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.
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.
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.
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