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Development of Retinal Degenerative Model Using Lead Acetate (PbAc) in Zebrafish: Morphological and Behavioral Aspects

Vincy Garg, Ravneet Kaur

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Abstract

Abstract Lead intoxication reduces cGMP phosphodiesterase activity and enhances the influx of Ca2+ in photoreceptor cells that trigger ATP loss. Thus, releasing proapoptotic factors and activating caspase cascade results in retinal cell apoptosis. In the current study, lead acetate (PbAc) induced retinal degenerative model which mimics ocular degenerative disorders like macular degeneration and retinitis pigmentosa. Qualitative and quantitative analysis of retinal histology, with dose and time response parameters, showed 0.08mg/L concentration for 15 days of treatment was the appropriate dose to develop the retinal degeneration model. Its intoxication affected the photoreceptor cells thus contributing to above mentioned disorders. At an ultrastructural level, it was observed that PbAc induce retinal degeneration by damaging outer and inner segments of the photoreceptors especially the rod cells. Escape response behavior also showed a significant decrease in visual response to changing contrasts. Thus, PbAc was inducing degeneration of retina between pigmented epithelium and photoreceptor layer for further retinal regenerative studies. Lead intoxication reduces cGMP phosphodiesterase activity and enhances the influx of Ca2+ in photoreceptor cells that trigger ATP loss. Thus, releasing proapoptotic factors and activating caspase cascade results in retinal cell apoptosis. In the current study, lead acetate (PbAc) induced retinal degenerative model which mimics ocular degenerative disorders like macular degeneration and retinitis pigmentosa. Qualitative and quantitative analysis of retinal histology, with dose and time response parameters, showed 0.08mg/L concentration for 15 days of treatment was the appropriate dose to develop the retinal degeneration model. Its intoxication affected the photoreceptor cells thus contributing to above mentioned disorders. At an ultrastructural level, it was observed that PbAc induce retinal degeneration by damaging outer and inner segments of the photoreceptors especially the rod cells. Escape response behavior also showed a significant decrease in visual response to changing contrasts. Thus, PbAc was inducing degeneration of retina between pigmented epithelium and photoreceptor layer for further retinal regenerative studies.

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Abstract Lead intoxication reduces cGMP phosphodiesterase activity and enhances the influx of Ca2+ in photoreceptor cells that trigger ATP loss. Thus, releasing proapoptotic factors and activating caspase cascade results in retinal cell apoptosis. In the current study, lead acetate (PbAc) induced retinal degenerative model which mimics ocular degenerative disorders like macular degeneration and retinitis pigmentosa. Qualitative and quantitative analysis of retinal histology, with dose and time response parameters, showed 0.08mg/L concentration for 15 days of treatment was the appropriate dose to develop the retinal degeneration model. Its intoxication affected the photoreceptor cells thus contributing to above mentioned disorders. At an ultrastructural level, it was observed that PbAc induce retinal degeneration by damaging outer and inner segments of the photoreceptors especially the rod cells. Escape response behavior also showed a significant decrease in visual response to changing contrasts. Thus, PbAc was inducing degeneration of retina between pigmented epithelium and photoreceptor layer for further retinal regenerative studies. Lead intoxication reduces cGMP phosphodiesterase activity and enhances the influx of Ca2+ in photoreceptor cells that trigger ATP loss. Thus, releasing proapoptotic factors and activating caspase cascade results in retinal cell apoptosis. In the current study, lead acetate (PbAc) induced retinal degenerative model which mimics ocular degenerative disorders like macular degeneration and retinitis pigmentosa. Qualitative and quantitative analysis of retinal histology, with dose and time response parameters, showed 0.08mg/L concentration for 15 days of treatment was the appropriate dose to develop the retinal degeneration model. Its intoxication affected the photoreceptor cells thus contributing to above mentioned disorders. At an ultrastructural level, it was observed that PbAc induce retinal degeneration by damaging outer and inner segments of the photoreceptors especially the rod cells. Escape response behavior also showed a significant decrease in visual response to changing contrasts. Thus, PbAc was inducing degeneration of retina between pigmented epithelium and photoreceptor layer for further retinal regenerative studies.

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Available abstract

Abstract Lead intoxication reduces cGMP phosphodiesterase activity and enhances the influx of Ca2+ in photoreceptor cells that trigger ATP loss. Thus, releasing proapoptotic factors and activating caspase cascade results in retinal cell apoptosis. In the current study, lead acetate (PbAc) induced retinal degenerative model which mimics ocular degenerative disorders like macular degeneration and retinitis pigmentosa. Qualitative and quantitative analysis of retinal histology, with dose and time response parameters, showed 0.08mg/L concentration for 15 days of treatment was the appropriate dose to develop the retinal degeneration model. Its intoxication affected the photoreceptor cells thus contributing to above mentioned disorders. At an ultrastructural level, it was observed that PbAc induce retinal degeneration by damaging outer and inner segments of the photoreceptors especially the rod cells. Escape response behavior also showed a significant decrease in visual response to changing contrasts. Thus, PbAc was inducing degeneration of retina between pigmented epithelium and photoreceptor layer for further retinal regenerative studies. Lead intoxication reduces cGMP phosphodiesterase activity and enhances the influx of Ca2+ in photoreceptor cells that trigger ATP loss. Thus, releasing proapoptotic factors and activating caspase cascade results in retinal cell apoptosis. In the current study, lead acetate (PbAc) induced retinal degenerative model which mimics ocular degenerative disorders like macular degeneration and retinitis pigmentosa. Qualitative and quantitative analysis of retinal histology, with dose and time response parameters, showed 0.08mg/L concentration for 15 days of treatment was the appropriate dose to develop the retinal degeneration model. Its intoxication affected the photoreceptor cells thus contributing to above mentioned disorders. At an ultrastructural level, it was observed that PbAc induce retinal degeneration by damaging outer and inner segments of the photoreceptors especially the rod cells. Escape response behavior also showed a significant decrease in visual response to changing contrasts. Thus, PbAc was inducing degeneration of retina between pigmented epithelium and photoreceptor layer for further retinal regenerative studies.

Key concepts: Retinitis pigmentosa, Retinal degeneration, Retinal, Retina, Photoreceptor cell, Macular degeneration, Outer nuclear layer, Biology

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Development of Retinal Degenerative Model Using Lead Acetate (PbAc) in Zebrafish: Morphological and Behavioral Aspects — Research Paper | ScholarLens