BackgroundRapid eye movement [REM] sleep deprivation is a stressor. It results in a predictable syndrome of physiological changes in rats. It has been proposed that reactive oxygen species and the resulting oxidative stress may be responsible for some of the effects of sleep deprivation.PurposeThe present study was undertaken to investigate the reversible nature of the effects of 96 hours of REM sleep deprivation on lipid peroxidation and total reduced glutathione level in the hypothalamus, midbrain and hindbrain of Wistar strain rats.MethodsThe rats were deprived of REM sleep using the inverted flowerpot technique. All the animals were maintained in standard animal house condition with 12-h light and 12-h dark cycles. At the end of the stipulated time Jugular venous blood sample of 2 ml was collected under mild ether anesthesia for the assay of stress index, plasma corticosterone. Lipid peroxidation using thiobarbituric acid, total reduced glutathione using DTNB (GSH) were assayed in the brain regions dissected out.ResultsThis study showed that 96 hours of REM sleep deprivation results in increased lipid peroxidation and reduction in total reduced glutathione level in the discrete regions of brain studied. However following restorative sleep for 24 hours all the changes reverts back to base line value. This study shows that oxidative stress produced by 96 hours of REM sleep deprivation is reversible.ConclusionFrom this study it is clear that, REM sleep deprivation is a potent oxidative stressor. This could probably play a role in the behavioral and performance alteration seen in both experimental animals as well as humans following REM sleep deprivation. Further investigations in this line are needed to highlight the importance of REM sleep.
Lipoma is the commonest benign tumour occurring at any anatomical site where fat is present. In oral cavity and oropharynx it is a relatively uncommon neoplasm.. Tongue which is totally devoid of fat cells is also a site for lipoma albeit very rarely. This is one such rare case of the universal tumour, presenting at the lateral margin of the tongue, for which complete tumour excision was done.
Recent studies revealed that alpha-ketoglutarate (A-KG) alone or with sodium thiosulfate (STS) provide significant protection against acute and sub-acute cyanide poisoning in rodents. This study addresses the protective effect of A-KG and/or STS in sub-chronic (90 days) cyanide poisoning. Wistar rats were divided into seven groups (n = 10): Control animals, potassium cyanide (KCN) A-KG, STS, KCN ? A-KG, KCN ? STS and KCN ? A-KG ? STS. Spontaneous motor activity and motor coordination were recorded every 15th day. Lipid peroxidation (LPO), reduced glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT) in blood, brain, liver and kidney, and glutamate, aspartate and dopamine in discrete regions of brain were measured following 90 days exposure. Cyanide significantly decreased motor coordination, accompanied by increase in LPO (blood, brain and liver) and dopamine (corpus striatum and cerebral cortex) levels, and depletion in GSH (blood, brain and liver), GPx (brain and liver), SOD (brain and liver), and CAT (blood and brain) levels. Although treatment of A-KG and STS alone significantly blunted the toxicity of KCN, concomitant use of both afforded the maximum protection. This study shows a promising role of A-KG and STS as treatment regime for long term cyanide exposure.
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