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Updated: Mar 19, 2026
Retinal Pathophysiological Evaluation in a Rat Model
Published on: May 6, 2022
Cadmium-induced systemic inflammation and retinal degeneration: histopathological and cytokine analysis in a rat
Selim Demirtaş1, Gül Şahika Gökdemir2, Uğur Şeker1
1Department of Histology and Embryology, Mardin Artuklu University, Faculty of Medicine, Mardin, Türkiye.
Clinical Relevance:
Cadmium causes systemic inflammation and retinal damage, posing a serious threat to visual and public health.
Background:
Cadmium is a harmful heavy metal that builds up in body tissues and cause systemic inflammation and organ damage. This research sought to explore the impact of subacute cadmium exposure on retinal morphology and inflammatory cytokine levels.
Method:
A total of fourteen male Wistar albino rats were randomized into control and cadmium-exposed groups within the scope of the experiment. 3 mg/kg cadmium (CdCl2) was administered intraperitoneally to the subjects in the cadmium group for 15 days. At the end of study, serum IL-6 and TNF-α levels were determined by ELISA method. In addition, retinal tissues were examined histopathologically after Hematoxylin and Eosin staining. Retinal apoptotic changes were assessed by semi-quantitative immunohistochemical analysis of Bax and Bcl-2 expression in the inner and outer nuclear layers.
Results:
According to the findings, cadmium exposure caused a statistically significant increase in serum IL-6 and TNF-α levels. Histopathological examination revealed a marked decrease in the thickness of the inner plexiform layer (IPL), inner nuclear layer (INL), and outer nuclear layer (ONL), as well as focal vacuolization and cellular disorganization. Cadmium exposure significantly increased Bax immunoreactivity and the Bax/Bcl-2 ratio in both the INL and ONL, while significantly decreasing Bcl-2 expression.
Conclusion:
In conclusion, cadmium exposure increased the systemic inflammatory response, leading to significant histopathological damage in the retinal layers and a dominant proapoptotic Bax/Bcl-2 balance, thereby triggering cellular apoptosis.
