Arsenic induces oxidative stress, sphingolipidosis, depletes proteins and some antioxidants in various regions of rat brain.

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dc.contributor.authorHaider, S Sen_US
dc.contributor.authorNajar, M Sen_US
dc.date.accessioned2009-05-28T03:59:31Z
dc.date.available2009-05-28T03:59:31Z
dc.date.issued2008-01-08en_US
dc.descriptionKathmandu University Medical Journal.en_US
dc.description.abstractOBJECTIVES: To seek an interrelationship, if any, between oxidant stress and neurochemical changes in various rat brain regions after arsenic exposure. MATERIALS AND METHODS: This study was carried out at the Department of Biochemistry, Al Arab Medical University, Benghazi, Libya. Seventy five male Spraque-Dawley rats were divided into three groups: CONTROL GROUP: Rats were administered 2 ml of normal saline solution/kg body weight (b.wt.) daily for 20 days by intraperitoneal (i.p.) route. ARSENIC-TREATED GROUP: Rats received elemental arsenic (as sodium arsenate) 2.0 mg/kg b.wt. daily for 20 days by i.p. route. RECOVERY GROUP: Rats received 2.0 mg/kg b.wt. elemental arsenic daily for 20 days by i.p. route and were allowed to recover for 20 days. Rats were sacrificed and brains were dissected into cerebral cortex, corpus striatum, cerebellum and brain stem. Tissue homogenized in respective mediums. And were analyzed for lipid classes, oxidative stress, concentration of proteins, glutathione and ascorbic acid by utilizing standard colorimetric procedures. RESULTS: Arsenic exposure increased the oxidant stress because lipid peroxidation was enhanced. And decreased the contents of lipid classes, proteins, glutathione and the ascorbic acid in various rat brain regions. However, thins-layer chromatography exhibited regional variations in phospholipids classes. CONCLUSION: These results suggested that arsenic-initiated oxidant stress by increasing lipid peroxidation. The losses of lipid classes, ascorbic acid and glutathione may be attributed to peroxidative damage and binding of arsenic with sulfhydryl groups of enzymes. Recovery of animals showed reversibility in most of studied parameters, but gangliosides and cerebrosides over shooted. And speculated "Sphingolipidosis". It is then likely that repeated exposures of humans to arsenic may result in hampering of cell signalling, apoptosis and mutagenesis.en_US
dc.description.affiliationDepartment of Biochemistry, Nepalgunj Medical College, Nepalgunj, Nepal. syedsaleemhaider@gmail.comen_US
dc.identifier.citationHaider SS, Najar MS. Arsenic induces oxidative stress, sphingolipidosis, depletes proteins and some antioxidants in various regions of rat brain. Kathmandu University Medical Journal. 2008 Jan-Mar; 6(1): 60-9en_US
dc.identifier.urihttps://imsear.searo.who.int/handle/123456789/46233
dc.language.isoengen_US
dc.source.urihttps://www.kumj.com.npen_US
dc.source.urihttps://kumj.com.np/ftp/issue/21/60-69.pdfen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntioxidants --metabolismen_US
dc.subject.meshArsenates --toxicityen_US
dc.subject.meshAscorbic Acid --metabolismen_US
dc.subject.meshBrain --metabolismen_US
dc.subject.meshChromatography, Thin Layeren_US
dc.subject.meshGlutathione --metabolismen_US
dc.subject.meshLipid Peroxidationen_US
dc.subject.meshMaleen_US
dc.subject.meshOxidative Stressen_US
dc.subject.meshProtein Biosynthesis --drug effectsen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshSphingolipidoses --chemically induceden_US
dc.subject.meshSulfhydryl Compounds --metabolismen_US
dc.titleArsenic induces oxidative stress, sphingolipidosis, depletes proteins and some antioxidants in various regions of rat brain.en_US
dc.typeJournal Articleen_US
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