Effect of Chronic Administration of the Vinyl Chalcogenide 3-Methyl-1-phenyl-2-(phenylseleno)oct-2-en-1-one on Oxidative Stress in Different Brain Areas of Rats

Abstract

Selenium (Se) is an essential mineral for mammals. It is a nutrient related to the complex metabolic and enzymatic functions. Although Se has important physiological functions in the cells, organic compounds of Se can be extremely toxic, and may affect the central nervous system. This study aims to investigate the effect of the chronic treatment with the vinyl chalcogenide 3-methyl-1-phenyl-2-(phenylseleno)oct-2-en-1-one on some parameters of oxidative stress in the brain of rats. Animals received the vinyl chalcogenide (125, 250 or 500 μg/kg body weight) intraperitoneally once a day during 30 days. 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) and glutathione peroxidase (GPx) activities were measured in the brain. Results showed that the organoselenium enhanced TBARS in the cerebral cortex of rats but the compound was not able to change carbonyl levels. Furthermore, the organoselenium reduced thiol groups measured by the sulfhydryl assay in all tissues studied. The activity of the antioxidant enzyme CAT was increased by the organochalcogen in the cerebral cortex and in the cerebellum, and the activity of SOD was increased in the hippocampus. On the other hand, the activity of the antioxidant enzyme GPx was reduced in all brain structures. Our findings indicate that this organoselenium compound induces oxidative stress in different brain regions of rats, corroborating to the fact that this tissue is a potential target for organochalcogen action.

Cerebrospinal fluid of newly diagnosed amyotrophic lateral sclerosis patients exhibits abnormal levels of selenium species including elevated selenite

“…Reasons for decreased organic Se levels in CSF of our ALS patients are unclear, since they cannot be ascribed to a low Se supply, due to the higher amount of inorganic Se available. Two possibly interrelated hypotheses may be advanced: the role of unknown genetic or non-genetic factors in reducing the antioxidant response, or the ability of pro-oxidant Se species, including selenite, to reduce expression of Se containing enzymes (Tallandini et al, 1996; Branco et al, 2012; Medeiros et al, 2012), possibly through the induction of oxidative stress (Suryo Rahmanto et al, 2012). On the other hand, in other investigations selenite has been shown to increase brain GPx activity as well as lipid perodixation (Glaser et al, 2010), the latter effect being possibly the cause of the former, and in human and in vitro studies it appears to increase SePP levels (Meplan et al, 2009; Hoefig et al, 2011).…”

Oxidant balance in brain of rats receiving different compounds of selenium

“…Administration of dl -selenomethionine to mercury-exposed rat pups whose mothers were also subjected to the same treatment during pregnancy resulted in significant increase in hippocampal SOD activity (Su et al 2008). Medeiros et al (2012) found that selenoorganic compound of chain structure increased SOD activity only in the rat hippocampus, whereas GPx was reduced in all studied brain structures (cerebral cortex, hippocampus and cerebellum). In the present experiment the same result was obtained with regard to GPx in group III receiving chain selenocompound.…”

“…Administration of selenium, in form of two organic compounds (selenones), to rats exposed to carcinogenic hydrocarbon resulted in distinct decrease in MDA concentration (Selamoglu Talas et al 2008). Organoselenium compound of chain structure did not influence in well-marked way TBARS in rat hippocampus and cerebellum, whereas enhancement in the cerebral cortex was observed (Medeiros et al 2012). Insignificant increase was observed in the present work in group IV, but the time of administration was considerably shorter (10 vs. 30 days).…”

“…The dose was chosen considering those applied by other authors which were included in the range from 1 × 10 −4  mg/g b.w. (Medeiros et al 2012) to 19.7 × 10 −4 mg/g b.w. (Selamoglu Talas et al 2008), mainly 2 × 10 −4 –3 × 10 −4 mg/g b.w.…”

Acute exposure to the vinyl chalcogenide 3‐methyl‐1‐phenyl‐2‐(phenylseleno)oct‐2‐en‐1‐one induces oxidative stress in different brain area of rats

“…The molecular mechanisms underlying Se toxicity is still not completely understood. The toxicology of organoselenium compounds is mediated at least in part by their ability to react with thiol groups from biologically active molecules and the capacity of the Se compounds to induce the formation of reactive species in many tissues such as brain, heart, liver and kidney …”