Tuning Cellular Power Production with Safety; Direct, Indirect Antioxidants and Proteostasis

Oxidative stress is harmful and increases with age and disease.

Anti oxidant capacity declines with age AND parallels the amount of Nrf2 activation.

In the abstract below showing that antioxidants disappoint in cardiovascular studies they do not acknowledge the importance of ROS as metabolic signaling.  One must increase antioxidant CAPACITY and activity without impacting signaling.

How?

Hydrogen rich water removes noise level oxidants only like a filter in a flow of signal rich electrons.

Secondly, sulforaphane increases antioxidant enzymes for PRN use with activation.

Finally, being able to translate signaling from genes requires proteostasis, making, refolding and removing proteins which is a function of wheat germ spermidine that declines with age in parallel to declining antioxidant CAPACITY.

One can measure direct antioxidant capacity and antioxidant stress in peripheral blood.

But can one measure available potential antioxidant capacity?

This would require a challenge or stress test.

These studies have already been performed in part.

E.g..  The product of order and power or speed parameters of HIIE sprints is increased by hydrogen rich water which preserves safe oxidation independent of baseline VO2 max.  The VO2 is directly proportional to the mass of mitochondria.  It had been shown that HYDROGEN RICH WATER makes each mitochondria more efficient and maintains a higher proton gradient which ultimately translates into POWER.

Homeostasis or balance of oxidative signaling or flux.

http://hyper.ahajournals.org/content/44/3/248.short

Abstract

Metabolism of oxygen by cells generates potentially deleterious reactive oxygen species (ROS). Under normal conditions the rate and magnitude of oxidant formation is balanced by the rate of oxidant elimination. However, an imbalance between prooxidants and antioxidants results in oxidative stress, which is the pathogenic outcome of oxidant overproduction that overwhelms the cellular antioxidant capacity. The kidney and vasculature are rich sources of NADPH oxidase–derived ROS, which under pathological conditions play an important role in renal dysfunction and vascular damage. Strong experimental evidence indicates that increased oxidative stress and associated oxidative damage are mediators of renovascular injury in cardiovascular pathologies. Increased production of superoxide anion and hydrogen peroxide, reduced nitric oxide synthesis, and decreased bioavailability of antioxidants have been demonstrated in experimental and human hypertension. These findings have evoked considerable interest because of the possibilities that therapies targeted against free radicals by decreasing ROS generation or by increasing nitric oxide availability and antioxidants may be useful in minimizing vascular injury and renal dysfunction and thereby prevent or regress hypertensive end-organ damage. This article highlights current developments in the field of ROS and hypertension, focusing specifically on the role of oxidative stress in hypertension-associated vascular damage. In addition, recent clinical trials investigating cardiovascular benefits of antioxidants are discussed, and some explanations for the rather disappointing results from these studies are addressed. Finally, important avenues for future research in the field of ROS, oxidative stress, and redox signaling in hypertension are considered.