The effect of sodium selenite (0.05, 0.1, and 0.2 mg/kg body weight, ip) on the contents of lipids (phospholipids, cholesterol, esterified fatty acids, gangliosides), thiobarbituric acid reactive substance (TBARS), and thiol group in circadian rhythm centers (preoptic area, brainstem, and posterior hypothalamus) of male Wistar rats was studied after 7 d of treatment. The content of phospholipids was elevated significantly with a dose of 0.1 mg/kg of selenite in the preoptic area and brainstem, but a 0.2-mg/kg dose has depleted its level significantly in these regions. The alteration of phospholipids in posterior hypothalamus was not significant with three doses of sodium selenite. The level of cholesterol in the preoptic area was inhibited significantly with a dose of 0.05 mg/kg sodium selenite, but its level was elevated significantly with a dose of 0.2 mg/kg selenite in the preoptic area and brainstem. Alteration with three doses of sodium selenite in the posterior hypothalamus was not significant. The ganglioside level in the preoptic area and brainstem was elevated significantly with a 0.1-mg dose of sodium selenite; conversely, a 0.2 mg dose of sodium selenite caused a significant depletion on its content in these areas. In the posterior hypothalamus, the ganglioside level was depleted significantly with a dose of 0.1 mg, but elevated significantly with a dose of 0.2 mg of sodium selenite. The level of esterified fatty acids was decreased significantly in the preoptic area and brainstem with a dose of 0.1 mg/kg sodium selenite, but in these regions, its level was elevated with a dose of 0.2 mg/kg sodium selenite and its elevation was significant in the preoptic area. In the posterior hypothalamus, the alteration of esterified fatty acids with three doses of sodium selenite was not significant. The effect of 0.1 and 0.2 mg/kg sodium selenite on the TBARS level and thiol group in sleep centers was significantly opposite to the wakefulness center. A sodium selenite dose of 0.1 mg/kg had depleted the content of TBARS in the preoptic area and brainstem but elevated the content of the thiol group significantly in the posterior hypothalamus. On the other hand, a 0.2-mg/kg dose of sodium selenite has significantly elevated the content of TBARS but depleted the content of the thiol group significantly in the posterior hypothalamus. No dose-dependent alteration was observed on the content of lipids, TBARS, and thiol group in the circadian rhythm centers of rats.
The effects of various doses of sodium selenite (0.05, 0.1, and 0.2 mg/kg body weight, i.p.) were studied on the content of phospholipids, cholesterol, esterified fatty acids (EFA), gangliosides, thiobarbituric acid reactive substance (TBARS), and sulfhydryl group in neuroendocrine centers of male Wistar rats for 7 d. The lowest dose of Se (0.05 mg/kg) did not alter the above parameters significantly in neuroendocrine centers. The content of phospholipids was depleted significantly in the pituitary and depletion in the pineal was 80.22% with a 0.1-mg/kg dose of Se, but this dose elevated its level significantly in the hypothalamus. Conversely, a 0.2-mg/kg dose of selenium elevated the level of phospholipids significantly in the pituitary and hypothalamus, the elevation in the pineal was 70%. Selenium, 0.1 mg/kg, elevated the level of cholesterol in the pituitary but depleted its level in the pineal (56.8%) and hypothalamus (13.60%). Selenium, 0.2 mg/kg, elevated the level of cholesterol significantly in the hypothalamus but its level was not significant in the pituitary and pineal. The depletion of esterified fatty acid in the pituitary and pineal with doses of 0.1 and 0.2 mg/kg was significant in the pituitary, whereas its depletion in the pineal was 85.4% and 69.26%, respectively. Selenium, 0.1 and 0.2 mg/kg, depleted the level of gangliosides significantly and dose dependently in the pituitary but has elevated its level significantly and dose dependently in the hypothalamus. Its depletion in the pineal was 87.1% and 67.8% with the 0.1- and 0.2-mg/kg dose of selenium, respectively. Selenium, 0.1 mg/kg, increased the content of TBARS significantly in neuroendocrine centers and its elevation in the pineal was 703.8%. Selenium, 0.2 mg/kg, elevated its level in the pituitary and it was 126.9% in the pineal, but this dose depleted its level significantly in the hypothalamus. The content of the sulfhydryl group with a 0.1-mg/kg dose of selenite was depleted significantly in neuroendocrine centers and it was 55.9% in the pineal. Selenium, 0.2 mg/kg, depleted the level of the sulfhydryl group more significantly in the pituitary and pineal, but its elevation in hypothalamus was significant.
The effect of sodium selenite (0.05, 0.1, and 0.2 mg/kg body weight, i.p.) on the lipid levels (total lipids, phospholipids, cholesterol, gangliosides), thiobarbituric acid reactive substance (TBARS), and sulfhydryl group (-SH) in the striatum and thalamus of a male Wistar rat was studied after 7 d of treatment. The level of total lipids and cholesterol was significantly and dose-dependently elevated in the striatum and thalamus with 0.1 and 0.2 mg/kg of sodium selenite. However, the cholesterol level was significantly increased only with 0.2 mg/kg of sodium selenite in the thalamus. The level of phospholipids and gangliosides was more significant with 0.1 mg/kg of sodium selenite as compared to 0.2 mg. No significant alteration on the gangliosides level was observed in the thalamus with various doses of sodium selenite although the elevation with 0.2 mg dose was 25.9%. The content of TBARS was elevated dose dependently in striatum, but its level was depleted significantly with 0.1-mg/kg dose of sodium selenite in the thalamus. The level of the -SH group was significantly depleted in the striatum with 0.1-mg/kg dose of sodium selenite; conversely, this dose has significantly elevated the levels of -SH group in the thalamus.
The effect of 0.05, 0.1, and 0.2 mg sodium selenite/kg body weight ip on the activities of neurobehavioral, acetyl cholinesterase, monoamine oxidase, and the content of dopamine and its metabolites in circadian rhythm centers of male Wistar rats was studied after 7 d of treatment. The results show an appreciable increase in locomotion, stereo-events, distance traveled, and average speed at the dose of 0.1 and 0.2 mg sodium selenite/kg. The data have shown hyperactivity of animals with various doses of sodium selenite, and it was significant and dose-dependent after 3 d of treatment. The activity of acetylcholinesterase (AChE) was inhibited dose dependently, and it was significant in preoptic area with 0.1 or 0.2 mg sodium selenite/kg. Conversely, in the posterior hypothalamus its activity was significantly elevated with the dose of 0.2 mg sodium selenite/kg, but its alteration in brain stem was not significant. Monoamine oxidase (MAO) activity was increased in preoptic area with the dose of 0.1 mg sodium selenite/kg, but its alteration in posterior hypothalamus and brain stem was not significant. The content of dopamine (DA), 3,4-dihydroxyphenyl acetic acid (DOPAC), and homovanilic acid (HVA) was elevated dose dependently and it was significant with the doss of 0.1 and 0.2 mg sodium selenite/kg, but the content of DOPAC and HVA in posterior hypothalamus was not significant with the dose of 0.1 mg sodium selenite/kg.
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