Can Persistent Blue Light Exposure Cause a Molecular Shift in the Vitreous of Rodents?

This experimental rodent study aimed to explore changes in the vitreous metabolome caused by prolonged chronic environmental blue light stress and to elucidate the underlying mechanisms. Four separate groups of control (NC), blue light (LE), two blue blocking lenses (blue light–blocking lenses (BBLs), BL + Crizal Prevencia (CP) and BL+Duravision Blue protect (DP) and 8‐week‐old albino male Wistar rats were used in this experiment. Animals were subjected to blue LED light, with and without BBLs, for 90 days under a 12:12‐h light:dark cycle and constant illumination at 450–500 lux. The control animals were maintained in standard laboratory conditions. Postexposure, the vitreous fluid (VF) was aspirated, stored at −20°C, and processed for LC‐MS. We observed significant variation in amino acid (AA) abundance across four groups: normal control (NC), light exposure (LE), light exposure with Duravision Blue (DB) and light exposure with CP lenses. Specifically, there was a significant difference in AA content between NC and LE [ F (21, 178) = 4.667, p < 0.0001], between LE and CP [ F (21, 181) = 7.971, p < 0.0001], between LE and DB [ F (21, 179) = 13.06, p < 0.0001], between NC and CP [ F (21, 184) = 11.46, p < 0.0001] and between all groups in general [ F (21, 182) = 14.22, p < 0.0001]. Pathway‐level analysis with false discovery rate (FDR) correction identified significant enrichment in phenylalanine and tyrosine metabolism, valine/leucine/isoleucine degradation and beta‐alanine metabolism pathways. From these results, it can be inferred that BBLs and light exposure significantly influence the presence of AAs compared with NC and LE. Persistent exposure to cumulative blue light can alter vitreous metabolites, potentially affect micro‐ and macromolecular components of the VF and carry functional consequences for vitreoretinal health.