Bromocriptine and Vitamin E were Protective Against Mercury-Induced Purkinje Neuron Injury in Male Wistar Rats
Mercuric chloride (HgCl2) is poisonous to both human and animals often causing systemic and nervous damage. The possible neuroprotective activity of bromocriptine (BRC), a dopamine agonist and alpha-tocopherol (TOCO) against mercuric chloride intoxication was investigated. Forty-two rats were randomized into six groups for this study. Group1 rats served as control; Group 2, TOCO (500 mg/kg); Group 3, BRC (10mg/kg); Group 4, HgCl2 (4mg/kg); Group 5, BRC (10mg/kg) + HgCl2 (4mg/kg); Group 6, TOCO (500 mg/kg) + HgCl2 (4mg/kg). HgCl2 and TOCO were administered with oral cannula for 14 days while BRC was given i.p. On day 15, behavioural studies were conducted and rats were euthanized by cervical dislocation the next day. Skulls were carefully dissected open and brains carefully extracted, rinsed, blotted with filter paper, weighed and fixed in 10% formalin. The cerebellum was separated from the brain and processed for paraffin wax embedment and slides stained with Haematoxylin and Eosin. There was significant difference in body weight of rats of TOCO group when compared with control. Behavioural results showed that HgCl2 treatment significantly (p<0.05) reduced the number of lines crossed, vertical movement (rearing) and forelimb grip when compared with the control. These parameters were significantly (p<0.05) elevated by BRC+HgCl2 treatment demonstrating the ameliorative effect of BRC co-treatment with HgCl2. The forelimb grip strength was elevated by BRC treatment while HgCl2 treatment elevated the duration recorded for negative geotaxis. Histological studies demonstrated degenerated Purkinje neurons in the cerebellum of HgCl2 -treated rats confirming neural damage. Mercuric chloride caused behavioural alterations in rats and was also toxic to rat Purkinje neurons. Both effects were mitigated by bromocriptine and alpha-tocopherol.
Keywords: Bromocriptine, alpha-tocopherol, mercuric chloride, Purkinje neurons, neuroprotection