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Pharmacological doses of vitamin A increase caspase‐3 activity selectively in cerebral cortex
Author(s) -
De Oliveira Marcos Roberto,
Oliveira Max William Soares,
Moreira José Cláudio Fonseca
Publication year - 2010
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.2009.00789.x
Subject(s) - hippocampus , cerebral cortex , striatum , vitamin , caspase , vitamin d and neurology , caspase 3 , cortex (anatomy) , apoptosis , biology , medicine , endocrinology , programmed cell death , neuroscience , biochemistry , dopamine
Vitamin A exerts a wide range of physiological roles from embryonic to adulthood stages of the mammalian life. However, there is a great concern regarding the deleterious effects of vitamin A use even therapeutically. It was shown that vitamin A induces behavioral impairments, for instance, anxiety‐like behavior and depression, in experimental animals and humans. Caspases are enzymes associated with cell death; however, there is a role for such enzymes also in synaptic plasticity. Then, based on previously published data, we have investigated the effects of vitamin A supplementation at clinical doses (1000–9000 IU/kg/day) for 28 days on caspase‐3 and caspase‐8 activities in adult rat cerebral cortex, cerebellum, striatum, and hippocampus. Furthermore, we have quantified TNF‐α levels, a pro‐inflammatory cytokine that, besides other biological roles, trigger the extrinsic apoptotic pathway in several cellular types, in those rat brain regions. Interestingly, we found increased caspase‐3 activity only in rat cerebral cortex. In all the other regions caspase‐3 and caspase‐8 activities did not change, as well as the levels of TNF‐α. The presented results, herein, indicate that more caution is needed regarding vitamin A clinical use and, also importantly, the consumption of vitamin A‐fortified foods, which are not exclusively distributed among vitamin A‐deficient subjects.