All cataracts involve damage of lens cells and/or lens proteins, leading to increased light scattering and opacification. Much of this damage can be traced, directly or indirectly, to oxidative or free radical-mediated effects. However, it has been difficult to show that oxidative damage initiates human cataract formation, rather than being the final “executioner” of transparency. In fact, the lens appears to be remarkably well protected from oxidative stress. It is essential to discover how these protective mechanisms are broken down or overcome to understand cataract etiology. We discuss some of the likely causes for different types of age-related cataracts, linking them to oxidative or free radical damage when appropriate.