Color vision and contrast sensitivity tests in early diagnosis of primary open-angle glaucoma.

Color vision was examined by the Farnsworth 100 hue test in 48 eyes with ocular hypertension (OHT). Thirteen eyes had a general loss of color discrimination and 8 had a blue-yellow axis. Spatial contrast sensitivity was tested in 31 eyes with OHT by the Mentor B-VAT and was reduced in 8 of them. Temporal contrast sensitivity was explored in 40 eyes with OHT by the Flickersyst&m and showed abnormal responses in 11 eyes. According to the lack of specificity of the responses and the overlapping of the results of normal eyes and OHT eyes, those tests are not useful for classifying an individual patient. Such investigations however have the interest to show that macular mediated functions may be impaired early in glaucoma.

Effect of visible light on benzo(a)pyrene binding to DNA of cultured human skin epithelial cells.

The ubiquity of the photosensitive carcinogen benzo(a)pyrene (BP) and visible light in the environment suggests that their interaction might lead to photoproducts harmful to humans. To test the combined impact of these two agents on human epithelial cells, binding of BP to cellular DNA was assessed following treatment of cultures with BP and low-intensity (4.6 watts/sq m) intermittent (12 hr daily, 3 to 5 days) cool white fluorescent light. Light exposure reduced the formation of covalent BP adducts 20-fold (from 150 to 7 pmol BP per mg DNA) in cells treated with 1 microgram BP per ml and completely inhibited cytotoxicity; even with 10 microgram BP per ml, light exposure markedly inhibited cytotoxicity. However, at low BP dosage (0.1 microgram/ml), covalent adducts (2 pmol/mg DNA) to cellular DNA are produced and their formation is not influenced by light. These adducts persisted for at least 7 days following treatment; this observation suggests that chronic low-level exposure of human epithelium to BP may lead to an accumulation of DNA damage.

Visible light-induced DNA crosslinks in cultured mouse and human cells.

Cool-white fluorescent light induces crosslinks in DNA when proliferating cells are exposed at 37 degrees C for 20 h to 4.6 J/m2/s in culture medium supplemented with fetal bovine serum. Using the Kohn alkaline elution technique, we now find that: 1. Increased light intensity increases DNA crosslinks. 2. The crosslinking is medium-mediated. 3. Oxygen enhances the crosslinking. 4. The extent of crosslinking is decreased at high cell density. 5. The crosslinks can be removed by digestion with proteinase K (0.02 to 0.50 mg/ml). 6. Human cell lines including those derived from adult prostate, fetal lung (IMR-90) and mixed fetal tissues are susceptible to light-induced crosslinks. 7. Crosslinkage is not decreased by addition of catalase to the medium and the effective wavelength is probably between 450 nm and 490 nm. From these results we conclude that the mechanism of light-induced crosslinks differs from that of light-induced chromatid breaks and that the major lesion observed is protein-DNA cross-linkage rather than DNA strand breaks.

Increased susceptibility of mouse cells to fluorescent light-induced chromosome damage after long-term culture and malignant transformation.

Exposure of mouse cells in culture to fluorescent light has been shown to produce chromatid breaks and exchanges. Hydrogen peroxide formed in the cell during illumination has been implicated as the causative agent. The present results indicate that susceptibility to light-induced chromosome damage increases with time in culture and seems to be associated with or requisite for the spontaneous malignant transformation of mouse cells. All three cell lines followed during long-term culture that either became tumorigenic or showed cytological evidence of neoplastic transformation developed a concomitant increase in susceptibility. In three additional cell lines, susceptibility to light-induced chromatid damage was significantly increased in the spontaneously transformed malignant cells as compared with their nonneoplastic precursors. The increased susceptibility is not simply the result of long-term culture, since three other nonneoplastic cell lines after prolonged culture were significantly less susceptible than their malignant counterparts. Increased susceptibility to light-induced chromatid damage could result from impaired DNA repair or from the loss of defense mechanisms for destroying H2O2 or scavenging free radicals.