Evidence suggests that prolonged blue-light exposure can impact vision; however, less is known about its impact on non-visual higher-order functions in the brain, such as learning and memory. Blue-light-blocking lenses (BBLs) claim to reduce these potential impacts. Hence, we assessed structural and functional hippocampal alterations following blue-light exposure and the protective efficacy of BBLs. Male Wistar rats were divided into (n = 6 in each group) normal control (NC), blue-light exposure (LE), and blue-light with BBLs (Crizal Prevencia, CP and DuraVision Blue, DB) groups. After 28 days of light exposure (12:12 light: dark cycle), rats were trained for the Morris water maze memory retention test, and brain tissues were sectioned for hippocampal neuronal analysis using Golgi and Cresyl violet stains. The memory retention test was significantly delayed (p < 0.05) in LE compared with DB groups on day 1 of training. Comparison of Golgi-stained neurons showed significant structural alterations, particularly in the basal dendrites of hippocampal neurons in the LE group, with BBLs significantly mitigating these structural changes (p < 0.05). Comparison of Cresyl-violet-stained neurons revealed significantly (p < 0.001) increased degenerated hippocampal neurons in LE rats, with fewer degenerated neurons in the CP lens group for CA1 neurons (p < 0.05), and for both CP and DB groups (p < 0.05) for CA3 neurons. Thus, in addition to documented effects on visual centers, high-level blue-light exposure also results in degeneration in hippocampal neurons with associated behavioral deficits. These changes can be partially ameliorated with blue-light-blocking lenses.

The exposure to blue and white Light emitting diodes (LED) light leads to damage in the visual system with short-term LED light exposure. Chronic exposure, adaptive responses to light, and self-protective mechanisms against LED light exposures need to be explored, and it would be essential to understand the repercussions of LED radiation on vitreous metabolites. A total of 24 male Wistar rats were used in this study, divided into four groups (n = 6 in each group). Three experimental groups of rats were exposed to either blue, white, or yellow LED light for 90 days (12:12 light-dark cycle routine) with uniform illumination (450–500 lux). Standard lab settings were used to maintain control rats. Vitreous fluids were subjected to untargeted metabolomics analysis using liquid chromatography-mass spectrometry (LC/MS). PLS-DA analysis indicated significant the separation of m metabolites among groups, suggesting that LED exposure induces metabolic reprogramming in the vitreous. Amino acids and their modifications showed significant alterations among groups which included D-alanine, D-serine (p < 0.05), lysine (p < 0.001), aspartate (p = 0.0068), glutathione (p = 0.0263), taurine (p = 0.007), and hypotaurine. In chronic light exposure, the self-protective or reworking system could be depleted, which may decrease the ability to compensate for the defending mechanism. This might fail to maintain the metabolomic structural integrity of the vitreous metabolites.