Astronauts on long-term space missions have a higher risk for the expression of radiation late effects
such as cancer or sub-capsular cortical eye lens opacities. This is due to higher dose and different patterns of cellular energy deposition from high-linear-energy-transfer (LET) components of galactic cosmic
radiation in space than that of terrestrial low-LET radiation on Earth. The eye lens is a radiation sensitive organ with radiation induced cataract to occur with a threshold absorbed dose of 0.5 Gy (0 - 1
Gy) of sparsely ionizing radiation. Doses perceived by astronauts on the International Space Station
(ISS) are in average 150 mSv per year (Cucinotta et al. (2001) Radiat Res. 156:460-466). Radiationinduced lens opacification is assumed to initiate from post irradiation proliferative activity of genetically
damaged lens epithelial cells with alterations in cell cycle control, apoptosis, differentiation, and cellular
disorganization, or other pathways controlling lens fiber cells’ differentiation. As the porcine eye lens is
similar to the human lens in size and anatomy, DNA damage response was investigated in ex-vivo porcine
lenses in organ culture, in in-vitro cultivated lens epithelial slabs (ES) and in porcine lens epithelial cells
(pLEC). Cell survival of proliferative cells was calculated from colony forming ability (CFA) assay. The
phosphorylated form of H2AX (γH2AX) was used as a molecular marker to visualize DNA double strand
breaks (DSB) and their repair. Propidium iodide based DNA staining for cellular DNA content marked
radiation-induced cell cycle disturbances. In pLEC the cell survival curve of immediate plated cells and
after a recovery period of 24 h follow the equation S=1.40xD+ln 1.47 and S=1.59xD+ln 1.79, respectively.
DNA DSB are induced in a dose-dependent manner ( 18 DSB/cell/Gy) and repaired during successive
recovery ( 5 DSB/cell/Gy residual damage after 24 h). For doses >2 Gy a cell cycle arrest in G2 phase
occurred 24 h after X-irradiation and persisted up to 72 h post-irradiation. DNA DSB induction and
repair could as well be documented for ES and whole lenses after X-irradiation. In whole lenses, the
amount of residual damage (after 24 h and 48 h) was highest in the equatorial zone while in the central
epithelial zone DSB repair seemed to proceed with time in a manner comparable to in-vitro cultivated
pLEC. Lens organ culture allows cellular metabolism and DNA synthesis in whole lenses. Repair of DNA
DSB takes place in the central epithelial layer and is reduced in the equatorial region of cultivated lenses