LONGECITY

Quotes are in black. My writing is in red.  

http://www.ncbi.nlm....es/PMC2916709/ 

This seems bad, right? On the other hand look at this study:  

http://onlinelibrary...12.00842.x/pdf 

We propose the following model for the nutrient-dependent role of SOD1 and ROS on lifespan (Fig. 6F). In wild-type flies, low TOR signaling in flies on the HS-LP and L-C diets increases activity of mitochondrial electron transport chain and produces more ROS, which induce defense response at the organismal level through mitohormesis and promote longevity. Although a higher sugar level in the HS-LP diet induces more ROS, ROS are partially detoxified by fully functional SOD1, which consequently results in no obvious detrimental effect of sugar on lifespan in wild-type flies. In contrast, high ROS and oxidative damage induced by the HS-LP not the L-C diet are insufficiently alleviated when SOD1 activity is low, although low protein levels in the HS-LP and L-C diets still reduce TOR signaling and promote longevity. This difference leads to differential lifespan response of sod1 mutant flies to the HS-LP and L-C diets. Consistent with this model, further reduction of TOR signaling by rapamycin shortens lifespan in flies with low SOD1 activity, and NAC has prolongevity effect on sod1RNAi flies fed the HS-LP but not other diets. 

http://www.ncbi.nlm....les/PMC4449467/

Dietary N-acetyl-L-cysteine supplementation significantly increased resistance to oxidative stress, heat stress, and UV irradiation in C. elegans. In addition, N-acetyl-L-cysteine supplementation significantly extended both the mean and maximum lifespan of C. elegans. 

Rapamycin and NAC seem to have opposing effects in many ways. On the other hand, they seem to both be capable of having pro-longevity effects in different ways. Also, they have both been suggested to treat progeria: (see http://www.ncbi.nlm....pubmed/21807766 (NAC) and http://www.ncbi.nlm.nih.gov/pubmed/21715679 (Rapamycin)) 

I'm wondering what all this means RE: Longevity.