Germanium compounds have been shown to be effective in preventing the formation of
advanced glycation end-products and for reversible solubilization of
glycated proteins. As protein glycation has been proposed to play a role in lens opacification, we initiated studies to evaluate the effects of 2-carboxyethyl
germanium sesquioxide (
germanium compound 132 or
Ge-132) on
galactose-induced cataractogenesis. For this study young Sprague-Dawley rats were fed a 50%
galactose diet. One group of rats received topical saline and another group was administered
Ge-132 in saline four times a day. The
lenses were periodically examined with an ophthalmoscope and at desired intervals processed for light and scanning electron microscopy. Our observations, beginning at 3 days and continuing to 21 days of
galactose feeding, exhibited the characteristic
galactose-induced morphological alterations, which include the formation of vacuoles,
cysts, membrane disruption and swelling of fibers and epithelial cells as well as disorganization of the bow in
lenses of rats in both groups. However, in the majority of rats administered
Ge-132 these alterations were delayed as compared to the
lenses of rats administered saline. Our findings show that, although the initiation, progression and pattern of lens opacification in rats receiving saline and
Ge-132 were similar, in the majority of
lenses the progression and establishment of mature
cataracts in the
Ge-132 group of rats were delayed. Analysis of the water-soluble and water-insoluble lens-
protein fractions for
glycated proteins showed increased levels of the Amadori products and advanced glycation related fluorescent products in galactosemic rats treated with saline
eye drops. In rats receiving the topical
Ge-132 treatment the levels of these glycation products were substantially reduced to levels lower than control values. Prevention of glycation seems to be a mechanism by which
cataract progression is delayed.