α-Tocopherol and ascorbic acid prevent memory deficits provoked by chronic hyperprolinemia in rats

Delwing, Débora; Bavaresco, Caren Serra; Monteiro, Siomara da Cruz; Matté, Cristiane; Netto, Carlos Alexandre; Wyse, Ângela T. S.

doi:10.1016/j.bbr.2005.08.014

Cited by 32 publications

(27 citation statements)

References 27 publications

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“…It was previously shown [8,9] that rats submitted to experimental hyperprolinemia in early life, during the period characterized by rapid brain development [5][6][7], presented cognitive deficits in adulthood, as assessed in the Morris water maze. We have here demonstrated that both protocols of experimental hyperprolinemia, namely partial time and full time hyperprolinemia, produced reference and working memory deficits, and confirming the working hypothesis, forced treadmill exercise training was able to prevent such deficits.…”

Section: Discussionmentioning

confidence: 99%

“…Considering that HP is an inherited disease, the animal model of hyperprolinemia was designed to sustain high levels of proline from the earliest days of life, comprising the period of rapid brain development with intense synaptogenesis and myelination in rats, which finalizes approximately at 21 days of life [5][6][7]. Rats chronically treated with proline following such experimental model present acquisition and memory deficits, as assessed in the Morris water maze, when they reach adulthood (approximately 30 days after the interruption of proline administration) [8,9].…”

Section: Introductionmentioning

confidence: 99%

“…The first protocol was designed to evaluate whether the exercise is able to recover the cognitive deficit already established by hyperprolinemia during the critical period of brain development [8,9], while the second protocol was performed to verify whether the putative beneficial cognitive effects of exercise would remain if hyperprolinemia is extended through adulthood. Furthermore, BDNF immunocontent and AChE activity were determined in cerebral cortex and the hippocampus, two cerebral structures known to participate in learning/memory modulation in experimental rats.…”

Section: Introductionmentioning

confidence: 99%

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Physical Exercise Reverses Cognitive Impairment in Rats Subjected to Experimental Hyperprolinemia

et al. 2011

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This study investigated whether physical exercise would reverse proline-induced performance deficits in water maze tasks, as well as its effects on brain-derived neurotrophic factor (BDNF) immunocontent and brain acetylcholinesterase (AChE) activity in Wistar rats. Proline administration followed partial time (6th-29th day of life) or full time (6th-60th day of life) protocols. Treadmill exercise was performed from 30th to 60th day of life, when behavioral testing was started. After that, animals were sacrificed for BDNF and AChE determination. Results show that proline impairs cognitive performance, decreases BDNF in cerebral cortex and hippocampus and increases AChE activity in hippocampus. All reported effects were prevented by exercise. These results suggest that cognitive, spatial learning/memory, deficits caused by hyperprolinemia may be associated, at least in part, to the decrease in BDNF levels and to the increase in AChE activity, as well as support the role of physical exercise as a potential neuroprotective strategy.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Physical Exercise Reverses Cognitive Impairment in Rats Subjected to Experimental Hyperprolinemia

et al. 2011

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“…By using this animal model, previous works showed that proline provokes several neurotoxic effects in rats, such as memory impairment [Delwing et al, 2006], inhibition of enzymes activities as acetylcholinesterase, Na þ ,K þ -ATPase, and aminotransferases [Pontes et al, 1999;Shanti et al, 2004;Delwing et al, 2005], energy deficit [Delwing et al, 2007;Ferreira et al, 2010], and induction of oxidative stress [Delwing et al, 2003a,b]. Herein, initially was investigated the effect of hyperprolinemia on several parameters of oxidative stress in liver tissue.…”

Section: Discussionmentioning

confidence: 98%

Experimental hyperprolinemia induces mild oxidative stress, metabolic changes, and tissue adaptation in rat liver

