Affiliation:
1. Department of Medicine, Rheumatology Division, College of Medicine, King Khalid University Hospital, King Saud University, Riyadh, Saudi Arabia, or
Abstract
Nickel intolerance owing to sensitization is a growing problem. The main objective of this study was to examine the relationship between nickel chloride and induction of autoimmunity in genetically susceptible rats. Thirty brown Norway rats were randomized into four treatment groups; the first and second groups received nickel chloride 4.5 mg in 0.2 ml normal saline either orally or subcutaneously, and the third and fourth groups (controls) received normal saline (0.9%) 0.2 ml through the same routes. A significant number of rats (P < 0.05) that received nickel chloride by the subcutaneous or oral routes showed a high level of serum antinuclear antibody (ANA) compared with controls. A significant number of rats (P < 0.05) that received nickel chloride by the subcutaneous route showed high serum anti-SSA, but the number of rats with anti-SSA was insignificant in the group that received nickel by the oral route. Other autoantibodies found in both groups (anti-double-stranded (ds)DNA, anti-Smith, anti-SSB) showed a gradual increase, but the number of rats with positive titers post exposure was not significant statistically. Nickel chloride exposure in the rats appeared to induce the development of autoimmunity. A longer duration following exposure to nickel chloride seems to be associated with greater risks. Lupus (2010) 19, 262—267. Key
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4 articles.
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