Osmotic cataract causes reduced vision in wild Atlantic salmon postsmolts

Osmotic cataracts were diagnosed in all of 191 Atlantic salmon Salmo salar L. postsmolts caught during 8 trawl hauls on the western side of the V?ringsplateau, Norwegian Sea, in June 2001. The changes varied from a hazy opacity in the anterior part of the lens to cataracts affecting the whole lens. Severely affected lenses appeared swollen and large vacuoles were visible in the opaque areas. Large vacuoles in otherwise clear lenses were diagnosed in 1 of 4 adult salmon examined. Histologically, widened sutures, vacuolation of lens epithelium and cortex, and proteinaceous lakes subjacent to the epithelium were the most frequent changes, while extensive cortical necroses and epithelial proliferation were seen in a few cases. UV-absorbance of the aqueous humor was determined and levels compared to plasma levels and also to levels in farmed Atlantic salmon of the same developmental stage. Wild salmon generally showed higher levels of protective factors than farmed fish. The osmotic type of cataract diagnosed leads to poor vision and is a potential cause of reduced survival in postsmolts. The cause of the cataracts could not be determined, but defective osmoregulation is suspected.     

Accelerated heavy ions and the lens. IV. Biomicroscopic and cytopathological analyses of the lenses of mice irradiated with 600 MeV/amu 56Fe ions

The lenses of mice exposed to 600 MeV/amu iron ions were evaluated by slit-lamp biomicroscopy and cytopathological analyses. The doses ranged from 0.05 to 1.6 Gy, and the lenses were assessed at several intervals postirradiation. Cataract, the development of which is dependent on both time and dose, is significantly more advanced in all of the exposed mice when compared to the unirradiated controls. The great difference between the severity of the cataracts caused by 0.05 Gy (the lowest dose used) and those that developed spontaneously in the control animals is an indication that 0.05 Gy may far exceed the threshold dose for the production of cataracts by accelerated iron ions. Cytopathologically, a similar dose dependence was observed for a number of end points including micronucleation, interphase death, and meridional row disorganization. In addition the exposure to the 56Fe ions produced a long-term effect on the mitotic population and a pronounced "focal" loss of epithelial cytoarchitecture. The microscopic changes support the view that the mechanism of heavy-ion-induced cataractogenesis is the same as that for cataracts caused by low-LET radiation.     

Reversible `fingerprint' cataract secondary to diabetes mellitus

Transient diabetic cataracts are generally located in the anterior and posterior subcapsular regions of the lens. The following case report describes a reversible diabetic cataract with a `fingerprint' like shape in the anterior adult nucleus. The etiology is unclear but may relate to protein modification and/or osmotic changes in the lens.     

Elevated Frequency of Cataracts in Birds from Chernobyl

Background

Radiation cataracts develop as a consequence of the effects of ionizing radiation on the development of the lens of the eye with an opaque lens reducing or eliminating the ability to see. Therefore, we would expect cataracts to be associated with reduced fitness in free-living animals.

Methodology/Principal Findings

We investigated the incidence of lens opacities typical of cataracts in more than 1100 free-living birds in the Chernobyl region in relation to background radiation. The incidence of cataracts increased with level of background radiation both in analyses based on a dichotomous score and in analyses of continuous scores of intensity of cataracts. The odds ratio per unit change in the regressor was 0.722 (95% CI 0.648, 0.804), which was less than odds ratios from investigations of radiation cataracts in humans. The relatively small odds ratio may be due to increased mortality in birds with cataracts. We found a stronger negative relationship between bird abundance and background radiation when the frequency of cataracts was higher, but also a direct effect of radiation on abundance, suggesting that radiation indirectly affects abundance negatively through an increase in the frequency of cataracts in bird populations, but also through direct effects of radiation on other diseases, food abundance and interactions with other species. There was no increase in incidence of cataracts with increasing age, suggesting that yearlings and older individuals were similarly affected as is typical of radiation cataract.

Conclusions/Significance

These findings suggest that cataracts are an under-estimated cause of morbidity in free-living birds and, by inference, other vertebrates in areas contaminated with radioactive materials.     

