Efeito biológico e comportamental da associação de ácido ascórbico, cetoprofeno e selênio

Abstract

Selenium is an essential nutrient for humans, supporting the functioning of enzymes involved in antioxidant defense, thyroid hormone metabolism, and the redox control of intracellular reactions. Vitamin C, also known as ascorbic acid, is a water-soluble vitamin essential for the growth, development, and maintenance of the human body. It is a powerful antioxidant that helps protect cells against damage caused by free radicals. Selenium and vitamin C supplementation are known to preserve the antioxidant system during stress induced by intense training in athletes. Ketoprofen, a nonsteroidal anti-inflammatory drug (NSAID), acts by inhibiting the enzyme cyclooxygenase (COX), responsible for the production of prostaglandins, which mediate inflammation. However, the use of NSAIDs, such as ketoprofen, can generate oxidative stress as a side effect. This study evaluated the effect of selenium and ascorbic acid supplementation on the oxidative effects of ketoprofen, oxidative stress in vitro and in vivo, and its impact on a possible depressive state in vivo. For this purpose, scavenger action experiments of the samples on the ABTS•+ radical and on the DPPH• radical were used, in addition to the action on human erythrocytes, to analyze the hemolytic activity. For the in vivo phase, 60 Wistar rats were used, which underwent an experiment receiving medication with ketoprofen, together with selenium and ascorbic acid supplementation. After administration of the substances, blood and tissue samples were collected to verify the expression of the DPPH• radical, as well as to evaluate the hemolytic activity on erythrocytes. For statistical analysis, one-way ANOVA with Tukey's Posthoc and the Kruskal-Wallis test were used. In the in vitro phase, this study observed a lower expression of ABTS•+ when the combination Selenium + Ketoprofen was used (0.13 ± 0.10) p=<0.001. For DPPH•, Ascorbic Acid (0.04 ± 0.01) presented the greatest antioxidant capacity, followed by the combination of Selenium + Ascorbic Acid (0.07 ± 0.06) p=<0.001. In relation to erythrocytes, the association of Selenium + Ketoprofen + Ascorbic Acid induced lower hemolytic activity in the time of 1h (0.27 ± 0.05) p = 0.038. In the in vivo phase for DPPH•, Selenium presented greater antioxidant capacity in its pure form (0.08 ± 0.01; p = <0.001) and in the proportion of 1:4 (0.23 ± 0.04; p = <0.001). In the proportion of 1:32, the lowest average was observed for the selenium group and for the ketoprofen + ascorbic acid group (0.03 ± 0.01; p = <0.001). In relation to erythrocytes at 6 hours, a lower average hemolysis was observed for the Selenium and Ascorbic Acid + Selenium groups (0.01 ± 0.01; p=0.036). It was possible to conclude that the association between Ascorbic Acid and Selenium generally reduces the oxidizing systems, generating a very effective antioxidant system.