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

creativeworkseries.issn1812-2027
dc.contributor.authorHaider, SS
dc.contributor.authorNajar, MSA
dc.date.accessioned2025-07-30T07:33:58Z
dc.date.available2025-07-30T07:33:58Z
dc.date.issued2008
dc.descriptionHaider SS1, Najar MSA2 1Associate Professor, Department of Biochemistry, Nepalgunj Medical College, Chisapani Campus, Nepalgunj, Nepal, 2Lecturer, Department of Biochemistry, Faculty of Medicine, Great Al-Fateh University, Tripoli, Libya
dc.description.abstractAbstract Objectives: 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.
dc.identifier.urihttps://hdl.handle.net/20.500.14572/971
dc.language.isoen_US
dc.publisherKathmandu University
dc.titleArsenic induces oxidative stress, sphingolipidosis, depletes proteins and some antioxidants in various regions of rat brain
dc.typeArticle
dspace.entity.typePublication
local.article.typeOriginal Article
oaire.citation.endPage69
oaire.citation.startPage60
relation.isJournalIssueOfPublication2ecff786-d17b-420c-b11e-19e392127b8d
relation.isJournalIssueOfPublication.latestForDiscovery2ecff786-d17b-420c-b11e-19e392127b8d
relation.isJournalOfPublicationa782b7ff-cf89-4178-ad1c-11ed89cfe1bd

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