An epidemiological study of cataracts in seawater farmed Atlantic salmon Salmo salar

Cataracts in farmed Atlantic salmon have been known for many years, but the aetiology and importance of the disease have not been clarified. A cross-sectional field study of 51 cages of Atlantic salmon at 49 randomly selected sea sites was performed during the summer of 1998. The target population was spring and autumn entry groups of the 1997 generation salmon. Approximately 15 fish from each cage, altogether 777 fish, were autopsied by the same person. Each eye of the fish was scored for cataracts on a scale from 0 to 4 using an otoscope lamp with magnification. The weight and length of each fish were measured. The prevalence of cataracts was 83 % and 79% in spring entry groups and autumn entry groups, respectively. The overall mean cataract index (mean score of both eyes) was 1.23, being significantly higher in the spring entry groups (1.36) than the autumn entry groups (0.85). The final results in the spring entry groups showed that the fish groups with higher weight at sea transfer also had a higher cataract index at inspection. The risk of development of cataracts varied significantly among the offspring from the 5 strains represented in the study. Fish from sites located in 2 counties in the southern part of Norway had a significantly higher cataract index than fish farmed in the northernmost county in the study. For the autumn entry groups none of the explanatory variables was significant. In the spring entry groups a significant negative relationship was observed between the cataract score and the weight of the fish at the time of inspection (Pearson's r = -0.17), while the corresponding correlation for the autumn released groups was r = -0.10. Among the spring entry groups the average weight of the fish with the highest cataract score was estimated to about a third of the weight of the fish with no visible cataracts.     

Multiple and additive functions of ALDH3A1 and ALDH1A1: cataract phenotype and ocular oxidative damage in Aldh3a1(-/-)/Aldh1a1(-/-) knock-out mice

ALDH3A1 (aldehyde dehydrogenase 3A1) is abundant in the mouse cornea but undetectable in the lens, and ALDH1A1 is present at lower (catalytic) levels in the cornea and lens. To test the hypothesis that ALDH3A1 and ALDH1A1 protect the anterior segment of the eye against environmentally induced oxidative damage, Aldh1a1(-/-)/Aldh3a1(-/-) double knock-out and Aldh1a1(-/-) and Aldh3a1(-/-) single knock-out mice were evaluated for biochemical changes and cataract formation (lens opacification). The Aldh1a1/Aldh3a1- and Aldh3a1-null mice develop cataracts in the anterior and posterior subcapsular regions as well as punctate opacities in the cortex by 1 month of age. The Aldh1a1-null mice also develop cataracts later in life (6-9 months of age). One- to three-month-old Aldh-null mice exposed to UVB exhibited accelerated anterior lens subcapsular opacification, which was more pronounced in Aldh3a1(-/-) and Aldh3a1(-/-)/Aldh1a1(-/-) mice compared with Aldh1a1(-/-) and wild type animals. Cataract formation was associated with decreased proteasomal activity, increased protein oxidation, increased GSH levels, and increased levels of 4-hydroxy-2-nonenal- and malondialdehyde-protein adducts. In conclusion, these findings support the hypothesis that corneal ALDH3A1 and lens ALDH1A1 protect the eye against cataract formation via nonenzymatic (light filtering) and enzymatic (detoxification) functions.     

Moderate caloric restriction delays cataract formation in the Emory mouse

Eye lens senile cataract is a major cause of blindness, affecting the elderly in particular. The etiology of the disorder has been elusive, and attempts to delay the onset of senile cataracts have been unsuccessful. The need for more information is underscored by epidemiologists who estimate that the ability to delay cataract formation in humans by only 10 years would eliminate the need for 50% of the cataract extractions performed annually in the United States. The Emory mouse provides the best model for human senile cataracts. Feeding Emory mice a diet that was restricted in calories by approximately 21% delayed the onset of cataracts. This is the first study that demonstrates in vivo the delay of senile-type cataracts. In these animals, aging and cataracts are associated with diverse changes in the proportion of various proteins (particularly 21, 22, 31-34 kDa) and with transformation of proteins from a soluble to an insoluble state. In advanced cataracts, there is a loss of total protein. Within a cataract grade, there is no difference between restricted and nonrestricted animals in relative proportion of specific lens proteins or in amounts of total or soluble proteins. The transition from a clear to cataractous lens appears when the soluble-to-total protein ratio falls below about 0.58. The exclusive use of gamma-crystallin as an indicator of lens viability is questioned. To the extent that cataract formation is due to lens protein oxidation and/or an inability to proteolytically remove damaged protein, it would appear that caloric restriction results in enhanced protection against lens oxidative stress or in prolonged proteolytic function.     

