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Neuroprotective role of Alpha lipoic acid (ALA) in arsenic (As) induced developmental neurotoxicity in rat pups
Author(s) -
Dhar Pushpa,
Kaushal Parul,
Mehra Raj D
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.921.9
Subject(s) - neurotoxicity , endocrinology , medicine , synaptophysin , oxidative stress , cerebellum , neuroprotection , striatum , chemistry , biology , immunohistochemistry , toxicity , dopamine
Aim To determine the role of exogenous ALA on arsenic induced morphological features and synaptophysin (SYP) expression in cerebellum of Wistar rat pups. Material and methods The experimental group of animals received either NaAsO 2 alone (1.5 or 2.5mg/kg bw) or NaAsO 2 + ALA (70 mg/kg bw) from postnatal day (PND) 1 to 21 by intraperitoneal (i.p) route whereas the controls received distilled water by the same route. Behavioral tests for evaluation of the arousal, cognition, vestibular and motor coordination ability (cliff avoidance, tail hung, negative geotaxis and midair righting) were carried out on PND 7, 9, 10 and 15 respectively. On PND 22, cerebellum obtained from perfusion fixed animals was processed for paraffin embedding and sectioning. Immunohistochemical localization (SYS) was carried out on cryostat sections. Results and conclusion During the experimental period, an apparent decrease (dose dependent) was noted in the performance of NaAsO 2 alone exposed pups as compared to the controls. The animals receiving ALA with NaAsO 2 showed an apparent improvement in these parameters. Substantial recovery was also evident in As induced disrupted cerebellar cytoarchitecture in animals receiving ALA with NaAsO 2. SYP expression, localized mainly in the molecular and granular layers showed an apparent decrease in the NaAsO 2 alone exposed animals as compared to control and ALA supplemented group, supporting the hypothesis of the important role of As induced oxidative stress in developmental neurotoxicity and the amelioration of these effects by exogenous ALA.