Relieved residual damage in the hematopoietic system of mice rescued by radiation-induced adaptive response (Yonezawa Effect)

Wang, Bing; Tanaka, Kaoru; Ninomiya, Yasuharu; Maruyama, Kouichi; Varès, Guillaume; Eguchi-Kasai, Kiyomi; Nenoi, Mitsuru

doi:10.1093/jrr/rrs077

Cited by 15 publications

(19 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although the results obtained in this phenomenal study clearly show that dietary fat has a big impact on mouse response to TIB, the underlying mechanisms remain unclear. It is well known that disturbance of hormonal balance, production and secretion of cytokines and growth factors could result in alterations in radiation susceptibility as these intercellular and intracellular messengers play important roles in preserving and restoring functions of tissues compromised by IR [44][45][46][47][48]. As dietary fat plays a critical role in such as physiological development and maintaining metabolic and immune function of the body [33][34][35][36][37], disturbed hormonal level, metabolic environment, and immune functions due to eating an unbalanced diet containing either very high fat or very low fat would be responsible for the altered response of the mice to TBI.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Dietary Modification of Mouse Response to Total-Body-Irradiation

Wang¹,

Tanaka²,

Katsube³

et al. 2015

Evolution of Ionizing Radiation Research

View full text Add to dashboard Cite

Exposure to ionizing radiation (IR) could induce deleterious effects including cancer. Diet, as one of the major factors to influence susceptibility to many diseases, plays a critical role in maintaining human heath. It is known that unbalanced diet could result in health consequences, for example, high-calorie diet could lead to obesity, which could increase the risk of diabetes, heart disease, fatty liver, and some forms of cancer. Although the impact of diet on susceptibility to IR is thought to be big, the evidence is not clear due to lack of study. In this work, effects from dietary fat on modulation of mouse responses to total-body-irradiation (TBI) were studied. The mice were fed after weaning at postnatal age of 4 weeks with a standard diet (MB-1), a very high-fat diet (HFD32), and a very low-fat diet (CE-2 Low Fat), containing of 4.4%, 32.0%, and 0.4% of crude fat, respectively. A mouse model for radiation-induced adaptive response (AR) was applied to this work. The priming low-dose TBI at a dose of 0.5 Gy from X-rays was given at postnatal age of 6 weeks, and the challenge high dose of TBI was given at postnatal age of 8 weeks. The mouse response to low dose of TBI was evaluated by the efficacy of the priming low dose to rescue the animals from bone marrow death induced by the challenge high dose in the 30-day survival test. The mouse response to high dose of TBI was evaluated by comparing the LD50 in the 30day survival test. In addition, dietary modulation of the residual (late) genotoxic effect from TBI was also evaluated by comparing the incidence of micronucleated erythrocytes in bone marrow using micronucleus test. Results showed that for the mice fed with the MB-1, a successful AR was demonstrated. While for the mice fed with either HFD32 or CE-2 Low Fat, no AR was observed, and all the animals died within 15 days after TBI with the challenge high dose at 7.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Micronucleus test: The bone marrow micronucleus test was carried out accordingly [42] with minor modifications [43,44]. Mice were sacrificed the following day after the 30-day survival test.…”

Section: Biological Endpointsmentioning

confidence: 99%

Dietary Modification of Mouse Response to Total-Body-Irradiation

Wang¹,

Tanaka²,

Katsube³

et al. 2015

Evolution of Ionizing Radiation Research

View full text Add to dashboard Cite

show abstract

“…A bone marrow micronucleus test was carried out according to Schmid [42] with minor modifications [43, 44]. Bone marrow smears prepared from both femurs were processed for the enumeration of micronucleated polychromatic erythrocytes (MNPCEs) and micronucleated normochromatic erythrocytes (MNNCEs).…”

Section: Methodsmentioning

confidence: 99%

Sodium orthovanadate (vanadate), a potent mitigator of radiation-induced damage to the hematopoietic system in mice