Conjunctival impression cytology in contact lens wearers

The upper tarsal conjunctiva is in constant friction with the surface of the contact lens. The conjunctival surfaces of 80 soft and gas-permeable contact lens wearers (40 each) and 20 controls were studied using biomicroscopy and impression cytology. A filter dissolution technique was used to process the conjunctival imprints. Biomicroscopic and cytologic grading of the conjunctivae was performed using four-tier grading systems. Impression cytology is a non-invasive, painless procedure. The altered technique of processing yielded better cellularity and excellent cellular detail. On biomicroscopy and cytology, all controls showed Grade 1 appearances. Soft lens wearers who were symptomatic were found to have a significant increase in both biomicroscopic and cytologic grades, when compared with their asymptomatic counterparts. No correlation was found between duration of lens use and biomicroscopic or cytologic grades. All changes were found to be more severe in soft lens wearers.     

An epidemiological assessment of lens opacifications that impaired vision in patients injected with radium-224

The incidence of lens opacifications that impaired vision (cataract) was analyzed among 831 patients who were injected with known dosages of 224Ra in Germany shortly after World War II. The dependence of the incidence on dosage, i.e., injected activity per unit body weight, and on time after treatment was determined. The observations are equally consistent with proportionality of the incidence of cataract to the square of dosage or with a linear dependence beyond a threshold of 0.5 MBq/kg. The possibility of a linear dependence without threshold was strongly rejected (P less than 0.001). The analysis of temporal dependences yielded a component that was correlated with the injected amount of 224Ra and a component that was uncorrelated. The former was inferred by a maximum likelihood analysis to increase approximately as the square of the time after treatment. The component unrelated to the treatment was found to increase steeply with age and to become dominant within the collective of patients between age 50 and 60. The relative magnitudes of the two components were such that a fraction of 55 to 60% of the total of 58 cataracts had to be ascribed to the dose-related incidence. Impaired vision due to cataract was diagnosed before age 54 in 25 cases. In terms of injected activity per unit body weight no dependence of the sensitivity on age was found; specifically there was no indication of a faster occurrence of the treatment-related cataracts in patients treated at older ages.     

In vivo inhibition of l-buthionine-(S,R)-sulfoximine-induced cataracts by a novel antioxidant, N-acetylcysteine amide

The effects of N-acetylcysteine amide (NACA), a free radical scavenger, on cataract development were evaluated in Wistar rat pups. Cataract formation was induced in these animals with an intraperitoneal injection of a glutathione (GSH) synthesis inhibitor, l-buthionine-(S,R)-sulfoximine (BSO). To assess whether NACA has a significant impact on BSO-induced cataracts, the rats were divided into four groups: (1) control, (2) BSO only, (3) NACA only, and (4) NACA+BSO. The control group received only saline ip injections on postpartum day 3, the BSO-only group was given ip injections of BSO (4mmol/kg body wt), the NACA-only group received ip injections of only NACA (250mg/kg body wt), and the NACA+BSO group was given a dose of NACA 30min before administration of the BSO injection. The pups were sacrificed on postpartum day 15, after examination under a slit-lamp microscope. Their lenses were analyzed for selective oxidative stress parameters, including glutathione (reduced and oxidized), protein carbonyls, catalase, glutathione peroxidase, glutathione reductase, and malondialdehyde. The lenses of pups in both the control and the NACA-only groups were clear, whereas all pups within the BSO-only group developed well-defined cataracts. It was found that supplemental NACA injections during BSO treatment prevented cataract formation in most of the rat pups in the NACA+BSO group. Only 20% of these pups developed cataracts, and the rest retained clear lenses. Further, GSH levels were significantly decreased in the BSO-only treated group, but rats that received NACA injections during BSO treatment had these levels of GSH replenished. Our findings indicate that NACA inhibits cataract formation by limiting protein carbonylation, lipid peroxidation, and redox system components, as well as replenishing antioxidant enzymes.     

