Germanium compounds have been shown to be effective in preventing the
formation of advanced glycation end-products and for reversible solubi
lization 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 compou
nd 132 or Ge-132) on galactose-induced cataractogenesis. For this stud
y young Sprague-Dawley rats were fed a 50% galactose diet. One group o
f rats received topical saline and another group was administered Ge-1
32 in saline four times a day. The lenses were periodically examined w
ith an ophthalmoscope and at desired intervals processed for light and
scanning electron microscopy. Our observations, beginning at 3 days a
nd continuing to 21 days of galactose feeding, exhibited the character
istic galactose-induced morphological alterations, which include the f
ormation of vacuoles, cysts, membrane disruption and swelling of fiber
s 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 ra
ts administered saline. Our findings show that, although the initiatio
n, progression and pattern of lens opacification in rats receiving sal
ine and Ge-132 were similar, in the majority of lenses the progression
and establishment of mature cataracts in the Ge-132 group of rats wer
e delayed. Analysis of the water-soluble and water-insoluble lens-prot
ein fractions for glycated proteins showed increased levels of the Ama
dori products and advanced glycation related fluorescent products in g
alactosemic rats treated with saline eye drops. In rats receiving the
topical Ge-132 treatment the levels of these glycation products were s
ubstantially reduced to levels lower than control values. Prevention o
f glycation seems to be a mechanism by which cataract progression is d
elayed. (C) 1995 Academic Press Limited