Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04040 (Catalase)
 3,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spatial memory is coordinated with different brain regions especially hippocampus (HIP) and medial prefrontal cortex (mPFC). Influence of noise stress on working and reference memory error in rats was evaluated by radial eight-arm maze experiment. Changes in the dendritic count were observed in the brain regions such as CA1, CA3 regions of HIP and layers II, III of mPFC. In order to understand the possible mechanism behind noise stress-induced changes, free radical status and acetylcholinesterase (AChE) activity in HIP and mPFC were evaluated. Plasma corticosterone level was also evaluated. Results obtained in this study showed that after noise-stress exposure, 100 dBA/4h per day for 30 days, working and reference memory error increased significantly (P < 0.05) when compared to control animals. Neuronal dendritic count in the HIP was reduced in the 2nd and 3rd order dendrites but not in the mPFC. Superoxide dismutase, lipid peroxidation, plasma corticosterone level and AChE activity were significantly increased in the 1 day, 15 days and 30 days stress groups animal significantly. Catalase and glutathione peroxidase activity were increased in the 1 day and 15 days noise-stress groups but decreased in the 30 days noise-stress group and GSH level was decreased in all the stress exposed animals. In conclusion, oxidative stress, increased AChE activity, reduced dendritic count in HIP, mPFC regions and elevated plasma corticosterone level which develops in long-term noise-stress exposed rats, might have caused the impairment of spatial memory.
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PMID:Effects of chronic noise stress on spatial memory of rats in relation to neuronal dendritic alteration and free radical-imbalance in hippocampus and medial prefrontal cortex. 1648 Nov 10

Curcuma comosa Roxb. is widely used as a gynaecological traditional medicine in South-East Asia and recent behavioral studies have shown that C. comosa extract significantly improved the spatial memory in rats. The present study investigated the protective effects of Curcuma comosa hexane extract on the ethanol (EtOH)-induced oxidation in rat brains. Young female Wistar rats were given 20% of EtOH intraperitoneally to induce the oxidative stress. Subsequently, C. comosa hexane extract was intraperitoneally co-administered at the doses of 100 and 250 mg kg(-1) b.wt. to the EtOH-induced rats for 14 days. The neuron densities of CA1, CA3 and CA4 areas of the hippocampus were counted and the activities of hippocampal Catalase (CAT), Glutathione Peroxidase (GPx) and Superoxide Dismutase (SOD) were determined. EtOH significantly decreased the neuron densities in Cornu Ammonis (CA), including CA1 and CA3 areas; however, the decrease was prevented by C. comosa co-administration. EtOH administration also increased the CAT and GPx activities in the hippocampus which were reversed by C. comosa co-administration. Moreover, C. comosa administration increased the SOD activity in a dose-dependent manner in the EtOH treated groups. C. comosa prevented the neuron loss in the hippocampus caused by EtOH. The possible neural protective mechanism may involve with the changes in activities of the antioxidant enzymes in the hippocampus.
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PMID:Curcuma comosa prevents the neuron loss and affects the antioxidative enzymes in hippocampus of ethanol-treated rats. 2419 65