title: Arsenic induces oxidative stress, sphingolipidosis, depletes proteins and some antioxidants in various regions of rat brain.
abstract: OBJECTIVE
  To seek an interrelationship, if any, between oxidant stress and neurochemical changes in various rat brain regions after arsenic exposure.
  
  
  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:
  
  
  METHODS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Biochemistry, Nepalgunj Medical College, Nepalgunj, Nepal. syedsaleemhaider@gmail.com
authors.forename: S S
authors.initials: SS
authors.lastname: Haider
authors.forename: M S
authors.initials: MS
authors.lastname: Najar
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001149:Arsenates / Q000633:toxicity*; D001205:Ascorbic Acid / Q000378:metabolism; D001921:Brain / Q000378:metabolism*; D002855:Chromatography, Thin Layer; D005978:Glutathione / Q000378:metabolism; D015227:Lipid Peroxidation; D008297:Male; D018384:Oxidative Stress; D014176:Protein Biosynthesis / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013106:Sphingolipidoses / Q000139:chemically induced*; D013438:Sulfhydryl Compounds / Q000378:metabolism
chemical_list: D000975:Antioxidants; D001149:Arsenates; D013438:Sulfhydryl Compounds; C009277:sodium arsenate; D005978:Glutathione; D001205:Ascorbic Acid