Hypoxia is a consistent challenge for aquatic animals. It is a pressing environmental problem; hypoxia can cause cranial edema and ovarium dysfunction in fish. Although several studies have reported the effect of hypoxic insult to the visual system, the hypoxic effect on perinatal animals and in particular their offspring has yet to be elucidated. In this study, activated caspase-3 activity was investigated using immunohistochemistry in order to examine the perinatal hypoxic damage in offspring fish. Offspring were divided into groups based on different time points of sacrifice. This allowed assessment of ocular development for different age groups. The results indicated that perinatal hypoxia induced ocular developmental defects in the offspring. The defects took the form of trabecular cell death and fibre degeneration, corneal thinning and lens fibre derangement. A concomitant change in intraocular pressure was recorded by tonometer in the experimental animals compared with the controls. Further investigation should be initiated to develop strategies to prevent developmental disability due to perinatal hypoxia and to increase survivability of the offspring.