Selected Topics in Ophthalmic Biochemistry

A Study of Diabetic and Non-diabetic Human Cataract Lens by Scanning Electron Microscopy

“…Characteristic findings of a completely developed diabetic cataract are snowflake-like opacifications of the anterior and posterior lens cortex. [9][10] Another proposed mechanism is non-enzymatic glycation. Advanced glycation arises during normal aging but to a greater degree in diabetic patients, contributing to lens opacity formation.…”

A Study of Diabetic and Non-diabetic Human Cataract Lens by Scanning Electron Microscopy

“…Characteristic findings of a completely developed diabetic cataract are snowflake-like opacifications of the anterior and posterior lens cortex. [9][10] Another proposed mechanism is non-enzymatic glycation. Advanced glycation arises during normal aging but to a greater degree in diabetic patients, contributing to lens opacity formation.…”

Oxidation-Induced Mixed Disulfide and Cataract Formation: A Review

“…The possible presence of protein-bound thiols in the lens was first suggested by Hermann and Moses in 1945 but no data were provided [21]. Kinoshita in his 1964 review [22] discussed the loss of GSH in ionizing and galactose cataracts and suggested that mixed disulfides might be formed, impairing metabolic functions. The observation of decreased levels of GSH in human cataractous lenses [23,24,25] led to the expectation that mixed disulfides could be generated during the development of senile cataracts.…”

“…With nuclear cataract development, the concentration of free GSH decreases even further than with age [13,22,23,24,26] falling below the suggested 1 mM threshold for cataract formation [40] and continuing to decrease with increasing nuclear color. In the most advanced cataract (dark brown, Type IV [8]), nuclear GSH drops to 0.15 mM [12,39].…”

Vitreoretinal Hemorrhages after Ingestion of Fava Beans in a G-6-PD-Deficient Subject

“…The enzyme deficiency, which is mainly evident at the level of RBC, involves also white blood cells (WBC), platelets, liver, and lens, where it has been related to the appearance of cataracts [.Zinkham, 1961;Kinoshita, 1964;Westring and Pisciotta, 1966;Charlton and Van Heyningen, 1971;Orzalesi et al, 1976). Ocular complications involving the posterior segment of the eye have been reported in G-6-PD-deficient sub jects following acute hemolytic crises [Pasca, 1945;Choremis et al, 1960;Bertoni et al, 1969).…”

A Study of Diabetic and Non-diabetic Human Cataract Lens by Scanning Electron Microscopy

“…Characteristic findings of a completely developed diabetic cataract are snowflake-like opacifications of the anterior and posterior lens cortex. [9][10] Another proposed mechanism is non-enzymatic glycation. Advanced glycation arises during normal aging but to a greater degree in diabetic patients, contributing to lens opacity formation.…”

Oxidation-Induced Mixed Disulfide and Cataract Formation: A Review

“…The possible presence of protein-bound thiols in the lens was first suggested by Hermann and Moses in 1945 but no data were provided [21]. Kinoshita in his 1964 review [22] discussed the loss of GSH in ionizing and galactose cataracts and suggested that mixed disulfides might be formed, impairing metabolic functions. The observation of decreased levels of GSH in human cataractous lenses [23,24,25] led to the expectation that mixed disulfides could be generated during the development of senile cataracts.…”

“…With nuclear cataract development, the concentration of free GSH decreases even further than with age [13,22,23,24,26] falling below the suggested 1 mM threshold for cataract formation [40] and continuing to decrease with increasing nuclear color. In the most advanced cataract (dark brown, Type IV [8]), nuclear GSH drops to 0.15 mM [12,39].…”

Vitreoretinal Hemorrhages after Ingestion of Fava Beans in a G-6-PD-Deficient Subject

“…The enzyme deficiency, which is mainly evident at the level of RBC, involves also white blood cells (WBC), platelets, liver, and lens, where it has been related to the appearance of cataracts [.Zinkham, 1961;Kinoshita, 1964;Westring and Pisciotta, 1966;Charlton and Van Heyningen, 1971;Orzalesi et al, 1976). Ocular complications involving the posterior segment of the eye have been reported in G-6-PD-deficient sub jects following acute hemolytic crises [Pasca, 1945;Choremis et al, 1960;Bertoni et al, 1969).…”

A Study of Diabetic and Non-diabetic Human Cataract Lens by Scanning Electron Microscopy

“…Characteristic findings of a completely developed diabetic cataract are snowflake-like opacifications of the anterior and posterior lens cortex. [9][10] Another proposed mechanism is non-enzymatic glycation. Advanced glycation arises during normal aging but to a greater degree in diabetic patients, contributing to lens opacity formation.…”

Oxidation-Induced Mixed Disulfide and Cataract Formation: A Review

“…The possible presence of protein-bound thiols in the lens was first suggested by Hermann and Moses in 1945 but no data were provided [21]. Kinoshita in his 1964 review [22] discussed the loss of GSH in ionizing and galactose cataracts and suggested that mixed disulfides might be formed, impairing metabolic functions. The observation of decreased levels of GSH in human cataractous lenses [23,24,25] led to the expectation that mixed disulfides could be generated during the development of senile cataracts.…”

“…With nuclear cataract development, the concentration of free GSH decreases even further than with age [13,22,23,24,26] falling below the suggested 1 mM threshold for cataract formation [40] and continuing to decrease with increasing nuclear color. In the most advanced cataract (dark brown, Type IV [8]), nuclear GSH drops to 0.15 mM [12,39].…”

Vitreoretinal Hemorrhages after Ingestion of Fava Beans in a G-6-PD-Deficient Subject

“…The enzyme deficiency, which is mainly evident at the level of RBC, involves also white blood cells (WBC), platelets, liver, and lens, where it has been related to the appearance of cataracts [.Zinkham, 1961;Kinoshita, 1964;Westring and Pisciotta, 1966;Charlton and Van Heyningen, 1971;Orzalesi et al, 1976). Ocular complications involving the posterior segment of the eye have been reported in G-6-PD-deficient sub jects following acute hemolytic crises [Pasca, 1945;Choremis et al, 1960;Bertoni et al, 1969).…”