A Role for Oxidative Stress in Suppressing Serum Immunoglobulin Levels in Lead-exposed Fisher 344 Rats
Evidence implicating oxidative stress in toxicity during lead intoxication in vivo has opened new avenues for investigation of the mechanisms of lead-induced immunosuppression. The current study explores the possibility that lead-induced oxidative stress contributes to the immunosuppression observed during lead poisoning. Fisher 344 rats were exposed to 2,000 ppm lead acetate in their drinking water for 5 weeks. One week following removal of lead from the drinking water, significant reductions in serum levels of IgA, IgM, and IgG were detected. Significant increases in oxidative damage, based on malondialdehyde (MDA) content, were observed in peripheral blood mononuclear cells (PMCs) collected during the same experiments. In addition, MDA content increased in livers from lead-exposed rats. Following 5 weeks of lead exposure, administration of either 5.5 mmol/kg N-acetylcysteine (NAC) or 1 mmol/kg meso-2,3-dimercaptosuccinic acid (DMSA) in the drinking water for 1 week significantly reversed the inhibitory effects of lead on serum immunoglobulin (Ig) levels. Also, all parameters indicative of oxidative stress returned to control levels. These results suggest that oxidative stress contributes to suppressed serum Ig levels during lead intoxication in vivo, and that intervention with either a thiol antioxidant (NAC) or a metal chelator (DMSA) will alleviate this lead-induced suppression by correcting the prooxidant/antioxidant imbalance caused by lead exposure.
N. Ercal et al., "A Role for Oxidative Stress in Suppressing Serum Immunoglobulin Levels in Lead-exposed Fisher 344 Rats," Archives of Environmental Contamination and Toxicology, vol. 39, no. 2, pp. 251-256, Springer Verlag, Aug 2000.
The definitive version is available at https://doi.org/10.1007/s002440010102
National Institutes of Health (U.S.)
University of Missouri--Rolla
International Standard Serial Number (ISSN)
Article - Journal
© 2000 Springer Verlag, All rights reserved.
01 Aug 2000