Gong H, Amemiya T
Department of Ophthalmology, Nagasaki University School of Medicine, Japan.
Invest Ophthalmol Vis Sci. 1996 Sep;37(10):1967-74.
To elucidate some biologic functions of manganese in the retina.
Three-week-old weanling Wistar Kyoto rats were used. Manganese-deficient rats were fed a manganese-deficient solid diet containing 0.23 mg manganese/100 g diet and all other nutrients. Control rats were fed a solid diet with 2.9 mg manganese/100 g diet. The retinas were examined by electron microscopy in the 12th, 18th, and 30th months of experimentation.
There was a statistically significant decrease in the plasma manganese levels in manganese-deficient animals compared to controls. In rats fed a manganese-deficient diet for 12 months, photoreceptor cells showed karyopyknosis-like changes of nuclei and a decrease in size and number of outer segments. Rats fed a manganese-deficient diet for 18 months showed a complete loss of photoreceptor cells, and the inner nuclear layer nuclei came in direct contact with the retinal pigment epithelium. Rats with manganese deficiency of 30 months showed invasion by capillaries and processes of Müller-like cells from the sensory retina into the retinal pigment epithelium. In the sensory retina, Müller-like cells proliferated, and neural cells disappeared.
Because manganese is related to Mn superoxide in the mitochondrial matrix and to protein and glycogen metabolism, manganese deficiency may disturb the renewal of photoreceptor outer segment discs, and the decrease in antioxidant action caused by a lower level of Mn superoxide dismutase may accelerate the damage to photoreceptor cells. After neural cell loss, Müller-like cells may proliferate. Manganese appears to be essential for maintaining photoreceptor cells.
