Endogenous antioxidants protect cells from
reactive oxygen species (ROS)-related deleterious effects, and an imbalance in the
oxidant/
antioxidant systems generates oxidative stress. Glyoxalase 1 (GLO1) is a ubiquitous cellular
enzyme involved in detoxification of
methylglyoxal (MG), a cytotoxic byproduct of glycolysis whose excess can produce oxidative stress. In
retinitis pigmentosa, one of the most diffuse cause of
blindness, oxidative damage leads to photoreceptor death. To clarify the role of GLO1 in
retinitis pigmentosa onset and progression, we treated human retinal pigment epithelium cells by the
oxidant agent A2E. Transcriptome profiles between treated and untreated cells were performed by
RNA-Seq, considering two time points (3 and 6 h), after the basal one. The exposure to A2E highlighted significant expression differences and splicing events in 370 GLO1 first-neighbor genes, and 23 of them emerged from pathway clustered analysis as main candidates to be associated with
retinitis pigmentosa. Such a hypothesis was corroborated by the involvement of previously analyzed genes in specific cellular activities related to oxidative stress, such as
glyoxylate and dicarboxylate metabolism, glycolysis, axo-dendritic transport,
lipoprotein activity and metabolism, SUMOylation and retrograde transport at the trans-Golgi network. Our findings could be the starting point to explore unclear molecular mechanisms involved in
retinitis pigmentosa etiopathogenesis.