Thiamine deficiency in vivo produces fiber cell degeneration in mouse lenses

• Published in: Biochemical and biophysical research communications 1999-05, Vol.258 (3), p.703-707
• Main Authors: Frederikse, P.H, Farnsworth, P, Zigler, J.S. Jr
• Format: Article
• Language: English
• Subjects: Amyloid beta-Peptides - metabolism; Amyloid beta-Protein Precursor - metabolism; Animals; eye lens; Immunohistochemistry; Lens, Crystalline - metabolism; Lens, Crystalline - pathology; Membrane Proteins - metabolism; Mice; Mice, Inbred BALB C; Oxidative Stress; Presenilin-1; thiamin; thiamin deficiency; Thiamine - antagonists & inhibitors; Thiamine Deficiency - metabolism; Thiamine Deficiency - pathology; vitamin deficiencies
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1006/bbrc.1999.0560

Thiamine (Vitamin B1) is a co-factor for enzymes key in bridging aerobic and anaerobic metabolism. One such enzyme, transketolase, catalyzes two of three reactions for entry into the pentose-phosphate pathway, a major source of chemical reducing power. Thus, thiamine deprivation (TD) is considered a classic model of systemic oxidative stress and is linked with degenerative diseases. TD in mice and rats produces neurodegeneration with Alzheimer's disease characteristics. Age-related disease of the lens, commonly cataract, is also linked with thiamine and oxidative stress. To test the effects of TD on mice, we used a previously defined protocol involving a thiamine free diet and a thiamine antagonist. After 12 days, lens fiber cell degeneration was observed primarily along the lens posterior beneath the intact capsule. These regions exhibited a localized increased expression of Alzheimer precursor protein, Abeta peptides, and presenilin 1. These data indicate that TD in mice produces fiber cell degeneration and suggest common mechanisms for TD-induced lens fiber and neuronal cell degeneration.