Autoantibodies against cytoskeletal neuronal proteins in sera of arsenic-exposed subjects correlate with neurological symptoms

Abstract

This descriptive study correlates the presence of serum autoantibodies to five neuronal cytoskeletal proteins with neurologic deficits in subjects exposed to arsenic (As). Arsenic exposure remains a serious problem in many countries producing skin lesions and hair loss. More serious manifestations include: liver and kidney damage, encephalopathy, peripheral neuropathy, gangrene of extremities, and cancer. Bangladesh represents one of the countries where high percentage of population is exposed to As through highly contaminated drinking groundwater. Autoantibodies were determined against the following proteins: neurofilament triplet proteins (NFP), microtubule associated protein-2 (MAP2), and microtubule associated protein tau (tau). Sera were obtained from 14 subjects in the severely affected village of Mianpur, Charghat Thana, Rajshahi. Individuals were further divided into group A with objective complaints of organic neurologic damage and group B without neurologic deficits manifestations and eight healthy controls from Rajshahi city. High levels of autoantibodies were detected in five subjects against low molecular weight neurofilaments (NFL) and in two subjects against high molecular weight neurofilament (NFH). Two subjects displayed significantly increased levels of MAP-2 autoantibodies and two others high levels of tau autoantibodies. All elevated autoantibodies were detected in group A subjects who were diagnosed with neurological disorders ranging from sleep disorders to paralysis. The results demonstrate a good correlation between neurologic defects in As-exposed subjects and presence of sera neuronal autoantibodies to cytoskeletal proteins.

Keywords:

• autoantibodies
• neurofilament
• microtubule associated protein-2
• microtubule associated protein-tau
• neuronal injury
• arsenic
• Bangladesh

Acknowledgements

The technical work of Elizabeth A. Herrick is appreciated. This study was supported in part by funds from the Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina, USA.