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Artemisinin mimics calorie restriction to trigger mitochondrial biogenesis and compromise telomere shortening in mice.

Wang DT, He J, Wu M, Li SM, Gao Q, Zeng QP - PeerJ (2015)

Bottom Line: Calorie restriction is known to extend lifespan among organisms by a debating mechanism underlying nitric oxide-driven mitochondrial biogenesis.We report here that nitric oxide generators including artemisinin, sodium nitroprusside, and L-arginine mimics calorie restriction and resembles hydrogen peroxide to initiate the nitric oxide signaling cascades and elicit the global antioxidative responses in mice.In conclusion, calorie restriction-triggered nitric oxide provides antioxidative protection and alleviates telomere attrition via mitochondrial biogenesis, thereby maintaining chromosomal stability and integrity, which are the hallmarks of longevity.

View Article: PubMed Central - HTML - PubMed

Affiliation: Tropical Medicine Institute, Guangzhou University of Chinese Medicine , Guangzhou , China.

ABSTRACT
Calorie restriction is known to extend lifespan among organisms by a debating mechanism underlying nitric oxide-driven mitochondrial biogenesis. We report here that nitric oxide generators including artemisinin, sodium nitroprusside, and L-arginine mimics calorie restriction and resembles hydrogen peroxide to initiate the nitric oxide signaling cascades and elicit the global antioxidative responses in mice. The large quantities of antioxidant enzymes are correlated with the low levels of reactive oxygen species, which allow the down-regulation of tumor suppressors and accessory DNA repair partners, eventually leading to the compromise of telomere shortening. Accompanying with the up-regulation of signal transducers and respiratory chain signatures, mitochondrial biogenesis occurs with the elevation of adenosine triphosphate levels upon exposure of mouse skeletal muscles to the mimetics of calorie restriction. In conclusion, calorie restriction-triggered nitric oxide provides antioxidative protection and alleviates telomere attrition via mitochondrial biogenesis, thereby maintaining chromosomal stability and integrity, which are the hallmarks of longevity.

No MeSH data available.


Related in: MedlinePlus

Determination of NO and ATP levels and electronic microscopic phenotyping of mitochondria in mouse skeletal muscles injected by ART, ARG, SNP, or H2O2.(A) The elevation of NO levels upon treatment by CR mimetics. (B) The elevation of ATP levels upon treatment by CR mimetics. (C)–(G) Mitochondrial density and structure in ART, ARG, SNP, H2O2, and AL, respectively. Samples were collected from mouse skeletal muscles after 6 h by one injection or by daily injection for three days by 260 µM ART, 67 µM SNP, 5.7 mM ARG, or 200 µM H2O2 (50 µl injection volume/20 g body weight).
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fig-7: Determination of NO and ATP levels and electronic microscopic phenotyping of mitochondria in mouse skeletal muscles injected by ART, ARG, SNP, or H2O2.(A) The elevation of NO levels upon treatment by CR mimetics. (B) The elevation of ATP levels upon treatment by CR mimetics. (C)–(G) Mitochondrial density and structure in ART, ARG, SNP, H2O2, and AL, respectively. Samples were collected from mouse skeletal muscles after 6 h by one injection or by daily injection for three days by 260 µM ART, 67 µM SNP, 5.7 mM ARG, or 200 µM H2O2 (50 µl injection volume/20 g body weight).

Mentions: The ELISA and Western blotting data have revealed the induced up-regulation of eNOS by CR mimetics, but direct evidence confirming the elevation of NO levels is still lacking. We monitored the NO levels in skeletal muscles of mice injected by ART, SNP, ARG, or H2O2. A NO burst was seen after treatment for six hours although a decline trend was observed after treatment for three days (Fig. 7A), addressing that all kinds of CR mimetics used in this study play their roles upon NO signaling. Furthermore, we also measured the ATP levels in the skeletal muscles of mice injected by ART, SNP, ARG, or H2O2. The results as depicted in Fig. 7B indicate that ATP is increased after treatment for six hours, but maintains a steady-state higher level after treatment for three days. These results provide support to the assumption of CR mimetics-enhanced mitochondrial functionality.


