ABSTRACT
Background: Studies suggest that vitamin A deficiency (VAD) can cause night blindness or xerophthalmia, hepatic and metabolic changes in the blood. Aim: Therefore, this work aimed to stablish a model of hypovitaminosis A in rats and to evaluate the effects of vitamin A deficiency on metabolic and oxidative parameters in the liver of rats. Methods: Male (n = 19), Wistar, rats (21-day-old) weighing 50g, divided into two experimental groups: Control Group (C), received AIN 93G diet and Vitamin A Deficiency Group (VAD), received AIN 93G vitamin A-free diet for 45 days. In this work, the parameters analyzed were: body mass, food and water intake, biochemical aspects in the blood, lipids and glycogen content, lipid peroxidation, carbonyl proteins and catalase activity in the liver. Results: In the VAD group, final body mass (9%), liver mass (28%), glycemia (14%), Total -cholesterol (17%), HDL -cholesterol (31%) and VLDL -cholesterol (30%) showed reduced (p < 0.05). The liver lipid (64%) and glyceride-fatty acid (74%) contents were higher in the VAD group. The carbonyl proteins in liver were increased by 171% (p < 0.05). Conclusion: In summary, these results suggest that the absence of vitamin A from the diet was effective in inducing characteristics of hypovitaminosis A in rats. This way, can be used for studies related to glucose and lipid metabolism.
ABSTRACT
The organosulfur compound sulforaphane (SFN; C6H11NOS2) is a potent cytoprotective agent promoting antioxidant, anti-inflammatory, antiglycative, and antimicrobial effects in in vitro and in vivo experimental models. Mitochondria are the major site of adenosine triphosphate (ATP) production due to the work of the oxidative phosphorylation (OXPHOS) system. They are also the main site of reactive oxygen species (ROS) production in nucleated human cells. Mitochondrial impairment is central in several human diseases, including neurodegeneration and metabolic disorders. In this paper, we describe and discuss the effects and mechanisms of action by which SFN modulates mitochondrial function and dynamics in mammalian cells. Mitochondria-related pro-apoptotic effects promoted by SFN in tumor cells are also discussed. SFN may be considered a cytoprotective agent, at least in part, because of the effects this organosulfur agent induces in mitochondria. Nonetheless, there are certain points that should be addressed in further experiments, indicated here as future directions, which may help researchers in this field of research.