Prevention of cataract development in severely galactosemic rats by the aldose reductase inhibitor, tolrestat

With a fixed time period of galactose feeding, the rate of appearance of lenticular opacities depended on the severity of galactosemia, while with a fixed amount of galactose fed, the rate was time dependent. The capacity of tolrestat, a structurally novel inhibitor of aldose reductase (AR), to control cataract development was assessed in rats fed 30-50% galactose with the diet for 7 to 277 days. In rats fed 30% galactose for 31 days, the controlling effect of tolrestat was dose dependent, and no cataracts were detected at a dose of 35 mg/kg/day. In rats given tolrestat with the diet for 14 days, then rendered severely galactosemic with a diet containing 50% galactose, and subjected to continued treatment with tolrestat at a dose of 43 mg/kg/day, no changes were detected by slit-lamp microscopy after 207 days. The preventive effect was also dose dependent. In view of the established similarity in the pathogenesis of galactosemic and diabetic cataracts, the results obtained with tolrestat support its potential for controlling cataract development in diabetics.     

Effect of estrogen on radiation-induced cataractogenesis

Cataractogenesis is a widely reported late effect that is observed in patients receiving total-body irradiation (TBI) prior to bone marrow transplantation or radiotherapy for ocular or head and neck cancers. Recent studies indicate that estrogens may protect against age-related and drug-induced cataracts. Moreover, other reports suggest that estrogen possesses antioxidant properties. Since the effect of estrogen on radiation cataractogenesis is unknown, we wished to determine whether estrogen modulates radiation-induced opacification of the lens. Intact or ovariectomized Sprague-Dawley rats were treated with either 17-beta-estradiol or an empty silastic capsule. The right orbit was then irradiated with either 10 or 15 Gy of (60)Co gamma rays using a Leksell Gamma Knife, and lenses were examined at various times postirradiation with a slit lamp or evaluated for light transmission. We found that for ovariectomized rats irradiated with 15 Gy, the lens opacity and the incidence of cataract formation in the estradiol-treated group were significantly increased compared to the control group at the end of the 25-week period of observation. Cataract incidence was also high in irradiated eyes of ovary-intact animals at 25 weeks postirradiation but was greatly reduced in the ovariectomized control group, with less than half of irradiated eyes showing evidence of cataractogenesis. Thus, after irradiation with 15 Gy of gamma rays, estrogen increased the incidence of cataract formation. We also observed that although the incidence of cataract formation in rats irradiated with 10 Gy and receiving continuous estrogen treatment was not altered compared to rats in the control group that did not receive estrogen, the latent period for posterior subcapsular cataract formation decreased and the severity of the anterior cataract increased. Taken together, our data suggest that estrogen accelerates progression of radiation-induced opacification.     

Diverse roles of Eph/ephrin signaling in the mouse lens

Recent genetic studies show that the Eph/ephrin bidirectional signaling pathway is associated with both congenital and age-related cataracts in mice and humans. We have investigated the molecular mechanisms of cataractogenesis and the roles of ephrin-A5 and EphA2 in the lens. Ephrin-A5 knockout (-/-) mice often display anterior polar cataracts while EphA2(-/-) lenses show very mild cortical or nuclear cataracts at weaning age. The anterior polar cataract of ephrin-A5(-/-) lenses is correlated with multilayers of aberrant cells that express alpha smooth muscle actin, a marker for mesenchymal cells. Only select fiber cells are altered in ephrin-A5(-/-) lenses. Moreover, the disruption of membrane-associated β-catenin and E-cadherin junctions is observed in ephrin-A5(-/-) lens central epithelial cells. In contrast, EphA2(-/-) lenses display normal monolayer epithelium while disorganization is apparent in all lens fiber cells. Immunostaining of ephrin-A5 proteins, highly expressed in lens epithelial cells, were not colocalized with EphA2 proteins, mainly expressed in lens fiber cells. Besides the previously reported function of ephrin-A5 in lens fiber cells, this work suggests that ephrin-A5 regulates β-catenin signaling and E-cadherin to prevent lens anterior epithelial cells from undergoing the epithelial-to-mesenchymal transition while EphA2 is essential for controlling the organization of lens fiber cells through an unknown mechanism. Ephrin-A5 and EphA2 likely interacting with other members of Eph/ephrin family to play diverse functions in lens epithelial cells and/or fiber cells.     