Artemisinin mimics calorie restriction to trigger mitochondrial biogenesis and compromise telomere shortening in mice.

Wang DT, He J, Wu M, Li SM, Gao Q, Zeng QP - PeerJ (2015)

Determination of NO and ATP levels and electronic microscopic phenotyping of mitochondria in mouse skeletal muscles injected by ART, ARG, SNP, or H2O2.(A) The elevation of NO levels upon treatment by CR mimetics. (B) The elevation of ATP levels upon treatment by CR mimetics. (C)–(G) Mitochondrial density and structure in ART, ARG, SNP, H2O2, and AL, respectively. Samples were collected from mouse skeletal muscles after 6 h by one injection or by daily injection for three days by 260 µM ART, 67 µM SNP, 5.7 mM ARG, or 200 µM H2O2 (50 µl injection volume/20 g body weight).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4358698&req=5

fig-7: Determination of NO and ATP levels and electronic microscopic phenotyping of mitochondria in mouse skeletal muscles injected by ART, ARG, SNP, or H2O2.(A) The elevation of NO levels upon treatment by CR mimetics. (B) The elevation of ATP levels upon treatment by CR mimetics. (C)–(G) Mitochondrial density and structure in ART, ARG, SNP, H2O2, and AL, respectively. Samples were collected from mouse skeletal muscles after 6 h by one injection or by daily injection for three days by 260 µM ART, 67 µM SNP, 5.7 mM ARG, or 200 µM H2O2 (50 µl injection volume/20 g body weight).
Mentions: The ELISA and Western blotting data have revealed the induced up-regulation of eNOS by CR mimetics, but direct evidence confirming the elevation of NO levels is still lacking. We monitored the NO levels in skeletal muscles of mice injected by ART, SNP, ARG, or H2O2. A NO burst was seen after treatment for six hours although a decline trend was observed after treatment for three days (Fig. 7A), addressing that all kinds of CR mimetics used in this study play their roles upon NO signaling. Furthermore, we also measured the ATP levels in the skeletal muscles of mice injected by ART, SNP, ARG, or H2O2. The results as depicted in Fig. 7B indicate that ATP is increased after treatment for six hours, but maintains a steady-state higher level after treatment for three days. These results provide support to the assumption of CR mimetics-enhanced mitochondrial functionality.

Bottom Line: Calorie restriction is known to extend lifespan among organisms by a debating mechanism underlying nitric oxide-driven mitochondrial biogenesis.We report here that nitric oxide generators including artemisinin, sodium nitroprusside, and L-arginine mimics calorie restriction and resembles hydrogen peroxide to initiate the nitric oxide signaling cascades and elicit the global antioxidative responses in mice.In conclusion, calorie restriction-triggered nitric oxide provides antioxidative protection and alleviates telomere attrition via mitochondrial biogenesis, thereby maintaining chromosomal stability and integrity, which are the hallmarks of longevity.

View Article: PubMed Central - HTML - PubMed

Affiliation: Tropical Medicine Institute, Guangzhou University of Chinese Medicine , Guangzhou , China.

ABSTRACT
Calorie restriction is known to extend lifespan among organisms by a debating mechanism underlying nitric oxide-driven mitochondrial biogenesis. We report here that nitric oxide generators including artemisinin, sodium nitroprusside, and L-arginine mimics calorie restriction and resembles hydrogen peroxide to initiate the nitric oxide signaling cascades and elicit the global antioxidative responses in mice. The large quantities of antioxidant enzymes are correlated with the low levels of reactive oxygen species, which allow the down-regulation of tumor suppressors and accessory DNA repair partners, eventually leading to the compromise of telomere shortening. Accompanying with the up-regulation of signal transducers and respiratory chain signatures, mitochondrial biogenesis occurs with the elevation of adenosine triphosphate levels upon exposure of mouse skeletal muscles to the mimetics of calorie restriction. In conclusion, calorie restriction-triggered nitric oxide provides antioxidative protection and alleviates telomere attrition via mitochondrial biogenesis, thereby maintaining chromosomal stability and integrity, which are the hallmarks of longevity.

No MeSH data available.


Related in: MedlinePlus