The fluorescent derivative of the actin-binding toxin phallacidin, 7-nitrobenz-2-oxa-1,3 diazole phallacidin, has been used to cytologically demonstrate the presence of actin in lens epithelium, corneal endothelium, and retinal pigment epithelium. In these noninjured tissues, no stress fibers are observed and fluorescence is confined mainly to an area at or near the cell membrane, although some diffuse cytoplasmic staining can also be seen. However, following injury to either the lens epithelium or corneal endothelium of rats and frogs, stress fibers are detected, but only in those cells that migrate into the wound area. Cells on the periphery of each tissue do not partake in would repair and thus maintain their normal appearance. After the tissue has regenerated, stress fibers disappear, and those cells involved in the injury response return to their normal morphology. When rabbit corneal endothelium is placed in tissue culture, stress fibers are observed as the cells migrate away from the initial explant. Upon reaching confluency, these cells spread out and each is surrounded by thick actin-containing bands. Furthermore, they exhibit some stress cables within their cytoplasm. This is in contrast to their appearance in vivo where stress fibers are absent and fluorescence is limited to a region near the cell membrane.

X-irradiation of frog eyes with natural and experimentally induced differences in lenticular mitotic activity reveals cataractogenesis to be dependent on the proliferative activity of the germinative zone of the lens epithelium. It has also been found that G₀ cells are sufficiently vulnerable to X-rays to cause opacity if cell division is allowed to occur following irradiation. In every case of X-ray-induced lens opacification, a disruption of the radiating columns shows a strong correlation to the severity of the associated cataract. It is suggested that lens cell damage from ionizing radiation is transduced by mitosis and expressed as an opacity by subsequent errant fiber genesis.

Exposure of the eyes of young frogs and rats to X-rays (12–25 Gy) causes posterior cataracts to appear several weeks later. Hypophysectomized frogs do not develop these opacities, but hypophysectomized rats do. In the former, but not the latter animals, the operation completely stops lens mitosis, the epithelial cells being largely confined to the G₀/ G₁ phase of the cell cycle.

Exposure to X-rays usually causes cataracts in frogs. These cataracts are always preceded by misalignment of the structures called meridional rows (MR). When cell division is completely halted by hypophysectomy, however, irradiation no longer disturbs the orientation of the MR. Since the MR are the structures formed as lens epithelial cells differentiate into lens fibres it is reasonable to propose that radiocataractogenesis depends upon a mitosis-driven formation of pathological fibres from epithelial cells that have been rendered abnormal by exposure to X-rays.