Vascular redox imbalance in rats submitted to chronic exercise.

Exercise training has been used for treatment/prevention of many cardiovascular diseases, but the mechanisms need to be clarified. Thus, our aim was to compare oxidative stress parameters between rats submitted to a swimming training and sedentary rats (control). Twelve male rats were divided into two groups: control and exercise training.

Pharmacological doses of vitamin A increase caspase-3 activity selectively in cerebral cortex.

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.

Vitamin A supplementation at pharmacological doses induces nitrosative stress on the hypothalamus of adult Wistar rats.

Vitamin A is a micronutrient involved in the regulation of a normal mammalian brain function. In spite of this, it has been demonstrated that vitamin A exerts a wide range of deleterious effects regarding neuronal homeostasis, for instance impairing brain metabolism and suppressing neurogenesis, to cite a few. In addition, vitamin A is a redox active molecule, i.

Increased receptor for advanced glycation endproducts immunocontent in the cerebral cortex of vitamin A-treated rats.

Vitamin A, beyond its biological role, is an alternative choice in treating some life threatening pathologies, for instance leukemia and immunodeficiency. On the other hand, vitamin A therapy at moderate to high doses has caused concern among public health researchers due to the toxicological aspect resulting from such habit. It has been described hepatotoxicity, cognitive disturbances and increased mortality rates among subjects ingesting increased levels of vitamin A daily.

Modulation in reproductive tissue redox profile in sexually receptive female rats after short-term exposure to male chemical cues.

It is well known that antioxidants play an important role in sperm fertility, but there is no data on the literature regarding the effect of male chemical cues in the antioxidant defenses of the female reproductive tract. Here, we evaluated oxidative parameters in ovaries and uterus of virgin female rats isolated from contact to males and exposed only to male-soiled bedding (MSB). Four-month-old Wistar (regular 4-day cyclic) virgin female rats were utilized from proestrus to estrus phase of the reproductive cycle for experimental exposure.

Evaluation of the effects of vitamin A supplementation on adult rat substantia nigra and striatum redox and bioenergetic states: mitochondrial impairment, increased 3-nitrotyrosine and alpha-synuclein, but decreased D2 receptor contents.

Vitamin A at moderate to high doses is applied in the treatment of some life threatening pathological conditions, for instance cancers. Additionally, vitamin A at low concentrations is a known antioxidant molecule. However, by increasing vitamin A (or its derivatives) concentrations, there is an increase in the levels of oxidative stress markers in several experimental models.

Decreased anxiety-like behavior and locomotor/exploratory activity, and modulation in hypothalamus, hippocampus, and frontal cortex redox profile in sexually receptive female rats after short-term exposure to male chemical cues.

Chemical cues are widely used for intraspecific social communication in a vast majority of living organisms ranging from bacteria to mammals. As an example, mammals release olfactory cues with urine that promote neuroendocrine modulations with changes in behavior and physiology in the receiver. In this work, four-month-old Wistar (regular 4-day cyclic) virgin female rats were utilized in the proestrus-to-estrus phase of the reproductive cycle for experimental exposure.

Short-term vitamin A supplementation at therapeutic doses induces a pro-oxidative state in the hepatic environment and facilitates calcium-ion-induced oxidative stress in rat liver mitochondria independently from permeability transition pore formation : detrimental effects of vitamin A supplementation on rat liver redox and bioenergetic states homeostasis.

There is a growing body of evidence showing that vitamin A induces toxic effects in several experimental models and in human beings. In the present work, we have investigated the effects of short-term vitamin A supplementation on the adult rat liver redox status. We have found that vitamin A at therapeutic doses induces a hepatic oxidative insult.

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

Vitamin A and its derivatives, the retinoids, exert modulatory roles on central nervous system (CNS) function. However, the clinical use of vitamin A at moderate to high doses induces serious side effects, including dysfunctional brain metabolism and mood disorders. Then, we have investigated in this work the effects of vitamin A supplementation at 1000, 2500, 4500, or 9000IU/kg/day for 28 days on redox and bioenergetics parameters in adult rat frontal cortex.