muscle evoked by stimulation of the inhibitory nitrergic nerves

Inhibition of Nitric Oxide Synthase with 7-Nitroindazole does not Modify Early Metabolic Recovery Following Focal Cerebral Ischemia in Rats

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