Glycosylation in vivo of human lens capsule (basement membrane) and diabetes mellitus

We have evaluated the levels of red blood cell galactose-1-phosphate uridyltransferase in 20 patients with cataract and in 15 subjects without cataract, suffering from compensated, noninsulin-dependent, type II diabetes. The diabetic patients were compared with a previously examined group of 65 age-matched nondiabetic subjects (25 of whom suffered from bilateral idiopathic cataract). In diabetic patients, the average galactose-1-phosphate uridyltransferase levels tended to be lower and the percentage of cases of reduced enzymatic activity tended to be higher than in the corresponding nondiabetic subjects.

“…the consequent formation of disulfide bridges is accelerated by nonenzymatic gly cosylation of proteins. This hypothesis has been confirmed by other authors [7,8,10].…”

Section: Introductionsupporting

confidence: 81%

Cataract Formation in Diabetic Patients and Galactose-1-Phosphate Uridyltransferase Deficiency

Simonelli¹,

Savastano²,

Rinaldi³

et al. 1987

“…The TBA assay implied that the amount of glycation in the 5.5-mM glucose medium is about the same as in the native lens capsule. The value obtained for the glycation of fresh bovine lens capsules, approximately 10 nmol glucose/mg dry weight of capsule, is of the same magnitude as Mandel et al [ 1983] found in nondiabetic human lens capsules, 29 nmol/mg protein. The 14C technique implied that the great increase in glycation occurred moving from 5.5 to 30 mM glucose solution irrespectively whether the incubation was for 18 or 32 days.…”

Section: Discussionsupporting

confidence: 57%

Bound Water Content of Bovine Lens Capsules

Popdimitrova

Bettelheim²

1989

The anterior parts of bovine lens capsules have been incubated in media with different glucose contents. The freezable water content of the lens capsule was obtained by differential scanning calorimetry and the total water content by thermogravimetric analysis. The bound (nonfreezable) water content was calculated as the difference between total and freezable water. The bound water as percent of the total water increases with the degree of glycosylation of the bovine lens capsules.

“…A number of diseases and their complications have been identified as risk factors for cataract formation [1], To solve and prevent the problem of cataracts exacer bated by different diseases, one of the most important research needs is to understand the role of individual components of the multifac torial etiology. Since cataractogenesis has been found to start from the lens fiber plasma membrane [2], the biochemical and structural changes of experimental lens opacification in the cortex and nucleus have been extensively studied [3,4], Although the lens of the eye is completely enclosed by an external lens cap sule which acts as the primary permeability barrier for substances entering and leaving the lens, there is scanty information about the relation between cataract formation and the lens capsule [5],…”

Section: Introductionmentioning

confidence: 99%

Possible Mechanism of Exacerbating Cataract Formation in Cataractous Human Lens Capsules Induced by Systemic Hypertension or Glaucoma

Lee¹,

Lin

et al. 1997

To clarify the role of the lens capsule in cataract formation, changes in the protein conformational structure of immature cataractous lens capsules from patients with systemic hypertension or glaucoma have been investigated, as compared to normal lens capsules. The protein secondary structure and composition of these capsular samples were determined using Fourier transform infrared microspectroscopy with second-derivative, deconvolution and curve-fitting methods. We found that the composition of both random coil and β-type (β-sheet and β-turn) structures in the immature cataractous human lens capsules was increasingly induced by systemic hypertension or glaucoma, but α-helix content clearly decreased, leading to the alteration of protein conformational structures in lens capsules. A possible pathway of cataract formation exacerbated by systemic hypertension or glaucoma is discussed. According to the results, we propose that systemic hypertension or glaucoma induce changes in the protein conformational structures of the lens capsule, then cause alteration of membrane transport and permeability for ions, and finally increase intraocular pressure, resulting in the exacerbation of cataract formation. The effect on the conformational structure of cataractous human lens capsules is more pronounced for systemic hypertension than for glaucoma. The present study implies that systemic hypertension or glaucoma can exacerbate cataract formation in senile patients by modifying the protein secondary structures in the lens capsule.