Publication: Arsenic induces oxidative stress, sphingolipidosis, depletes proteins and some antioxidants in various regions of rat brain
Date
2008
Authors
Journal Title
Journal ISSN
Volume Title
Publisher
Kathmandu University
Abstract
Abstract
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.
Description
Haider 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