Proline impairs energy metabolism in cerebral cortex of young rats

Ferreira, Andréa G. K.; Lima, Daniela Delwing-de; Delwing, Débora; Mackedanz, Vanize; Tagliari, Bárbara; Kolling, Janaína; Schuck, Patrícia Fernanda; Wajner, Moaçir; Wyse, Ângela T. S.

doi:10.1007/s11011-010-9193-y

Cited by 21 publications

(12 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…-ATPase and consequently, on glutamate uptake. Results showed that both acute and chronic proline administration increased TBARS, in accordance to our previous data [28,52]. Moreover, guanosine treatment was able to prevent both acute and chronic proline-mediated effects on TBARS.…”

Section: Discussionsupporting

confidence: 91%

Evidence that Hyperprolinemia Alters Glutamatergic Homeostasis in Rat Brain: Neuroprotector Effect of Guanosine

et al. 2011

Self Cite

View full text Add to dashboard Cite

This study investigated the effects of acute and chronic hyperprolinemia on glutamate uptake, as well as some mechanisms underlying the proline effects on glutamatergic system in rat cerebral cortex. The protective role of guanosine on effects mediated by proline was also evaluated. Results showed that acute and chronic hyperprolinemia reduced glutamate uptake, Na(+), K(+)-ATPase activity, ATP levels and increased lipoperoxidation. GLAST and GLT-1 immunocontent were increased in acute, but not in chronic hyperprolinemic rats. Our data suggest that the effects of proline on glutamate uptake may be mediated by lipid peroxidation and disruption of Na(+), K(+)-ATPase activity, but not by decreasing in glutamate transporters. This probably induces excitotoxicity and subsequent energy deficit. Guanosine was effective to prevent most of the effects promoted by proline, reinforcing its modulator role in counteracting the glutamate toxicity. However, further studies are needed to assess the modulatory effects of guanosine on experimental hyperprolinemia.

show abstract

Section: Discussionsupporting

confidence: 91%

Evidence that Hyperprolinemia Alters Glutamatergic Homeostasis in Rat Brain: Neuroprotector Effect of Guanosine

et al. 2011

Self Cite

View full text Add to dashboard Cite

show abstract

“…It should be borne in mind that effects of dietary supplementation with any AA depend on its supplemental dose and the content of other AA in the diet (Ferreira et al 2010; Stipanuk et al 2009; Tan et al 2009a, b). For example, when the basal diet contained no glutamine, proline supplementation had no effect on piglet growth (Chung and Baker 1993).…”

Section: Proline and Hydroxyproline Nutritionmentioning

confidence: 99%

Proline and hydroxyproline metabolism: implications for animal and human nutrition

et al. 2010

View full text Add to dashboard Cite

Proline plays important roles in protein synthesis and structure, metabolism (particularly the synthesis of arginine, polyamines, and glutamate via pyrroline-5-carboxylate), and nutrition, as well as wound healing, antioxidative reactions, and immune responses. On a pergram basis, proline plus hydroxyproline are most abundant in collagen and milk proteins, and requirements of proline for whole-body protein synthesis are the greatest among all amino acids. Therefore, physiological needs for proline are particularly high during the life cycle. While most mammals (including humans and pigs) can synthesize proline from arginine and glutamine/glutamate, rates of endogenous synthesis are inadequate for neonates, birds, and fish. Thus, work with young pigs (a widely used animal model for studying infant nutrition) has shown that supplementing 0.0, 0.35, 0.7, 1.05, 1.4, and 2.1% proline to a proline-free chemically defined diet containing 0.48% arginine and 2% glutamate dose dependently improved daily growth rate and feed efficiency while reducing concentrations of urea in plasma. Additionally, maximal growth performance of chickens depended on at least 0.8% proline in the diet. Likewise, dietary supplementation with 0.07, 0.14, and 0.28% hydroxyproline (a metabolite of proline) to a plant protein-based diet enhanced weight gains of salmon. Based on its regulatory roles in cellular biochemistry, proline can be considered as a functional amino acid for mammalian, avian, and aquatic species. Further research is warranted to develop effective strategies of dietary supplementation with proline or hydroxyproline to benefit health, growth, and development of animals and humans.

show abstract

“…We believe that it is not altered this way because no changes were observed in the activity of the cytochrome c oxidase, a marker of oxidative phosphorylation. Similar results have been shown in other tissues by our group . Creatine plus Hcy maintain the increase in succinate dehydrogenase‐SDH activity.…”

Section: Discussionmentioning

confidence: 99%

“…Impaired energy metabolism may trigger proapoptotic signalling (programmed cell death), oxidative damage to lipids, protein and DNA, and impair mitochondrial DNA repair. 14,15 It has been demonstrated that alterations in energy metabolism seem to be implicated in the pathogenesis of a number of muscle and neurological complications, [16][17][18] metabolic disorders, [19][20][21][22] aging [23][24][25] and neuromuscular diseases. 26,27 Mitochondrial function and structure/integrity is crucial to maintaining the energy supply for optimal function and maintenance of homeostasis in some tissues.…”

Section: Introductionmentioning

confidence: 99%

Homocysteine induces energy imbalance in rat skeletal muscle: Is creatine a protector?

Kolling¹,

Scherer²,

Siebert³

et al. 2012

Cell Biochemistry & Function

Self Cite

View full text Add to dashboard Cite

Homocystinuria is a neurometabolic disease caused by a severe deficiency of cystathionine beta-synthase activity, resulting in severe hyperhomocysteinemia. Affected patients present several symptoms including a variable degree of motor dysfunction. In this study, we investigated the effect of chronic hyperhomocysteinemia on the cell viability of the mitochondrion, as well as on some parameters of energy metabolism, such as glucose oxidation and activities of pyruvate kinase, citrate synthase, isocitrate dehydrogenase, malate dehydrogenase, respiratory chain complexes and creatine kinase in gastrocnemius rat skeletal muscle. We also evaluated the effect of creatine on biochemical alterations elicited by hyperhomocysteinemia. Wistar rats received daily subcutaneous injections of homocysteine (0.3-0.6 µmol/g body weight) and/or creatine (50 mg/kg body weight) from the 6th to the 28th days of age. The animals were decapitated 12 h after the last injection. Homocysteine decreased the cell viability of the mitochondrion and the activities of pyruvate kinase and creatine kinase. Succinate dehydrogenase was increased other evaluated parameters were not changed by this amino acid. Creatine, when combined with homocysteine, prevented or caused a synergistic effect on some changes provoked by this amino acid. Creatine per se or creatine plus homocysteine altered glucose oxidation. These findings provide insights into the mechanisms by which homocysteine exerts its effects on skeletal muscle function, more studies are needed to elucidate them. Although creatine prevents some alterations caused by homocysteine, it should be used with caution, mainly in healthy individuals because it could change the homeostasis of normal physiological functions.

show abstract

Proline impairs energy metabolism in cerebral cortex of young rats

Cited by 21 publications

References 39 publications

Evidence that Hyperprolinemia Alters Glutamatergic Homeostasis in Rat Brain: Neuroprotector Effect of Guanosine

Evidence that Hyperprolinemia Alters Glutamatergic Homeostasis in Rat Brain: Neuroprotector Effect of Guanosine

Proline and hydroxyproline metabolism: implications for animal and human nutrition

Homocysteine induces energy imbalance in rat skeletal muscle: Is creatine a protector?

Contact Info

Product

Resources

About