Studies on the Mechanisms of Estradiol-Induced Radioprotection

Thompson, John S.; Simmons, Eric L.; Crawford, Margaret K.; Severson, Charles D.

doi:10.2307/3572984

Cited by 16 publications

(7 citation statements)

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“…E3 may encourage the differentiation of certain stem cells in the direction of erythroid series at the expense of their differentiation toward the lymphocyte >opu!ations, as suggested by Batchelor [1968] for testosterone. The stimulating effects of estrogens on erythropoiesis have been re ported by other investigators [Frulmian, 1966;Thompson et al, 1969;Lord and Murphy, 1972].…”

Section: Discussionmentioning

confidence: 86%

Effects of estrogen on the lymphoid regeneration and immune response in irradiated and marrow-reconstituted mice

Kotani

Fujii

Tsuchiya

et al. 1979

Cells Tissues Organs

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Various doses of estriol (E₃) were given to mice intraperitoneally, immediately after lethal irradiation and marrow reconstitution. The assessment of the plaque-forming cell (PFC) response to sheep erythrocytes in the spleen and the histological assessment of lymphoid tissues were carried out 30 days later. The effects appeared to be dose-dependent and resulted in a marked suppression of the PFC response. The depletion of lymphocytes was dramatic and dose-dependent in the thymus, and in the thymus-dependent and in the thymus-indepen-dent areas of the peripheral lymphoid tissues. These results suggest that E₃ acts on the differentiation of stem or precursor cells toward both the populations of T and B lymphocytes. Although E₃, given on day 7 after irradiation and marrow reconstitution, suppressed the lymphoid regeneration and PFC response markedly, E₃ given on day 14 had no effect. On day 7 the majority of regenerating lymphoid tissues were large pyroninophilic cells and on day 14, small lymphocytes. These results suggest that the precursor or immature lymphocytes are sensitive to E₃, while mature lymphocytes are resistant. Lymphoid regeneration and PFC response were retarded in mice irradiated and reconstituted with bone marrow cells from donors pretreated with E₃. These results suggest that E₃ acts on the stem or precursor cells capable to differentiate in the direction of lymphoid populations and reduce their number in the bone marrow.

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Section: Discussionmentioning

confidence: 86%

Effects of estrogen on the lymphoid regeneration and immune response in irradiated and marrow-reconstituted mice

Kotani

Fujii

Tsuchiya

et al. 1979

Cells Tissues Organs

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“…ER␣ Ϫ/Ϫ mice have increased circulating sex steroid levels due to disturbed negative feedback (12). Since sex steroids have been shown to protect HC against irradiation (5,24), all mice were OVX prior to irradiation to prevent unequal protection of HC in WT and ER␣ Ϫ/Ϫ recipients.…”

Section: Generation Of Chimeric Mice With Selective Inactivation Of Ementioning

confidence: 99%

The effect of estrogen on bone requires ERα in nonhematopoietic cells but is enhanced by ERα in hematopoietic cells

Henning¹,

Ohlsson²,

Engdahl³

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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The effects of estrogen on bone are mediated mainly via estrogen receptor (ER)α. ERα in osteoclasts (hematopoietic origin) is involved in the trabecular bone-sparing effects of estrogen, but conflicting data are reported on the role of ERα in osteoblast lineage cells (nonhematopoietic origin) for bone metabolism. Because Cre-mediated cell-specific gene inactivation used in previous studies might be confounded by nonspecific and/or incomplete cell-specific ERα deletion, we herein used an alternative approach to determine the relative importance of ERα in hematopoietic (HC) and nonhematopoietic cells (NHC) for bone mass. Chimeric mice with selective inactivation of ERα in HC or NHC were created by bone marrow transplantations of wild-type (WT) and ERα-knockout (ERα(-/-)) mice. Estradiol treatment increased both trabecular and cortical bone mass in ovariectomized WT/WT (defined as recipient/donor) and WT/ERα(-/-) mice but not in ERα(-/-)/WT or ERα(-/-)/ERα(-/-) mice. However, estradiol effects on both bone compartments were reduced (∼50%) in WT/ERα(-/-) mice compared with WT/WT mice. The effects of estradiol on fat mass and B lymphopoiesis required ERα specifically in NHC and HC, respectively. In conclusion, ERα in NHC is required for the effects of estrogen on both trabecular and cortical bone, but these effects are enhanced by ERα in HC.

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“…DES was subcutaneously injected 24 h before irradiation, a single dose of 5 mg/kg b.w.. 4) Control animals received sesame oil orally or saline for injection, respectively, in the same volume and at the same time as the treated group. Therefore, mice used for this study were divided in five groups: normal nonirradiation control (Group N), sesame oil plus irradiation control (Group O), genistein plus irradiation group (Group G), saline plus irradiation control (Group S), and DES plus irradiation group (Group D).…”

Section: Radiation and Administrationmentioning

confidence: 99%

“…Both the natural estrogens like estradiol and the synthetic estrogens like diethylstilbestrol (DES) exerted radioprotective actions on radiation sickness of experimental animals including improving the survival and accelerating the recovery of hematopoiesis. [3][4][5] Moreover, estrogens also ameliorated hematopoietic suppression induced by caner radiotherapy or chemotherapy in the clinic. 6,7) However, the inherent toxicities of these agents at the radioprotective concentration warranted further search of safer and more effective radioprotectors.…”

Section: Introductionmentioning

confidence: 99%

Genistein Stimulates Hematopoiesis and Increases Survival in Irradiated Mice

Zhou

2005

JRR

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Radiation protection from death and stimulating hematopoietic recovery by oral administrations of genistein, 160 mg/kg b.w., once daily for seven consecutive days before whole-body gamma-rays irradiation, were confirmed by tests with adult male BALB/c mice. Moreover, the protective action of genistein was compared to that of diethylstilbestrol (DES). Based on the studies of survival, behavior of hematograms, endogenous hematopoietic spleen colony formation (endoCFUs), and numbers of nucleated cell, granulocyte-macrophage colony forming units (CFU-GM) in bone marrow following irradiation, it was demonstrated that genistein was an effective radioprotector. The survival of irradiated mice protected by genistein was significantly increased and statistically higher than that of mice pre-treated with DES. Stimulated recovery of leukocytes, erythrocytes, lymphocytes and thrombocytes were observed in mice pre-treated with genistein or DES, however, the effects of genistein on promoting recovery of bone marrow nucleated cells, leukocytes and lymphocytes were significantly higher than those of DES. Enhanced endoCFUs, numbers of bone marrow nucleated cells and CFU-GM were also found in mice pre-treated with genistein as well as DES. Meanwhile, endoCFU numbers in mice pre-treated with genistein was 3.47-fold higher than that in the irradiated control group, although no significant difference was found between genistein administration and DES administration. It could be deduced that the radioprotective action against death is induced by a possible process of enhanced regeneration of the hematopoietic stem cells due to not only strengthened radioresistance and increased numbers of remained hematopoietic cells, but also enhanced post-irradiation repair or promoted proliferation of the hematopoietic stem cells. These effects of genistein may have some therapeutic implications for radiation-induced injuries.

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Studies on the Mechanisms of Estradiol-Induced Radioprotection

Cited by 16 publications

References 0 publications

Effects of estrogen on the lymphoid regeneration and immune response in irradiated and marrow-reconstituted mice

Effects of estrogen on the lymphoid regeneration and immune response in irradiated and marrow-reconstituted mice

The effect of estrogen on bone requires ERα in nonhematopoietic cells but is enhanced by ERα in hematopoietic cells

Genistein Stimulates Hematopoiesis and Increases Survival in Irradiated Mice

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