Wang¹,

Tanaka²,

Morita

et al. 2013

Journal of Radiation Research

View full text Add to dashboard Cite

Previous in vitro and in vivo studies have shown that sodium orthovanadate (vanadate), an inorganic vanadium compound, could effectively suppress radiation-induced p53-mediated apoptosis via both transcription-dependent and transcription-independent pathways. As a potent radiation protector administered at a dose of 20 mg/kg body weight (20 mg/kg) prior to total body irradiation (TBI) by intra-peritoneal (ip) injection, it completely protected mice from hematopoietic syndrome and partially from gastrointestinal syndrome. In the present study, radiation mitigation effects from vanadate were investigated by ip injection of vanadate after TBI in mice. Results showed that a single administration of vanadate at a dose of 20 mg/kg markedly improved the 30-day survival rate and the peripheral blood hemogram, relieved bone marrow aplasia and decreased occurrence of the bone marrow micronucleated erythrocytes in the surviving animals. The dose reduction factor was 1.2 when a single dose of 20 mg/kg was administered 15 min after TBI in mice using the 30-day survival test as the endpoint. Results also showed that either doubling the vanadate dose (40 mg/kg) in a single administration or continuing the vanadate treatment (after a single administration at 20 mg/kg) from the following day at a dose of 5 mg/kg per day for 4 consecutive days further significantly improved the efficacy for rescuing bone marrow failure in the 30-day survival test. Taken together, these findings indicate that vanadate would be a potent mitigator suppressing the acute lethality (hematopoietic syndrome) and minimizing the detrimental effects (anhematopoiesis and delayed genotoxic effects) induced by TBI in mice.

show abstract

“…65 - 68 The mouse RAR model (Yonezawa Effect) is a well-designed system in investigating response of the mice to IR of both low and high doses using endpoints at molecular, cellular and whole body levels. 38 , 69 - 74 There are 2 different phenotypes of RAR in this model involving different mechanisms: the first phenotype could be induced by a low priming dose at 0.30-0.50 Gy leading to radioresistance in blood forming tissues 2 weeks later, and the second phenotype could be induced by a very low priming dose at 0.05-0.10 Gy 2 months later. The model for the first phenotype was used to comparatively study the response in the GFP transgenic mice to TBI with that in their wild type counterparts.…”

Section: Discussionmentioning

confidence: 96%

Altered Response to Total Body Irradiation of C57BL/6-Tg (CAG-EGFP) Mice

et al. 2020

View full text Add to dashboard Cite

Application of green fluorescent protein (GFP) in a variety of biosystems as a unique bioindicator or biomarker has revolutionized biological research and made groundbreaking achievements, while increasing evidence has shown alterations in biological properties and physiological functions of the cells and animals overexpressing transgenic GFP. In this work, response to total body irradiation (TBI) was comparatively studied in GFP transgenic C57BL/6-Tg (CAG-EGFP) mice and C57BL/6 N wild type mice. It was demonstrated that GFP transgenic mice were more sensitive to radiation-induced bone marrow death, and no adaptive response could be induced. In the nucleated bone marrow cells of GFP transgenic mice exposed to a middle dose, there was a significant increase in both the percentage of cells expressing pro-apoptotic gene Bax and apoptotic cell death. While in wild type cells, lower expression of pro-apoptotic gene Bax and higher expression of anti-apoptotic gene Bcl-2, and significant lower induction of apoptosis were observed compared to GFP transgenic cells. Results suggest that presence of GFP could alter response to TBI at whole body, cellular and molecular levels in mice. These findings indicate that there could be a major influence on the interpretation of the results obtained in GFP transgenic mice.

show abstract

Relieved residual damage in the hematopoietic system of mice rescued by radiation-induced adaptive response (Yonezawa Effect)

Cited by 15 publications

References 26 publications

Dietary Modification of Mouse Response to Total-Body-Irradiation

Dietary Modification of Mouse Response to Total-Body-Irradiation

Sodium orthovanadate (vanadate), a potent mitigator of radiation-induced damage to the hematopoietic system in mice

Altered Response to Total Body Irradiation of C57BL/6-Tg (CAG-EGFP) Mice

Contact Info

Product

Resources

About