10 1 Background
We are very confident to conclude that ROS should be reversely correlated with
lifespan, i.e., a higher level of ROS that has not been scavenged by antioxidants deter-
mines a shortened lifespan due to the damage of DNA and telomeres, whereas a lower
level of ROS that can induce antioxidants confers an extended lifespan upon the pro-
tection of telomeres and chromosomes. Mitochondria are the main organelles respon-
sible for ROS generation, but CR-triggered optimal NO can promote the generation of
sublethal ROS and induce the activation of antioxidant enzymes for ROS scavenging.
On the other hand, immune stress from chronic pathogenic infections or by
overgrown gut microbiota, especially LPS that is leaked into the bloodstream from
G− bacteria, can activate proinflammatory cytokines and subsequently stimulate
iNOS for triggering potent NO bust. High-level NO may competitively occupy the
O 2 binding site within hemoglobin/myoglobin, leading to a hypoxic milieu, which
can drive angiogenesis, hyperplasia, and inflammatory lesions.
This book is devoted to discuss both beneficial and harmful aspects (so-called
“Yin-Yang effects”) of NO on the biology and medicine, and is also dedicated
to review an up-to-date literature and prospecting the future application of ART
in many pathological conditions. I explain why you should keep a steady-state
level of aging-suppressed NO and avoid an extremely high level of infection- and
inflammation-triggered NO. In the final part of the book, I suggest a hypothesis of
healthy/unhealthy obesity and also provide a clue to CSC origin.
The book with a brief description of the multiple implications of ART in com-
bating tumor/cancer, pathogenic bacteria, chronic inflammation, and aging/aging-
associated disorders is written for medical researchers and students, clinicians,
biologists, and other people interested in NO-driven healthy and pathological
effects and ROS-involved aging processes.
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