Total and Mitochondrial Nitrosative Stress,Decreased Brain-Derived Neurotrophic Factor (BDNF) Levels and Glutamate Uptake,and Evidence of Endoplasmic Reticulum Stress in the Hippocampus of Vitamin A-Treated Rats |
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Authors: | Marcos Roberto de Oliveira Ricardo Fagundes da Rocha Laura Stertz Gabriel Rodrigo Fries Diogo Losch de Oliveira Flávio Kapczinski José Cláudio Fonseca Moreira |
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Institution: | Centro de Estudos em Estresse Oxidativo (Lab. 32), Departamento de Bioquímica, ICBS, Universidade Federal do Rio Grande do Sul, Av. Ramiro Barcelos, 2600-Anexo, Porto Alegre, RS, CEP 90035-003, Brazil. mrobioq@yahoo.com.br |
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Abstract: | Vitamin A supplementation has caused concern among public health researchers due to its ability in decreasing life quality
from acute toxicological effects to increasing mortality rates among vitamin supplement users. For example, it was described
cognitive decline (i.e. irritability, anxiety, and depression) in patients subjected to long-term vitamin A therapy, as occurs
in cancer treatment. However, the mechanism by which vitamin A affects mammalian cognition is not completely understood. Then,
we performed the present work to investigate the effects of vitamin A supplementation at clinical doses (1,000–9,000 IU/kg day−1) for 28 days on rat hippocampal nitrosative stress levels (both total and mitochondrial), bioenergetics states, brain-derived
neurotrophic factor (BDNF), alpha- and beta-synucleins, BiP and dopamine receptor 2 (D2 receptor) contents, and glutamate
uptake. We observed mitochondrial impairment regarding respiratory chain function: increased complex I-III, but decreased
complex IV enzyme activity. Also, decreased BDNF levels were observed in vitamin A-treated rats. The present data demonstrates,
at least in part, that mitochondrial dysfunction and decreased BDNF and D2 receptors levels, as well as decreased glutamate
uptake may take an important role in the mechanism behind the previously reported cognitive disturbances associated to vitamin
A supplementation. |
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