Evaluation of the effects induced by dietary diphenyl diselenide on common carp Cyprinus carpio.

Several diets employed in aquaculture are enriched with selenium (Se), as it is a fundamental element to aquatic vertebrates. Diphenyl diselenide [(PhSe)2], which is a synthetic organoselenium compound, has been considered a potential antioxidant agent in different experimental models. Thus, the aim of this study was to evaluate the effects of dietary diphenyl diselenide at concentrations of 1.5, 3.0, and 5.0 mg/kg for 60 days and to determine its optimal supplemental level for carp, Cyprinus carpio. Neither growth retardation nor hepatoxicity was induced by the inclusion of diphenyl diselenide at concentrations ranging from 1.5 to 5.0 mg/kg. In addition, the inclusion of 3.0 mg/kg of diphenyl diselenide stimulated the weight and length of the carp. The supplementation with 1.5 and 3.0 mg/kg of diphenyl diselenide did not produce oxidative damage in the tissues, verified by peroxidation lipid and protein carbonyl assays. However, at 5.0 mg/kg, it caused an increase of the lipid peroxidation in the liver, brain, and muscle, and inhibited the cerebral acetylcholinesterase activity. An increase of the hepatic superoxide dismutase activity and non-protein thiols content in all tissues and ascorbic acid in the liver, gills, and brain was verified in carp fed with the diet containing 3.0 mg/kg of diphenyl diselenide. This diet had advantageous effects for the fish used in experiments. Therefore, this compound could be considered a beneficial dietary supplement for carp nutrition.

Diphenyl diselenide supplemented diet reduces depressive-like behavior in hypothyroid female rats.

Hypothyroidism has been associated to psychiatric disorder development and tissue oxidative damage. In this study, we evaluated the effect of diphenyl diselenide supplementation on depressive-like behavior triggered by methimazole exposure in female rats. Additionally, thiobarbituric acid reactive substances (TBARS), reactive oxygen species (ROS) and non-protein thiol (NP-SH) levels were analyzed in cerebral cortex, hippocampus and striatum structures of rats. Monoamine oxidase (MAO) activity was evaluated in total brain. Firstly, female rats received methimazole (MTZ) 20mg/100ml in the drinking water for 30days and were evaluated in open-field and forced swimming tests (FST). In this set of experiments, the rats exposed to MTZ presented a depressive-like behavior, which was evidenced by a significant increase in the immobility time when compared to control group. Thereafter, MTZ-induced hypothyroid rats received either a standard or a diet containing 5ppm of diphenyl diselenide, and then they were evaluated monthly in open-field and FST tests during 3months. No alteration on the locomotor performance was observed among the groups. The depressive-like behavior of hypothyroid rats was blunted by diphenyl diselenide supplementation during all experimental periods. The levels of thyroid hormones remained low in MTZ exposed groups until the end of experimental period. The MTZ group had an increase in TBARS and ROS levels that were restored by diphenyl diselenide supplementation. NP-SH content of cerebral structures was not modified by MTZ exposure and/or diphenyl diselenide supplementation. Diphenyl diselenide supplementation restored the MAO B activity that was decreased in MTZ group. In summary, our results show that hypothyroidism induced by MTZ methimazole triggers a depressive-like behavior in female rats and that dietary diphenyl diselenide was able to reduce this effect.

Comparative study on effects of dietary with diphenyl diselenide on oxidative stress in carp (Cyprinus carpio) and silver catfish (Rhamdia sp.) exposed to herbicide clomazone.

The study investigated the capacity of diphenyl diselenide [(PhSe)2] (3.0mg/kg), on reduce the oxidative damage in liver, gills and muscle of carp and silver catfish exposed to clomazone (192h). Silver catfish exposed to clomazone showed increased thiobarbituric acid-reactive substance (TBARS) in liver and muscle and protein carbonyl in liver and gills. Furthermore, clomazone in silver catfish decrease non-protein thiols (NPSH) in liver and gills and glutathione peroxidase and ascorbic acid in liver. (PhSe)2 reversed the effects caused by clomazone in silver catfish, preventing increases in TBARS and protein carbonyl. Moreover, NPSH and ascorbic acid were increased by values near control. The results suggest that (PhSe)2 attenuated the oxidative damage induced by clomazone in silver catfish. The clomazone no caused an apparent situation of oxidative stress in carp, showing that this species is more resistant to this toxicant. Altogether, the containing (PhSe)2 diet helps fish to increase antioxidants defenses.

Effect of repeated restraint stress and clomipramine on Na+/K+-ATPase activity and behavior in rats.

Activation of the limbic-hypothalamic-pituitary-adrenal axis (LHPA) and the release of glucocorticoids are fundamental for the adaptive response and immediate survival of an organism in reaction to acute stimuli. However, high levels of glucocorticoids in the brain may produce neuronal injury and a decrease of Na(+)/K(+)-ATPase activity, with effects on neurotransmitter signaling, neural activity, as well as the whole animal behavior. Clomipramine is a tricyclic antidepressant that inhibits the reuptake of serotonin and norepinephrine by indirect actions on the dopaminergic system and LHPA axis. Its chronic use increases the body's ability to cope with stress; however, high doses can potentiate its side effects on memory, learning, and sensory motor function. The purpose of the present study was to compare the effect of repeated restraint stress and clomipramine treatment on Na(+)/K(+)-ATPase activity and on the behavior of male rats. Changes in the behavioral response were evaluated by measuring the memory, learning, anxiety, and exploratory responses. Our results showed that exposure to repeated restraint stress reduced levels of Na(+)/K(+)-ATPase in brain structures and changed short and long-term memory, learning, and exploratory response when compared to the control group. Exposure to clomipramine treatment increased anxiety levels and reduced Na(+)/K(+)-ATPase activity in the cerebral cortex as well as short term memory, learning, and exploratory response. In conclusion, the present results provide additional evidence concerning how repeated restraint stress and clomipramine chronically administered at higher dose levels affect the neural activity and behavior of male rats.

Resveratrol protects against a model of vacuous chewing movements induced by reserpine in mice.

Reserpine treatment is a putative animal model of orofacial dyskinesia, tremor, and Parkinsonism. Here, we examined the effects of resveratrol, a polyphenol with neuroprotective properties primarily contained in red grapes and red wine, in an animal model of vacuous chewing movements (VCMs) induced by treatment with reserpine. Mice were treated with reserpine (1 mg/kg, subcutaneously on days 1 and 3) and/or resveratrol (5 mg/kg, intraperitoneally 3 consecutive days). VCM, locomotor, and exploratory performance were evaluated. Reserpine treatment produced an increase in VCM intensity, which was significantly reduced by resveratrol co-treatment. Reserpine also decreased locomotor and exploratory activity in the open field test. However, resveratrol co-treatment was not able to protect against these effects. The data suggest that resveratrol could be a promising pharmacological tool for studying VCM in rodents. However, further investigations are needed to understand the exact mechanisms involved in the neuroprotective effects of resveratrol.