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Citation |
de Oliveira MR, da Rocha RF, Schnorr CE, Moreira JCF. Fundam. Clin. Pharmacol. 2012; 26(4): 513-529. |
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Copyright |
(Copyright © 2012, John Wiley and Sons) |
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DOI |
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PMID |
21521362 |
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Abstract |
Vitamin A has been characterized as a potential neurotoxin, because ingestion of such vitamin - or its derivatives, the retinoids - at moderate to high doses elicits a myriad of deleterious effects, from acute intoxication involving head-ache, confusion, and 'pseudo tumor cerebri' to chronic, and perhaps irreversible, abnormalities, including irritability, anxiety, depression, and suicide ideation. Nevertheless, it still remains to be found the mechanism by which vitamin A induces cognitive decline. Based on the fact that vitamin A at clinical doses is a potent pro-oxidant agent to the central nervous system, we performed the present work to analyze whether a cotreatment with L-NAME at 30 mg/kg (four times a week) was able to prevent (or minimize) the biochemical and/or behavioral disturbances resulting from a 28-day daily supplementation with retinol palmitate at doses from 1000 to 9000 IU/kg/day. Then, we investigated mitochondrial function, redox parameters, and the levels of proteins potentially involved in neurodegenerative events, as for instance α-synuclein and receptor for advanced glycation endproducts. Besides, monoamine oxidase enzyme activity was quantified in this work. We observed that L-NAME cotreatment was not completely effective in preventing the redox disturbances induced by vitamin A supplementation. Moreover, L-NAME cotreatment did not affect the behavioral deficits elicited by vitamin A supplementation. We conclude that other parameters rather than NO levels or its derivatives, as for example ONOO(-), take a more important role in mediating the negative effects triggered by vitamin A supplementation. Language: en |
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Keywords |
Male; Animals; Rats; Anxiety Disorders; Central Nervous System; Mitochondria; Manganese; Oxidation-Reduction; Neurodegenerative Diseases; Vitamin A; Tyrosine; Monoamine Oxidase; Receptors, Dopamine; Behavior, Animal; Dietary Supplements; Glutathione Transferase; Superoxide Dismutase; Rats, Wistar; Nitric Oxide; Locomotion; Electron Transport; Superoxides; NG-Nitroarginine Methyl Ester; Diterpenes; Illness Behavior; alpha-Synuclein; Heat-Shock Proteins; Receptor for Advanced Glycation End Products; Receptors, Immunologic; Retinyl Esters |