UV-B and early cortical and nuclear changes in the human lens

Abstract

Experimental studies in mice and rats have shown that UV (B) irradiation leads to specific lens changes, viz. yellowing of the nucleus and a multilayered epithelium in the anterior pole with disrupted cortical fibres underneath. Biomicroscopic and ultrastructural studies on ageing human lenses revealed yellowing of the lens nucleus and locally ruptured membranes and small opacities in the equatorial cortex. No changes in the anterior pole were ever observed. This discrepancy between the human and animal lens, contraindicating UV as an important risk factor for human cataract, is discussed and may be due to several factors: (1) a difference between the high level acute and low level chronic irradiation; (2) species differences: nocturnal animals may be unable to cope with bright light exposure; (3) differences in scavenger and other defense mechanisms between humans and animals.

Redox Regulation in Age-Related Cataracts: Roles for Glutathione, Vitamin C, and the NRF2 Signaling Pathway

“…Analysis of age-related cataractous lenses from human diabetic or non-diabetic samples showed decreased methylation of the KEAP1 promoter, which in turn upregulates KEAP1 expression, and inhibits the NRF2 antioxidant response [111,115]. Downstream targets of NRF2, including glutathione synthesis, thioredoxin reductase, glutathione reductase, thioltransferases, and levels of all these antioxidant enzymatic functions have been shown to be decreased in cataracts [28,32,[116][117][118]. We recently demonstrated that male and female NRF2 knockout mice (Nrf2-/-) have increased We previously demonstrated that low glycemic index diets protect mice from agerelated macular degeneration-like phenotypes [119][120][121][122].…”