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Healing Radiation-Induced Senescence aka Aging-

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“Senescence (/sɪˈnɛsəns/) or biological aging is the gradual deterioration of functional characteristics in living organisms. The word senescence can refer to either cellular senescence or to senescence of the whole organism.”

According to research, chemotherapy and radiation cause pre-mature aging of the patient.

I was diagnosed with multiple myeloma in early 1994. I underwent the FDA approved, safe and effective, standard-of-care therapy plan.

The radiation to my neck and to my iliac crest caused damage that I could feel as well as damage that I could not feel. Healing radiation-induced senescence has been an ongoing effort of mine in the same way that I work to build my bone health, my kidney health, etc.


The Science of Aging


According to the research linked below, curcumin may be able to alleviate radiation-induced senescence.

To be clear, I’m not trying to fight the normal aging process. I’m simply trying to heal some/all/a little of the senescence caused by radiation therapy.

Email me at David.PeopleBeatingCancer@gmail.com with questions about your MM, your side effects, etc.

Hang in there,

David Emerson

  • MM Survivor
  • MM Cancer Coach
  • Director PeopleBeatingCancer

Cancer Treatment-Induced Accelerated Aging in Cancer Survivors: Biology and Assessment

“In brief, future research is warranted to better understand the biological mechanisms of aging. Since anti-aging drugs are available, a deeper understanding of aging-related consequences of cancer and cancer treatments would lead to new strategies to mitigate or even reverse aging and will eventually improve the quality of life of cancer survivors…”

Curcumin nanoparticles alleviate brain mitochondrial dysfunction and cellular senescence in γ-irradiated rats

Abstract

Despite the diverse applications of γ radiation in radiotherapy, industrial processes, and sterilization, it causes hazardous effects on living organisms, such as cellular senescence, persistent cell cycle arrest, and mitochondrial dysfunction.

This study evaluated the efficacy of curcumin nanoparticles (CNPs) in mitigating mitochondrial dysfunction and cellular senescence induced by γ radiation in rat brain tissues.

Four groups of male Wistar albino rats (n = 8 per group) were included:

  • (Gr1) the control group;
  • (Gr2) the CNPs group (healthy rats receiving oral administration of curcumin nanoparticles at a dose of 10 mg/kg/day, three times per week for eight weeks);
  • (Gr3) the irradiated group (rats exposed to a single dose of 10 Gy head γ irradiation); and
  • (Gr4) the irradiated + CNPs group (irradiated rats treated with CNPs).

The data obtained demonstrated that oral administration of CNPs for eight weeks attenuated oxidative stress in γ-irradiated rats by lowering the brain’s lipid peroxidation level [malondialdehyde (MDA)] and enhancing antioxidant markers [superoxide dismutase (SOD), reduced glutathione (GSH), and total antioxidant capacity (TAC)] (P < 0.05).

In addition, CNPs significantly increased mitochondrial function by improving complex I, complex II, and ATP production levels compared to the irradiated group.

In irradiated rats, CNPs also showed anti-neuroinflammatory effects by reducing brain interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-α), and nuclear factor-kappa B (NF-ĸB) levels (P < 0.05).

Moreover, CNPs administered to irradiated rats significantly reduced brain β-galactosidase activity and the expression levels of p53, p21, and p16 genes (P < 0.05) while concurrently inducing a significant increase in AMPK mRNA expression compared to the irradiated group.

In conclusion, CNPs ameliorated the neurotoxicity of γ radiation and hold promise as a novel agent to delay cellular senescence via their combined antioxidant, anti-inflammatory, and mitochondrial-enhancing properties.

Conclusion

Our study concluded that oral administration of CNPs (10 mg/kg) in γ-irradiated rats attenuates brain mitochondrial dysfunction and cellular senescence by enhancing the oxidant/antioxidant status, increasing the activity of mitochondrial complexes I and II, and boosting ATP production.

Additionally, it reduces the levels of brain inflammatory mediators (TNF-α, IL-6, and NF-κB) and β-galactosidase while downregulating the gene expression of senescence pathway activators (p53-p21/p16 signaling pathway) and simultaneously elevating AMPK mRNA expression levels.

According to our findings, CNPs act as an anti-senescence agent, delaying cellular senescence and enhancing mitochondrial function.

radiation-induced senescence radiation-induced senescence

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