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A recent documentary (skip to 58:20) discusses the possibility that hibernation, if it could be induced in extrasolar astronauts, would reduce damage from cosmic radiation. The obvious reason this could happen is the shielding of hibernation chambers, but the documentary reviews evidence that even hibernation in the wild (e.g. bears) reduces radiation damage due to a slowed metabolism.

I would assume the connection is that reduced need for enzyme synthesis keeps DNA coiled up most of the time so its nucleotides are less exposed to radiation, but even if this is true it raises the question of how coiling shields radiation. (For example, is it less able to penetrate histones or the phosphorylated deoxyribose backbone?) Adding to my confusion, the documentary claims the mechanism is rooted in hydrogen sulphide, but doesn't explain either why this is more concentrated in the cells of hibernating animals nor how it reduces mutations.

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This is still an area of active research, and there doesn't appear to be a single definitive answer for the mechanisms behind the reduction in radiation-damage during hibernation.

A recent review by Cerri et al. (2016) covers a lot of the known biology behind hibernation and resistance to radiation damage.

A few select quotes from this review:

At the cellular level, it is well known that cells irradiated in resting state, and left undisturbed for 24 h after irradiation, are more resistant than cells re-plated immediately after exposure. This effect is known as delayed plating, and is generally attributed to the potentially lethal damage repair (PLDR) in resting phase.

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The oxygen level during hibernation may contribute to the enhanced radioresistance. Hypoxia is a well know protective mechanism, and is arguably the main reason of local control failure in radiotherapy.

Rockwell et al. (2009) discuss the underlying reason behind reduced radiation sensitivity in a hypoxic environment:

Molecular oxygen (O2) is a potent chemical radiosensitizer. This radiosensitization does not result from any of the metabolic or physiological effects of oxygen, but instead reflects the fact that O2 is an extremely electron-affinic molecule that participates in the chemical reactions that lead to the production of DNA damage after the absorption of energy from ionizing radiation [21,22].

My personal take would be that the reduced risk of radiation-induced damage is probably not due to the structural arrangement of DNA, but rather the overall cellular environment. This is perhaps linked to an enhanced ability to repair damaged DNA, but is also likely to be highly dependent on cellular oxygen levels.

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