thiobarbituric-acid and Cataract

Previous studies have suggested that free radicals and related species play a role in lens damage. The molecules involved may include proteins, lipids and DNA. Focal cortical changes and cortical liquefaction have been reported in patients with Down's syndrome over the age of 15 years. There is evidence supporting the hypothesis that trisomy 21 patients have an increase in free radical reactions and lipoperoxidation susceptibility. This could be due to an increase in the H2O2 generation catalysed by CuZn SOD although the activity of other gene products coded for on chromosome 21 cannot be excluded. Thiobarbituric acid reactive products were measured in human erythrocytes of nine DS patients and nine age-matched controls. There was a significant increase in the first group (21.0 +/- 2.3 nmol MDA/g Hb vs 16.4 +/- 2.9 nmol MDA/g Hb; p less than or equal to 0.01). In plasma, however, TBA products and antioxidant levels (ascorbic acid, tocopherol and uric acid) were not significantly different. Further studies should be carried out, namely through the use of more specific and sensitive methods, to assess the possible association between oxidative stress and cortical lens damage in DS patients.

Topics: Adolescent; Adult; Ascorbic Acid; Cataract; Child; Child, Preschool; Down Syndrome; Erythrocytes; Free Radicals; Humans; Infant; Lipid Peroxidation; Oxygen; Superoxide Dismutase; Thiobarbiturates; Uric Acid; Vitamin E

Investigations of aqueous humor in primary open-angle glaucoma have shown a change in its normal contents: decreased ascorbic acid in it and increased secondary products of lipid peroxidation. In patients with glaucoma of stages III and IV, a correlative relationship between them is recorded (r = -0.78). It is suggested that in the pathomechanism of increased intraocular pressure in primary glaucoma activation of the process of lipid peroxidation plays a role due to decreased concentration of ascorbic acid in the aqueous humor, being one of the most important components of antioxidative system of the eye.

Topics: Aged; Aqueous Humor; Ascorbic Acid; Cataract; Female; Glaucoma, Open-Angle; Humans; Lipid Peroxidation; Male; Middle Aged; Spectrophotometry; Thiobarbiturates

The Royal College of Surgeons (RCS) rat has been extensively studied as a model system for inherited retinal degeneration. As in a number of human retinal degenerative diseases, posterior subcapsular cataracts (PSC) are associated with the retinal changes. It has been hypothesized recently that such cataracts may be initiated by toxic products generated by the peroxidation of polyunsaturated lipid components from degenerating photoreceptor outer segments. In the present study, the possibility that such a mechanism might be responsible for cataract initiation in the RCS rat has been investigated. The degeneration of the rod outer segments (ROS) occurs rapidly in these animals, beginning a few weeks after birth. Due to the failure of the retinal pigmented epithelium to phagocytize normally, ROS degeneration is accompanied by an accumulation of debris in the eye. During the brief period of maximal debris accumulation there is a marked increase in lipid peroxidation products in the vitreous. Cataract formation is correlated temporally with these events, becoming evident immediately following the time during which peroxidation products are present in the vitreous. In addition, the primary damage detected in the RCS lenses is an increase in the passive permeability of the lens membranes. Similar lens damage has been found in studies in which normal rat lenses were exposed to degenerating ROS in vitro. These findings are consistent with the hypothesis that cataracts in the RCS rat may be initiated by toxic lipid peroxidation products.

Topics: Aging; Animals; Cataract; Cell Membrane Permeability; In Vitro Techniques; Lipid Peroxides; Photoreceptor Cells; Rats; Rats, Inbred Strains; Retinal Degeneration; Rod Cell Outer Segment; Spectrometry, Fluorescence; Thiobarbiturates