晶状体生化的研究 平阳霉素诱发大鼠白内障的研究

 本文报道间日经皮下注射平阳霉素(Pingyangmycin)(25μg/10g体重)于出生后四日之乳鼠可诱发白内障,其诱发率为84.6％。患白内障时晶状体中可溶性蛋白质含量明显降低。经Sephadex G-200柱层析可见βH,γ晶体蛋白降低,α晶体蛋白则相对升高。经10％聚丙烯酰胺凝胶电泳及等电聚焦电泳可见γ晶体蛋白改变明显,这些结果和我们用半乳糖及亚硒酸钠诱发白内障所得结果一致。     

先天性与后天性大鼠白内障晶体中游离氨基酸含量变化的研究

用药物诱发大鼠先天性白内障动物模型,检测了晶体中１８种游离氨基酸（ＦＡＡ）含量,并与大鼠硒性和半乳糖性白内障晶体中ＦＦＡ含量进行了比较,发现：仔一代和仔二代先天性白内障晶体中各ＦＡＡ含量接近;先天性白内障晶体内,酪氨酸和羟脯氨酸含量明显高于正常对照组（Ｐ＜０．０５）;谷氨酸,甘氨酸等９种ＦＡＡ明显低于硒性白内障（Ｐ＜０．０５）;而酪氨酸高于半乳糖性白内障组,半胱氨酸等５种ＦＡＡ含量均低于半乳糖性白内障组。同时还发现：硒性和半乳糖性白内障晶体内一些ＦＡＡ变化与以往报道不同,这些现象提示先天性与后天性白内障病变过程可能不同。     

Expression changes in mRNAs and mitochondrial damage in lens epithelial cells with selenite

An overdose of sodium selenite induces cataracts in young rats. The mid-stage events producing the cataract include calpain-induced hydrolysis and precipitation of lens proteins. Apoptosis in lens epithelial cells has been suggested as an initial event in selenite cataracts. Expression levels of two genes associated with apoptosis were altered in lens epithelial cells from selenite-injected rats. The purpose of the present experiment was to perform a more comprehensive search for changes in expression of mRNAs in lens epithelial cells in order to more fully delineate the early events in selenite-induced cataracts. Lens epithelial cells were harvested at 1 and 2 days after a single subcutaneous injection of sodium selenite (30 mumol/kg body weight) into 12-day-old rats. Gene expression was analyzed using a commercial DNA array (Rat Genome U34A GeneChip array, Affymetrix). Of approximately 8000 genes assayed by hybridization, 13 genes were decreased and 27 genes were increased in the rat lens epithelial cells after injection of selenite. Some of the up-regulated genes included apoptosis-related genes, and a majority of the down-regulated genes were mitochondrial genes. Previously observed changes in expression of EGR-1 mRNA were also confirmed. Changes in the expression patterns of mRNAs were also confirmed by RT-PCR. To determine the mechanism for damage of lens epithelial cells (alpha TN4 cell) by culture in selenite, leakage of cytochrome c from mitochondria was measured. Selenite caused significant leakage of cytochrome c into the cytosol of alpha TN4 cells. Our data suggested that the loss of integrity of lens epithelial cells by selenite might be caused by preferential down-regulation of mitochondrial RNAs, release of cytochrome c, and impaired mitochondrial function. Up-regulation of mRNAs involved in maintenance of DNA, regulation of metabolism, and induction of apoptosis may also play roles.     

Platelet-derived growth factor D, tissue-specific expression in the eye, and a key role in control of lens epithelial cell proliferation

Platelet-derived growth factor D (PDGF-D), also known as Iris-expressed growth factor, is a member of the PDGF/vascular endothelial growth factor family. The expression of PDGF-D in the eye is tissue-specific. In the anterior segment, it is localized to iris and ciliary body, whereas in the retina, PDGF-D is restricted to the outer plexiform layer. PDGF-D is present in aqueous humor but is not detectable in mature lens or in mouse lens-derived alphaTN4-1 cells. However, it is expressed in rabbit lens-derived N/N1003A cells. N/N1003A cell-conditioned medium stimulates proliferation in rat lens explants, and this is blocked by immunodepletion of PDGF-D. Immunopurified PDGF-D also stimulates cell proliferation in rat lens explants and in NIH 3T3 cells. In organ culture of rat eye anterior segments, anti-PDGF-D strongly inhibits lens epithelial cell proliferation. This finding suggests a major in vivo role for PDGF-D in the mechanisms of coordinated growth of eye tissues. Intervention in the PDGF-D pathway in the eye, perhaps by antibody or blocking peptide, could be useful in the treatment of certain cataracts, including post-operative secondary cataract.     

