Relato de experiência do profissional farmacêutico inserido no apoio as equipes de saúde da família no município do Rio de Janeiro

Este relato de caso descreve os serviços realizados pelo farmacêutico ao apoio das equipes da estratégia de saúde da família (ESF) no Município do Rio de Janeiro, no âmbito da assistência farmacêutica local (territórios de saúde das comunidades assistidas), bem como expõe a importância da formação especializada, residência em saúde da família e comunidade, para o trabalho no âmbito da estratégia da saúde da família e comunidade.

The organochalcogen 3-methyl-1-phenyl-2-(phenylseleno)oct-2-en-1-one induces oxidative stress in heart, liver, and kidney of rats.

The objective of this study was to investigate the in vitro effects of the organochalcogen 3-methyl-1-phenyl-2-(phenylseleno)oct-2-en-1-one on some parameters of oxidative stress in liver, kidney, and heart of 10-day-old rats. The homogenates of liver, kidney, and heart were incubated for 1 h in the absence (control) or in the presence of 1, 10, or 30 µM of the organoselenium and thiobarbituric acid reactive substances, carbonyl, and the activity of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) were measured. First, we tested the influence of the compound on 1,1-diphenyl-2-picrylhydrazyl (DPPH(•)) radical scavenging and verified that the organochalcogen did not have any antioxidant properties. We observed an increase of lipid peroxidation in all concentrations tested in heart and kidney, while in liver only in the concentrations of 10 and 30 µM. Moreover, we also verified an enhance of protein oxidation in the concentrations of 10 and 30 µM in kidney. On the other hand, the compound caused a reduction on the activity of CAT in heart (10 and 30 µM), liver (30 µM), and kidney (30 µM). The activity of SOD was increased in heart (10 and 30 µM), while in liver (30 µM) and in kidney (10 and 30 µM) the activity was reduced. Our findings indicate that this organoselenium compound induces oxidative stress in liver, heart, and kidney of immature rats, collaborating to the fact that these tissues are potential targets for the organochalcogen action.

Effect of acute administration of 3-butyl-1-phenyl-2-(phenyltelluro)oct-en-1-one on oxidative stress in cerebral cortex, hippocampus, and cerebellum of rats.

Organotellurium compounds have been synthesized since 1840, but pharmacological and toxicological studies about them are still incipient. Therefore, the objective of this study was to verify the effect of acute administration of the organochalcogen 3-butyl-1-phenyl-2-(phenyltelluro)oct-en-1-one on some parameters of oxidative stress in the brain of 30-day-old rats. Animals were treated intraperitoneally with a single dose of the organotellurium (125, 250, or 500 µg/kg body weight) and sacrificed 60 min after the injection. The cerebral cortex, the hippocampus, and the cerebellum were dissected and homogenized in KCl. Afterward, thiobarbituric acid reactive substances (TBARS), carbonyl, sulfhydryl, catalase (CAT), superoxide dismutase (SOD), nitric oxide (NO) formation, and hydroxyl radical production were measured in the brain. The organotellurium enhanced TBARS in the cerebral cortex and the hippocampus, and increased protein damage (carbonyl) in the cerebral cortex and the cerebellum. In contrast, the compound provoked a reduced loss of thiol groups measured by the sulfhydryl assay in all the tissues studied. Furthermore, the activity of the antioxidant enzyme CAT was reduced by the organochalcogen in the cerebral cortex and the cerebellum, and the activity of SOD was inhibited in all the brain tissues. Moreover, NO production was increased in the cerebral cortex and the cerebellum by this organochalcogen, and hydroxyl radical formation was also enhanced in the cerebral cortex. Our findings indicate that this organotellurium compound induces oxidative stress in the brain of rats, corroborating that this tissue is a potential target for organochalcogen action.

Effect of in vitro exposure of human serum to 3-butyl-1-phenyl-2-(phenyltelluro)oct-en-1-one on oxidative stress.

The objective of this study was to verify the effect of the organochalcogen 3-butyl-1-phenyl-2-(phenyltelluro)oct-en-1-one on some parameters of oxidative stress in human serum. Serum of volunteers were incubated for 30 min in the presence or absence of 1, 10, or 30 microM of 3-butyl-1-phenyl-2-(phenyltelluro)oct-en-1-one and oxidative stress was measured. First, we tested the influence of the compound on 1,1-diphenyl-2-picrylhydrazyl (DPPH(*)) radical-scavenging and verified that the organotellurium did not have any antioxidant properties. The organochalcogen was capable to enhance TBARS but the compound was not able to alter carbonyl assay. Furthermore, the organochalcogen provoked a reduction of protein thiol groups measured by the sulfhydryl assay. Moreover, the organotellurium enhanced the activity of catalase and superoxide dismutase, inhibited the activity of glutathione peroxidase and did not modify the glutathione S-transferase activity. Furthermore, nitric oxide production and hydroxyl radical activity were not affected by the compound. Our findings showed that this organochalcogen induces oxidative stress in human serum, indicating that this compound is potentially toxic to human beings.

Effect of 3-butyl-1-phenyl-2-(phenyltelluro)oct-en-1-one on oxidative stress in cerebral cortex of rats.

The objective of this study was to verify the effect of the organochalcogen 3-butyl-1-phenyl-2-(phenyltelluro)oct-en-1-one on some parameters of oxidative stress in the brain of 10-day-old rats. Cerebral cortex was incubated for 1h in the presence or absence of 1, 10 or 30 microM of 3-butyl-1-phenyl-2-(phenyltelluro)oct-en-1-one and thiobarbituric acid reactive substances (TBARS), carbonyl, sulfhydryl, catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione S-transferase (GST), nitric oxide (NO) production and the release of the cytosolic enzyme lactate dehydrogenase (LDH) were measured. The organotellurium was not capable to alter TBARS and carbonyl assays. In contrast, the compound at 10 and 30 microM provoked a reduced of protein thiol groups measured by the sulfhydryl assay. Furthermore, the activity of the antioxidant enzyme CAT (10 and 30 microM) and GPx (1, 10 and 30 microM) was reduced by the organochalcogen. On the other hand, the activity of SOD and GST were enhanced respectively by 1, 10 and 30 microM of the compound. Furthermore, NO production was also increased by 30muM of this organochalcogen. Finally, we verified that the organotellurium was capable of enhance the LDH release at 30 microM concentration. Our findings indicate that this organotellurium compound induces in vitro oxidative stress in the cerebral cortex of rats being potentially toxic for the brain of rats.