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B. C. Lane; Defining Stages of Fish-Methylmercury-Induced Cataract. Invest. Ophthalmol. Vis. Sci. 2010;51(13):4559.
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To recognize clinical signs and document initiation and progression of a fish-methylmercury (MeHg) induced cataract and to differentiate it from similar-appearing lens anomalies.
This survey included more than 300 cataract cases and more than 150 controls from our Fish MeHg Cataract Open Panel Study. We studied biomicroscopic and ophthalmoscopic findings and lens photos of these patients, ages 9-96, as they changed over time, totalling more than 1300 patient visits, followed for as much as 14 years. We tabulated each patient's customary intake of individual species of large fish, organic mercury measured in nape-of-neck hair and in erythrocyte (rbc) specimens. We also recorded associated estimated average intake of ascorbic acid and selenium and rbc-concentration of glutathione peroxidase, possibly protective against MeHg cataractogenesis.
Stage 1: Hg elevation in diet, hair, urine, blood, but no signs in lenses. Stage 2: Anterior Subcapsular vacuoles (ASC) start as widely separated single vacuoles in central 6 mm and then begin to aggregate. Stage 3: Migrated ASC appear as Posterior Subcapsular vacuoles (PSC) and may acquire a ruddy color. Stage 4: In an average of approximately 5 years after start of Stage 3 with continuing Hg intake, nucleus becomes severely involved with myopic shift in focus. Differential Dx: Sun-induced cortical-spicule vacuoles start behind the iris, not in central 6 mm, and are attributed to transmission of infrared radiation from overheating of the sun-exposed iris. Steroid-induced PSC starts as PSC and progresses to ASC. Vitamin C and other chelators can chelate with Hg and mitigate the effect of fish MeHg intake. Lutein and zeaxanthin intakes appear associated with mitigation of Stage 4. It is our observation that eating fish can be healthy. The cataractogenesis problem derives from eating those larger fish that are rich in organic mercury.
Stages can be identified in the induction of a fish-MeHg-induced cataract. Vacuoles first appear at the germinative anterior pole of the lens where new epithelial cells arise as the lens grows through life. Hg-toxicity damages the protective enzymes, especially Glutathione Peroxidase, an effect we measured and reported previously. The Hg-induced vacuoles (ASC & PSC) and toxicity are associated with damage to the Na,K ATP-ase ion pump. The data shows the progression from ASC (vacuoles) visible in the undilated pupil to PSC and eventually to the compromised nucleus metabolism.
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