Vitamin A supplementation at clinical doses induces a dysfunction in the redox and bioenergetics states, but did change neither caspases activities nor TNF-α levels in the frontal cortex of adult Wistar rats

Increased blood oxidative stress in experimental menopause rat model: the effects of vitamin A low‐dose supplementation upon antioxidant status in bilateral ovariectomized rats

“…Therefore, in our own breeding colony, the dietary consumption of vitamin A in food is around to 375–625 IU per rat. In addition, several works originating within our research group demonstrated that vitamin A supplementation in higher doses (up to 2500 IU/kg/day) potentially induces dysfunctions in the redox and bioenergetics states of different tissues in healthy male rats [66–69]. It is important to emphasize that here we tested the supplementation of vitamin A in a totally distinct rat model, with clearly noticeable gender and physiological differences being considered.…”

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

“…Indeed, we have experimentally demonstrated that vitamin A (retinol palmitate) at clinical doses induced anxiety-related behavior in adult Wistar rats. Furthermore, we have observed decreased locomotory and exploratory activities performed by such animals in an open field apparatus [9][10][11][12][13][14][15]. Recently, it was reported decreased brain metabolism in patients subjected to daily retinoid therapy [16] and, more concerning, increased mortality rates among vitamin supplements users even when ingesting low daily vitamin A doses (mainly as retinol palmitate) [17].…”

“…Our research group recently reported that clinical vitamin A doses induced an imbalance in the adult rat hippocampal redox environment [9]. Furthermore, we have observed anxietylike, but not depression-related behavior, in vitamin Atreated rats [15]. However, the exact mechanism behind this effect remains to be elucidated.…”

Increased susceptibility of mitochondria isolated from frontal cortex and hippocampus of vitamin A-treated rats to non-aggregated amyloid-β peptides 1–40 and 1–42

“…Decreased metabolic rates were observed in the cerebral cortex of patients under retinoid treatment against acne (29). In addition, vitamin A supplementation is able to impair METC enzyme activity in vivo, which may give rise to free radical production (3)(4)(5)(6)(7)(8)(9)(10). Nonetheless, it still remains on debate by which mechanisms such vitamin elicits neurotoxicity.…”

“…On the other hand, vitamin A-related toxicity has long been investigated, but the mechanisms by which it acts are not completely understood (2). We have shown that vitamin A supplementation at pharmacological doses induces a pro-oxidant effect in some rat brain regions and impaired rat performance in different behavioural tests (3)(4)(5)(6)(7)(8)(9)(10). We have shown that vitamin A supplementation at pharmacological doses induces a pro-oxidant effect in some rat brain regions and impaired rat performance in different behavioural tests (3)(4)(5)(6)(7)(8)(9)(10).…”