Ferreira

Cunha

Machado

et al. 2011

J of Cellular Biochemistry

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The present study investigated the effects of chronic hyperprolinemia on oxidative and metabolic status in liver and serum of rats. Wistar rats received daily subcutaneous injections of proline from their 6th to 28th day of life. Twelve hours after the last injection the rats were sacrificed and liver and serum were collected. Results showed that hyperprolinemia induced a significant reduction in total antioxidant potential and thiobarbituric acid-reactive substances. The activities of the antioxidant enzymes catalase and superoxide dismutase were significantly increased after chronic proline administration, while glutathione (GSH) peroxidase activity, dichlorofluorescin oxidation, GSH, sulfhydryl, and carbonyl content remained unaltered. Histological analyses of the liver revealed that proline treatment induced changes of the hepatic microarchitecture and increased the number of inflammatory cells and the glycogen content. Biochemical determination also demonstrated an increase in glycogen concentration, as well as a higher synthesis of glycogen in liver of hyperprolinemic rats. Regarding to hepatic metabolism, it was observed an increase on glucose oxidation and a decrease on lipid synthesis from glucose. However, hepatic lipid content and serum glucose levels were not changed. Proline administration did not alter the aminotransferases activities and serum markers of hepatic injury. Our findings suggest that hyperprolinemia alters the liver homeostasis possibly by induction of a mild degree of oxidative stress and metabolic changes. The hepatic alterations caused by proline probably do not implicate in substantial hepatic tissue damage, but rather demonstrate a process of adaptation of this tissue to oxidative stress. However, the biological significance of these findings requires additional investigation.

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“…Tierexperimentelle Demenzmodelle [28,29] zeigten für Vitamin C und Vitamin E eine signifikante Schutzwirkung. Auch Menschen scheinen in dieser Hinsicht von Vitamin E zu profitieren: In einer Studie [30] …”

Section: Alzheimer-krankheit Und Demenzunclassified

Vitamin E - Antioxidans «par excellence»

Saller¹,

Römer-Lüthi²,

Brignoli³

et al. 2007

Schweiz Z Ganzheitsmed

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Hintergrund: Der Begriff "Vitamin E" ist ein Oberbegriff fÜr mindestens sieben komplexe fettlÖsliche Vitamine, die unter dem Namen Tocopherole zusammengefasst werden. Tocopherole finden sich besonders in PflanzenÖlen, Weizenkeimen, BlattgemÜse, Eigelb und HÜlsenfrÜchten. Vitamin E ist das wichtigste fettlÖsliche Antioxidans im menschlichen KÖrper. Zielsetzung: Erstellung eines systematischen Review zur klinischen Bedeutung von Vitamin E. Methoden: Systematische Analyse und Bewertung von Humanstudien (prospektive Doppelblindstudien, epidemiologische und retrospektive Studien, kurzfristige biochemische/hÄmatologische Studien ("Surrogate Markers")) der letzten 10 Jahre aus den gÄngigen elektronischen Datenbanken sowie der Angaben von Standardwerken und publizierten Monographien. Ergebnisse und Schlussfolgerungen: Vitamin E verhindert die Verklumpung der BlutplÄttchen und reguliert die AktivitÄt von Enzymen, die an EntzÜndungsreaktionen beteiligt sind. Neuere gross angelegte Studien konnten nicht bestÄtigen, dass durch die Einnahme von Vitamin E das Risiko fÜr Herzkrankheiten oder Krebserkrankungen verringert werden kann. Eine allgemeine NahrungsergÄnzung mit Vitamin E wird deshalb nicht empfohlen. Ob Vitamin E Augenkrankheiten wie der altersbedingten Makuladegeneration oder dem grauen Star vorbeugen beziehungsweise den Krankheitsverlauf verzÖgern kann, lÄsst sich nach dem derzeitigen Stand des Wissens nicht schlÜssig beantworten. Hinweise auf andere Einsatzgebiete mÜssen noch durch grÖssere Studien bestÄtigt werden. Dazu gehÖrt der Einsatz von Vitamin E bei Patienten mit Arteriosklerose, nach Herztransplantation, bei Demenzen sowie bei spezifischen Nervenerkrankungen. Die Einnahme von Vitamin E in hohen Dosen sollte deshalb nur nach RÜcksprache mit dem Arzt erfolgen.

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α-Tocopherol and ascorbic acid prevent memory deficits provoked by chronic hyperprolinemia in rats

Cited by 32 publications

References 27 publications

Physical Exercise Reverses Cognitive Impairment in Rats Subjected to Experimental Hyperprolinemia

Physical Exercise Reverses Cognitive Impairment in Rats Subjected to Experimental Hyperprolinemia

Experimental hyperprolinemia induces mild oxidative stress, metabolic changes, and tissue adaptation in rat liver

Vitamin E - Antioxidans «par excellence»

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