The effects of lutein on cisplatin-induced retinal injury: an experimental study

Aim: Lutein is one of the most common carotenoids defined in human plasma as having potent anti-oxidant effects. We aimed to determine the biochemical and histopathological effects of lutein on cisplatin-induced oxidative retinal injury in rats. Materials and methods: Twenty-four rats were equally divided into four groups as healthy controls (HC group), only cisplatin (5 mg/kg) administered group (CIS group), Lutein (0.5 mg/kg) + cisplatin (5 mg/kg) administered group (LC group), and only Lutein (0.5 mg/kg) (LUT group) administered group. From the blood samples obtained, serum malondialdehyde (MDA), total glutathione (tGSH), interleukin 1 beta (IL-1β), and tumor necrosis factor alpha (TNF-α) levels were investigated. In histopathological analyses, the total retinal thickness, retinal pigment epithelium (RPE), photoreceptor layer (PL), outer nuclear layer (ONL), outer plexiform layer (OPL), inner nuclear layer (INL), inner plexiform layer (IPL), and ganglion cell layer (GCL) were evaluated. Results: MDA, IL-1β, and TNF-a levels were statistically significantly higher (p < 0.001) in CIS group compared with other three groups while tGSH levels were statistically significantly lower (p < 0.001). In subgroup analyses, there was no any statistically significant difference regarding all four parameters analyzed between HC, LC, and LUT groups. In histopathological analyses, cisplatin-induced retinal damage included atrophy and disorganization on outer segment, degeneration and detachment of RPE and PL from choroid, degeneration and edema of INL and IPL, total degeneration of GCL; while cisplatin-induced retinal damage was determined to be significantly prevented with 0.5 mg lutein treatment on histopathological evaluations. Conclusions: Lutein co-administration was highly effective in prevention of cisplatin-induced retinal damage due to the anti-oxidant and anti-inflammatory effects of lutein. © 2018, © 2018 Informa UK Limited, trading as Taylor & Francis Group.