3 replies to this topic

[ta5]

This study suggests CR might help delay sarcopenia and that's nice. But, if superoxide, or the lack of SOD, is a cause, then I wonder what we could do for that directly.

 

Geroscience. 2017 Apr 13.

A new mouse model of frailty: the Cu/Zn superoxide dismutase knockout mouse.

Deepa SS1, Bhaskaran S2, Espinoza S3,4, et al.

Frailty is a geriatric syndrome that is an important public health problem for the older adults living in the USA. Although several methods have been developed to measure frailty in humans, we have very little understanding of its etiology. Because the molecular basis of frailty is poorly understood, mouse models would be of great value in determining which pathways contribute to the development of frailty. More importantly, mouse models would be critical in testing potential therapies to treat and possibly prevent frailty. In this article, we present data showing that Sod1KO mice, which lack the antioxidant enzyme, Cu/Zn superoxide dismutase, are an excellent model of frailty, and we compare the Sod1KO mice to the only other mouse model of frailty, mice with the deletion of the IL-10 gene. Sod1KO mice exhibit four characteristics that have been used to define human frailty: weight loss, weakness, low physical activity, and exhaustion. In addition, Sod1KO mice show increased inflammation and sarcopenia, which are strongly associated with human frailty. The Sod1KO mice also show alterations in pathways that have been proposed to play a role in the etiology of frailty: oxidative stress, mitochondrial dysfunction, and cell senescence. Using Sod1KO mice, we show that dietary restriction can delay/prevent characteristics of frailty in mice.

PMID: 28409332

Edited by ta5, 15 April 2017 - 04:35 PM.

[corb]

SOD mimetics.

I'm not convinced this is a valid model of age related muscle wasting though - it replicates the increase in ROS but that's about it.

 

[zorba990]

Copper Salicylate

https://www.ncbi.nlm...pubmed/22313179
The complexes [Cu(salH)(2)(H(2)O)] (1), [Cu(dipsH)(2)(H(2)O)] (2), {Cu(3-MeOsal)(H(2)O)(0.75)}(n) (3), [Cu(dipsH)(2)(BZDH)(2)] (4), [Cu(dipsH)(2)(2-MeOHBZDH)(2)]·EtOH (5), [Cu(sal)(phen)] (6), [Cu(dips)(phen)]·H(2)O (7), and [Cu(3-MeOsal)(phen)]·H(2)O (8) (salH(2) = salicylic acid; dipsH(2) = 3,5-diisopropylsalicylic acid; 3-MeOsalH(2) = 3-methoxysalicylic acid; BZDH = benzimidazole; 2-MeOHBZDH = 2 methanolbenzimidazole and phen =1,10-phenanthroline) were prepared and characterized. Structures of 4, 5, and 8 were determined by X-ray crystallography. Compounds 1-8 are potent superoxide dismutase mimetics, and they are inactive as inhibitors of COX-2 activity. Compounds 1, 4, and 5 exhibit moderate inhibition of COX-1. Complexes 6-8 display rapid micromolar cytotoxicity against cisplatin sensitive (breast (MCF-7), prostate (DU145), and colon (HT29)) and cisplatin resistant (ovarian (SK-OV-3)) cell lines compared to 1-5, and they exhibit potent in vitro DNA binding and cleavage capabilities

[corb]

I'm not ill informed. If anything I'm starting to become too well informed to the point of spending less than 5 seconds on a paper like this before I see it's bullshit.

 

>delete antioxidant gene

>ROS increases

>low calorie diet is known to decrease ROS

>it does in fact decrease it

A pat on the back and funds well spent...

 

Ok... but what exactly is this proving?
That CR reduces MTOR activity and MTOR inhibition lowers ROS production. As I said, all well known information.

OK. Great.

 

So where is the proof this is a valid model of sarcopenia? Or any age related illness for that matter?

It's not in the paper.

Edited by corb, 17 April 2017 - 02:24 AM.