Vascular leakage is a characteristic incident that occurs with autoimmune uveitis-related breakdown of the blood-retinal barrier. Therefore, additional investigations on the expression of osteopontin and fibronectin within the retinal pigment epithelium in association with autoimmune uveitis are needed to further assess their role in disease pathogenesis. Investigations of molecular mechanisms in autoimmune uveitis are mainly focused on cell-associated proteins, whereas the knowledge about ECM protein expression in disease pathogenesis is limited. We aimed to determine the role of ECM in autoimmune uveitis-related tissues by investigating expression profiles of relevant ECM proteins. The results indicate severe ECM remodeling in autoimmune uveitis highlighted by reduced neuroprotection mediated by Muiller cell-derived osteopontin and a loss of Muiller cell adhesion through fibronectin. Thus the investigation of ECM proteins is particularly worthwhile to gain further insight into the molecular pathomechanisms occurring in autoimmune uveitis affected tissues. The impact of ECM re-modeling and its consequences for the surrounding tissue in autoimmune uveitis merits further investigation. Cadmium, a toxic and nonessential element, pigments, paints, welding, and batteries, which results in both biotic and BAY 43-9006 284461-73-0 abiotic environments. Unlike organic compounds, Cd is not biodegradable and has a very long biological half-life. Cd has been found to produce wide ranges of biochemical and physiological dysfunctions in humans and laboratory animals. Many mammalian organs are adversely affected by Cd, which include kidney, liver, testis, lung, pancreas, prostate, ovary, and placenta, and several studies have illustrated that the testis is exceedingly sensitive to Cd toxicity. It is reported that spermatogenesis was disturbed by free radical. Mounting evidence has also shown that Cd alters antioxidant defense systems and increases production of cellular reactive oxygen species, such as singlet oxygen, hydrogen peroxide, and hydroxyl radicals. ROS can lead to oxidative stress within cells by reacting with macromolecules and cause damages, such as mutations in DNA, destruction of protein function and structure, and peroxidation of lipids as well as alterations in gene expression and apoptosis. Tissue levels of malondialdehyde and the activities of superoxide dismutase, glutathione peroxidase and catalase are proven indicators of oxidative stress. Investigations by our lab have found that Cd changed antioxidant defense systems and induced apoptosis in the hepatopancreas of S. henanense, suggesting that Cd-induced apoptosis may be connected with oxidative stress. Several reports have shown that oxidative stress is an important mechanism of Cd toxicity. In male experimental animals, Cd exposure can reduce testis weight and cause histopathological lesions leading to reduced sperm counts and impaired sperm motility and adversely affect male fertility, and several reports have shown that Cd can induce apoptosis in testis.