Mutation in LIM2 Is Responsible for Autosomal Recessive Congenital Cataracts

PurposeTo identify the molecular basis of non-syndromic autosomal recessive congenital cataracts (arCC) in a consanguineous family.MethodsAll family members participating in the study received a comprehensive ophthalmic examination to determine their ocular phenotype and contributed a blood sample, from which genomic DNA was extracted. Available medical records and interviews with the family were used to compile the medical history of the family. The symptomatic history of the individuals exhibiting cataracts was confirmed by slit-lamp biomicroscopy. A genome-wide linkage analysis was performed to localize the disease interval. The candidate gene, LIM2 (lens intrinsic membrane protein 2), was sequenced bi-directionally to identify the disease-causing mutation. The physical changes caused by the mutation were analyzed in silico through homology modeling, mutation and bioinformatic algorithms, and evolutionary conservation databases. The physiological importance of LIM2 to ocular development was assessed in vivo by real-time expression analysis of Lim2 in a mouse model.ResultsOphthalmic examination confirmed the diagnosis of nuclear cataracts in the affected members of the family; the inheritance pattern and cataract development in early infancy indicated arCC. Genome-wide linkage analysis localized the critical interval to chromosome 19q with a two-point logarithm of odds (LOD) score of 3.25. Bidirectional sequencing identified a novel missense mutation, c.233G>A (p.G78D) in LIM2. This mutation segregated with the disease phenotype and was absent in 192 ethnically matched control chromosomes. In silico analysis predicted lower hydropathicity and hydrophobicity but higher polarity of the mutant LIM2-encoded protein (MP19) compared to the wild-type. Moreover, these analyses predicted that the mutation would disrupt the secondary structure of a transmembrane domain of MP19. The expression of Lim2, which was detected in the mouse lens as early as embryonic day 15 (E15) increased after birth to a level that was sustained through the postnatal time points.ConclusionA novel missense mutation in LIM2 is responsible for autosomal recessive congenital cataracts.     

A juvenile-onset, progressive cataract locus on chromosome 3q21-q22 is associated with a missense mutation in the beaded filament structural protein-2

Juvenile-onset cataracts are distinguished from congenital cataracts by the initial clarity of the lens at birth and the gradual development of lens opacity in the second and third decades of life. Genomewide linkage analysis in a multigenerational pedigree, segregating for autosomal dominant juvenile-onset cataracts, identified a locus in chromosome region 3q21.2-q22.3. Because of the proximity of the gene coding for lens beaded filament structural protein-2 (BFSP2) to this locus, we screened for mutations in the coding sequence of BFSP2. We observed a unique C-->T transition, one that was not observed in 200 normal chromosomes. We predicted that this led to a nonconservative R287W substitution in exon 4 that cosegregated with cataracts. This mutation alters an evolutionarily conserved arginine residue in the central rod domain of the intermediate filament. On consideration of the proposed function of BFSP2 in the lens cytoskeleton, it is likely that this alteration is the cause of cataracts in the members of the family we studied. This is the first example of a mutation in a noncrystallin structural gene that leads to a juvenile-onset, progressive cataract.     

Increased content of zinc and iron in human cataractous lenses

The purpose of the study was to examine the zinc and iron content of human lenses in different types of cataract and to investigate the possible influence of diabetes on the zinc and iron content of the lens. Iron and zinc of 57 human lenses (28 corticonuclear cataracts and 29 mature cataracts with a mean age of 70.6±16.1 and 74.7±11.1 yr, 41 nondiabetics and 16 diabetics) were determined by atomic absorption spectroscopy. The zinc content of human lenses was significantly increased in mature cataracts compared to corticonuclear cataracts (0.51±0.33 vs 0.32±0.20 μmol/g dry mass, p=0.012). The iron content of mature cataracts was also higher than in corticonuclear cataracts (0.11±0.09 vs 0.07±0.05 μmol/g dry mass, p=0.071). Furthermore, a significant increase of the lens zinc content could be observed with increasing lens coloration (light brown 0.33±0.17 vs dark brown 0.52±0.35 μmol/g dry mass, p=0.032). Diabetic patients seem to have both increased zinc and iron contents in the lens compared to nondiabetic subjects (zinc: 0.45±0.42 vs 0.40±0.22 μmol/g dry mass; iron: 0.12±0.10 vs 0.08±0.05 μmol/g dry mass). These data suggest a possible influence of the lens zinc and iron content on the development of lens opacification. Especially advanced forms of cataract and dark brown colored lenses show significantly increased zinc and iron content.