Why doesn't Cu/ZnSOD affect lifespan in mice?

%expand% Why doesn't Cu/ZnSOD affect lifespan in mice? %set(body,%html-clean({

Superoxide dismutase is a critical factor in reducing damage to cells. So why isn't more better?

Looking at the pathways, it's possible that overexpression of SOD in mice merely creates a bottleneck at the pathways for conversion of hydrogen peroxide. In other words, in accordance with Kascer's enzyme activity predictions, without overexpression of GSHPx (and others perhaps) no lifespan increase need be observed. This was proposed by Kurata, et al in 1993 (1)

This argument is sound, but there's more to it.

There are multiple pathways of aging. Just as a single enzyme's activity cannot predict the flux of a pathway, so too a single aging vector (mitochondrial damage) might not impact the overall lifespan of a complex organism. If the mitochondrial damage doesn't kill you the advanced glycation end-products will.

I would image that the more complex the organism, the more pathways of aging there are. Thus the more "multipath" an intervention would have to be in order to have an effect.

(1) HUANG et al. (2000) "Ubiquitous overexpression of CuZn superoxide dismutase does not extendlife span in mice"
(2) Kurata, Masatoshi Suzuki, et al (1993) "Antioxidant systems and erythrocyte life-span in mammals"

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Friday, April 30, 2010

Why doesn't Cu/ZnSOD affect lifespan in mice?
Posted 10:10 AM

Superoxide dismutase is a critical factor in reducing damage to cells. So why isn't more better?

Looking at the pathways, it's possible that overexpression of SOD in mice merely creates a bottleneck at the pathways for conversion of hydrogen peroxide. In other words, in accordance with Kascer's enzyme activity predictions, without overexpression of GSHPx (and others perhaps) no lifespan increase need be observed. This was proposed by Kurata, et al in 1993 (1)

This argument is sound, but there's more to it.

There are multiple pathways of aging. Just as a single enzyme's activity cannot predict the flux of a pathway, so too a single aging vector (mitochondrial damage) might not impact the overall lifespan of a complex organism. If the mitochondrial damage doesn't kill you the advanced glycation end-products will.

I would image that the more complex the organism, the more pathways of aging there are. Thus the more "multipath" an intervention would have to be in order to have an effect.

(1) HUANG et al. (2000) "Ubiquitous overexpression of CuZn superoxide dismutase does not extendlife span in mice"
(2) Kurata, Masatoshi Suzuki, et al (1993) "Antioxidant systems and erythrocyte life-span in mammals"

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