Radiation-Induced Change in Lymphocyte Proliferation and its Neuroendocrine Regulation: Dose-Response Relationship and Pathophysiological Implications

Liu, Shuzheng

doi:10.1080/15401420490507486

Cited by 13 publications

(8 citation statements)

References 20 publications

(28 reference statements)

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“…• Extend tumor latency in cancer-prone mice (Mitchel et al 2003;Mitchel 2004Mitchel , 2005 • Activate the immune response (Liu et al 1987;Makinodan and James 1990;Sakamoto et al 1997;Liu 2003Liu , 2004 and suppress lung and lymph node metastasis in vivo (Hosoi and Sakamoto 1993;Hashimoto et al 1999;Sakamoto 2004). • Suppress spontaneous cancers in humans (Howe, 1995;Rossi and Zaider 1997;Scott 2005aScott , 2006a).…”

Section: B R Scott and J DI Palmamentioning

confidence: 97%

“…As previously indicated, low doses and dose rates of low-LET radiation activate a system of cooperative protective processes in the body. The protective processes include (1) defenses such as scavenging of reactive oxygen species and other toxins, (2) presumably p53 related activated high-fidelity DNA repair/apoptosis, (3) a novel auxiliary protective apoptosis mediated (PAM) process that selectively eliminates aberrant cells, and (4) induced immunity (Liu et al 1994; Liu, 2004). The PAM process has been demonstrated to involve reactive oxygen and nitrogen chemical species, specific cytokines (e.g., transforming growth factor beta in the case of fibroblast cells), and can occur independently of the p53 gene (Scott 2004, 2005a; Scott et al 2006).…”

Section: Low-dose/dose-rate Low-let Radiation-induced System Of Protementioning

confidence: 99%

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Sparsely Ionizing Diagnostic and Natural Background Radiations are Likely Preventing Cancer and other Genomic-Instability-Associated Diseases

Scott¹,

Palma²

2007

Dose-Response

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Routine diagnostic X-rays (e.g., chest X-rays, mammograms, computed tomography scans) and routine diagnostic nuclear medicine procedures using sparsely ionizing radiation forms (e.g., beta and gamma radiations) stimulate the removal of precancerous neo-plastically transformed and other genomically unstable cells from the body (medical radiation hormesis). The indicated radiation hormesis arises because radiation doses above an individual-specific stochastic threshold activate a system of cooperative protective processes that include high-fidelity DNA repair/apoptosis (presumed p53 related), an auxiliary apoptosis process (PAM process) that is presumed p53-independent, and stimulated immunity. These forms of induced protection are called adapted protection because they are associated with the radiation adaptive response. Diagnostic X-ray sources, other sources of sparsely ionizing radiation used in nuclear medicine diagnostic procedures, as well as radioisotope-labeled immunoglobulins could be used in conjunction with apoptosis-sensitizing agents (e.g., the natural phenolic compound resveratrol) in curing existing cancer via low-dose fractionated or low-dose, low-dose-rate therapy (therapeutic radiation hormesis). Evidence is provided to support the existence of both therapeutic (curing existing cancer) and medical (cancer prevention) radiation hormesis. Evidence is also provided demonstrating that exposure to environmental sparsely ionizing radiations, such as gamma rays, protect from cancer occurrence and the occurrence of other diseases via inducing adapted protection (environmental radiation hormesis).

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Section: B R Scott and J DI Palmamentioning

confidence: 97%

Section: Low-dose/dose-rate Low-let Radiation-induced System Of Protementioning

confidence: 99%

Sparsely Ionizing Diagnostic and Natural Background Radiations are Likely Preventing Cancer and other Genomic-Instability-Associated Diseases

Scott¹,

Palma²

2007

Dose-Response

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“…This result further supports the idea that glucocorticoids may be involved in in vivo RAR after low-dose-rate IR. However, the level of the dose response of GR and glucocorticoids after exposure to IR seems complicated, as Liu 63 has shown a decreased GR level in splenic T cells after a low-dose (30–75 mGy) X-irradiation. It is also elusive whether activated GR suppresses IR carcinogenesis.…”

Section: Evidence Of In Vivo Rarsmentioning

confidence: 99%

In vivo radioadaptive response

Nenoi¹,

Wang²,

Varès³

2014

Hum Exp Toxicol

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Radioadaptive response (RAR) describes phenomena where small conditioning doses of ionizing radiation (IR) reduce detrimental effects of subsequent higher IR doses. Current radiation protection regulations do not include RAR because of the large variability in expression among individuals and uncertainties of the mechanism. However, RAR should be regarded as an indispensable factor for estimation and control of individual IR sensitivity. In this article, RAR studies relevant to individual cancer risk are reviewed. Using various stains of mice, carcinogenic RAR has been demonstrated. Consistently much in vivo evidence for RAR with end points of DNA and chromosome damage is reported. Most in vivo RAR studies revealed efficient induction of RAR by chronic or repeated low-dose priming irradiation. Chronic IR-induced RAR was observed also in human individuals after environmental, occupational, and nuclear accident radiation exposure. These observations may be associated with an intrinsically distinct feature of in vivo experimental systems that mainly consist of nonproliferating mature cells. Alternatively, induction of RAR by gap junction-mediated bystander effects suggests that multicellular systems comprising densely communicating cells may be capable of responding to long-lasting low-dose-rate priming irradiation. Regulation by endocrine factors is also a plausible mechanism for RAR at an individual level. Emerging evidence suggests that glucocorticoids, known as stress hormones, participate in in vivo RAR induction following long-term low-dose-rate exposure to IR.

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“…Cell proliferation is a basic biological process that occurs continuously in higher organisms in response to changes in their external and internal environments. In the immune system, lymphocyte proliferation is an important parameter indicating the status of the body's defenses [ 1 ]. Recent evidence from both animal and human studies further supports the concept that lymphopenia can drive homeostatic proliferation and the development of autoimmune disease [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

Walterinnesia aegyptia venom combined with silica nanoparticles enhances the functioning of normal lymphocytes through PI3K/AKT, NFkappaB and ERK signaling

et al. 2012

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Background: The toxicity of snake venom varies over time in some species. The venom of newborn and small juvenile snakes appears to be more potent than adults of the same species, and a bite from a snake that has not fed recently, such as one that has just emerged from hibernation, is more dangerous than one that has recently fed due to the larger volume of venom injected. Therefore, the potency of a snake's venom is typically determined using the LD 50 or IC 50 tests. In the present study, we evaluated the anti-tumor potential of snake venom from Walterinnesia aegyptia (WEV) on the human breast carcinoma cell line MDA-MB-231, as well as its effect on the normal mice peripheral blood mononuclear cells (PBMCs).

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Radiation-Induced Change in Lymphocyte Proliferation and its Neuroendocrine Regulation: Dose-Response Relationship and Pathophysiological Implications

Cited by 13 publications

References 20 publications

Sparsely Ionizing Diagnostic and Natural Background Radiations are Likely Preventing Cancer and other Genomic-Instability-Associated Diseases

Sparsely Ionizing Diagnostic and Natural Background Radiations are Likely Preventing Cancer and other Genomic-Instability-Associated Diseases

In vivo radioadaptive response

Walterinnesia aegyptia venom combined with silica nanoparticles enhances the functioning of normal lymphocytes through PI3K/AKT, NFkappaB and ERK signaling

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