Long-Term Toxic Effects of Low-Dose Lead Exposure on the Retina of Albino Rats and the Possible Protective Role of Vitamin C Versus Vitamin E: A Toxicological Ultrastructural Biochemical Study

The study was conducted to determine if there was a selective change in the retina following low-level lead exposure and to correlate these changes with ultrastructural observations as well as, explaining these histological and ultrastructural alterations in the light of the biochemical results. In addition, the possible protective role of vitamin C or E at this level of exposure is to be obviated. Finally, it is done to elucidate the possible mechanisms by which low doses of lead induce retinal toxicity on long-term exposure. For these objectives, the study included 36 Wistar albino rats were studied for 16 weeks and which were divided into 6 groups, 6 in each group. Group (1) received water (control); group (2) received lead acetate; group (3) received vitamin C; group (4) received lead acetate and vitamin C; group (5) received vitamin E and group (6) received lead acetate and vitamin E. Semithin sections of the retinae were prepared from all groups, while ultrathin sections were done from groups (2) and (6) only. Retinal tissue homogenates were examined for the estimation of glutathione (GSH), superoxide dismutase (SOD), catalase (Cat), malondialdehyde (MDA) and lead concentrations. It was found that long-term exposure to low levels of lead affected all the retinal layers; however, the most striking deleterious effect was on the mitochondria. In addition, it also damaged the phagocytic activity of the Muller cells which are quite diverse throughout the different layers of the retina. These histological changes were proved to be resulting from a positive oxidative stress status presented in the form of reduced activity of endogenous antioxidants as (SOD), (GSH) and (Cat) and increased levels of the lipid peroxidation product (MDA). Supplementation with exogenous antioxidahts as vitamins C or E potentiated a significant harmonical interaction among the endogenous antioxidants. However, it has been proved that vitamin E can restore the retinal histological pattern better than vitamin C. The possible roles by which lead induced retinal damage included the lead-induced reduction of the antioxidant defences indicating a possible role of free radicals in the pathogenesis of lead toxicity. Another role was through the damage of the phagocytic activity of the Muller cells by depleting these cells from their (GSH) content. This consequently, affected the harmonical action of the other endogenous antioxidants as (SOD) and (Cat.).